The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index; none of the 29 sources its claims cite is checked for support yet.
Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity
Open accessAbstract
Visceral adipose tissue (VAT) is an important risk factor for obesity-related metabolic disorders. Therefore, a reduction in VAT has become a key goal in obesity management. However, VAT is correlated with intrahepatic triglyceride (IHTG) content, so it is possible that IHTG, not VAT, is a better marker of metabolic disease. We determined the independent association of IHTG and VAT to metabolic function, by evaluating groups of obese subjects, who differed in IHTG content (high or normal) but matched on VAT volume or differed in VAT volume (high or low) but matched on IHTG content. Stable isotope tracer techniques and the euglycemic–hyperinsulinemic clamp procedure were used to assess insulin sensitivity and very-low-density lipoprotein–triglyceride (VLDL-TG) secretion rate. Tissue biopsies were obtained to evaluate cellular factors involved in ectopic triglyceride accumulation. Hepatic, adipose tissue and muscle insulin sensitivity were 41, 13, and 36% lower ( P < 0.01), whereas VLDL-triglyceride secretion rate was almost double ( P < 0.001), in subjects with higher than normal IHTG content, matched on VAT. No differences in insulin sensitivity or VLDL-TG secretion were observed between subjects with different VAT volumes, matched on IHTG content. Adipose tissue CD36 expression was lower ( P < 0.05), whereas skeletal muscle CD36 expression was higher ( P < 0.05), in subjects with higher than normal IHTG. These data demonstrate that IHTG, not VAT, is a better marker of the metabolic derangements associated with obesity. Furthermore, alterations in tissue fatty acid transport could be involved in the pathogenesis of ectopic triglyceride accumulation by redirecting plasma fatty acid uptake from adipose tissue toward other tissues.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
In obese nondiabetic adults, intrahepatic triglyceride (IHTG) content, rather than visceral adipose tissue (VAT) volume, was independently linked to multiorgan insulin resistance and increased hepatic VLDL-triglyceride secretion. The authors conclude that VAT’s association with metabolic disease may reflect its correlation with IHTG.
Key findings
- When subjects were matched on VAT volume, those with high IHTG had 41%, 13%, and 36% lower hepatic, adipose tissue, and skeletal muscle insulin sensitivity, respectively (P < 0.01), and nearly double the VLDL-TG secretion rate (23 ± 2 vs. 12 ± 1 µmol/min; P < 0.001).
- When subjects were matched on IHTG content, no differences in insulin sensitivity or VLDL-TG secretion were observed between low- and high-VAT groups.
- In multivariate regression including age, sex, BMI, body fat percentage, IHTG, VAT, and subcutaneous abdominal adipose tissue, IHTG was the best predictor of insulin action in liver, skeletal muscle, and adipose tissue and of VLDL-TG secretion, accounting for 21%, 45%, 38%, and 21% of variability, respectively (P ≤ 0.01); VAT was not a predictor of any dependent variable.
- Skeletal muscle CD36 gene expression was almost 3-fold greater with high IHTG (0.82 ± 0.16 vs. 0.34 ± 0.05 AU; P < 0.05), while adipose tissue CD36 gene expression was 35% lower and adipose CD36 protein was 43% lower in the high-IHTG group.
Methods
- A total of 42 obese men and women were screened; 31 participated (mean BMI 35.7 ± 0.8 kg/m²), with 9 subjects assigned to more than one group. Subjects were nondiabetic and had no liver disease other than NAFLD.
- Groups were matched either on VAT volume with normal vs. high IHTG, or on IHTG content with low vs. high VAT. Body composition was assessed by DXA, MRI, and proton magnetic resonance spectroscopy.
- Metabolic function was assessed with stable isotope tracer techniques and a two-stage euglycemic-hyperinsulinemic clamp; VLDL-TG kinetics were measured with glycerol and palmitate tracers. Adipose and muscle biopsies were used for CD36 gene expression and protein analysis. Comparisons used t tests and stepwise linear regression.
Limitations
- The paper states that the data cannot determine whether the IHTG–metabolic dysfunction association is cause-and-effect, and that insulin resistance could be a cause rather than a consequence of IHTG accumulation; other mechanisms for insulin resistance are also noted.
- The authors state they did not measure CD36 gene expression or protein content in the liver, and instead infer likely hepatic CD36 changes from other studies.
- Evident from the text: the sample was small (31 participants, generally 10 per group), and 9 subjects were assigned to more than one group to achieve matching, which may limit generalizability and independence of group comparisons.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
37 Own result · 16 Not checked yet · 13 Own interpretation · 9 Own method
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“VAT was not a predictor of any of the dependent variables.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Predictors of Insulin Sensitivity and VLDL-TG Kinetics.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, abdominal s.c.adipose tissue CD36 gene expression was 35% lower in the high IHTG than in the normal IHTG group (0.09 Ϯ 0.01 and 0.14 Ϯ 0.01 AU; P Ͻ 0.05) (Fig. 3C)”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Muscle and Adipose Tissue Regulation of Fatty Acid Trafficking.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hepatic VLDL-TG secretion rate was almost double in subjects with high than in those with normal IHTG content (23 Ϯ 2 and 12 Ϯ 1 mol/min, respectively; P Ͻ 0.001), when matched on VAT volume (Fig. 2A).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > VLDL-TG Kinetics.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, VLDL-TG secretion rate was not different in subjects with low or high VAT volume, when matched on IHTG content (Fig. 2 A).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > VLDL-TG Kinetics.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Plasma insulin concentration was inversely correlated with adipose tissue CD36 expression (r ϭ 0.56, P Ͻ 0.01)”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Muscle and Adipose Tissue Regulation of Fatty Acid Trafficking.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hepatic, adipose tissue and muscle insulin sensitivity were 41, 13, and 36% lower (P < 0.01), whereas VLDLtriglyceride secretion rate was almost double (P < 0.001), in subjects with higher than normal IHTG content, matched on VAT.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hepatic, adipose tissue and muscle insulin sensitivity were 41, 13, and 36% lower (P < 0.01), whereas VLDLtriglyceride secretion rate was almost double (P < 0.001), in subjects with higher than normal IHTG content, matched on VAT.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Skeletal muscle CD36 gene expression was almost 3-fold greater in subjects with high IHTG than in those with normal IHTG content, matched on VAT volume (0.82 Ϯ 0.16 and 0.34 Ϯ 0.05 arbitrary units; P Ͻ 0.05) (Fig. 3A).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Muscle and Adipose Tissue Regulation of Fatty Acid Trafficking.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and adipose tissue CD36 protein content was 43% lower in subjects with high IHTG than in those with normal IHTG (0.19 Ϯ 0.03 and 0.33 Ϯ 0.05 AU; P Ͻ 0.05) (Fig. 3D).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Muscle and Adipose Tissue Regulation of Fatty Acid Trafficking.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and directly correlated with muscle insoluble CD36 content (r ϭ 0.58, P ϭ 0.02).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Muscle and Adipose Tissue Regulation of Fatty Acid Trafficking.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 10
- Probably not a substantial claim. 9
- The quote only partly states this claim. 7
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“No differences in CD36 adipose tissue gene expression and protein content and in muscle gene expression were detected between subjects with low or high VAT volume, when matched on IHTG content (Fig. 3).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Muscle and Adipose Tissue Regulation of Fatty Acid Trafficking.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“VAT volume (cm 3 ) | 1290 Ϯ 238 | 1335 Ϯ 178 | 766 Ϯ 77 | 1946 Ϯ 319 †”
- Also stated in: § ACKNOWLEDGMENTS. · plain
“† Value is significantly different from the corresponding value in the low VAT groups, P Ͻ 0.01.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > ACKNOWLEDGMENTS.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Also stated in: § ACKNOWLEDGMENTS. · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hepatic (A), skeletal muscle (B), and adipose tissue (C) insulin sensitivity in subjects matched on visceral adipose tissue (VAT) volume with either normal or high intrahepatic triglyceride (IHTG) content and subjects matched on IHTG content who had either low or high VAT volume.”
- Also stated in: § ACKNOWLEDGMENTS. · plain
“*, value is significantly different from the corresponding value in the normal IHTG group, P Ͻ 0.05.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > ACKNOWLEDGMENTS.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § ACKNOWLEDGMENTS. · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hepatic (A), skeletal muscle (B), and adipose tissue (C) insulin sensitivity in subjects matched on visceral adipose tissue (VAT) volume with either normal or high intrahepatic triglyceride (IHTG) content and subjects matched on IHTG content who had either low or high VAT volume.”
- Also stated in: § ACKNOWLEDGMENTS. · plain
“*, value is significantly different from the corresponding value in the normal IHTG group, P Ͻ 0.05.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > ACKNOWLEDGMENTS.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § ACKNOWLEDGMENTS. · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hepatic (A), skeletal muscle (B), and adipose tissue (C) insulin sensitivity in subjects matched on visceral adipose tissue (VAT) volume with either normal or high intrahepatic triglyceride (IHTG) content and subjects matched on IHTG content who had either low or high VAT volume.”
- Also stated in: § ACKNOWLEDGMENTS. · plain
“*, value is significantly different from the corresponding value in the normal IHTG group, P Ͻ 0.05.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > ACKNOWLEDGMENTS.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § ACKNOWLEDGMENTS. · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Skeletal muscle (A) and s.c.abdominal adipose tissue (C) CD36 gene expression and skeletal muscle (B) and adipose tissue CD36 protein content (D) in subjects matched on visceral adipose tissue (VAT) volume with either normal or high intrahepatic triglyceride (IHTG) content and in subjects matched on IHTG content who had either low or high VAT volume.”
- Also stated in: § ACKNOWLEDGMENTS. · plain
“*, value is significantly different from corresponding value in the normal IHTG group, P Ͻ 0.05.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > ACKNOWLEDGMENTS.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § ACKNOWLEDGMENTS. · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Skeletal muscle (A) and s.c.abdominal adipose tissue (C) CD36 gene expression and skeletal muscle (B) and adipose tissue CD36 protein content (D) in subjects matched on visceral adipose tissue (VAT) volume with either normal or high intrahepatic triglyceride (IHTG) content and in subjects matched on IHTG content who had either low or high VAT volume.”
- Also stated in: § ACKNOWLEDGMENTS. · plain
“*, value is significantly different from corresponding value in the normal IHTG group, P Ͻ 0.05.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > ACKNOWLEDGMENTS.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § ACKNOWLEDGMENTS. · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Skeletal muscle (A) and s.c.abdominal adipose tissue (C) CD36 gene expression and skeletal muscle (B) and adipose tissue CD36 protein content (D) in subjects matched on visceral adipose tissue (VAT) volume with either normal or high intrahepatic triglyceride (IHTG) content and in subjects matched on IHTG content who had either low or high VAT volume.”
- Also stated in: § ACKNOWLEDGMENTS. · plain
“*, value is significantly different from corresponding value in the normal IHTG group, P Ͻ 0.05.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > ACKNOWLEDGMENTS.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § ACKNOWLEDGMENTS. · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Skeletal muscle (A) and s.c.abdominal adipose tissue (C) CD36 gene expression and skeletal muscle (B) and adipose tissue CD36 protein content (D) in subjects matched on visceral adipose tissue (VAT) volume with either normal or high intrahepatic triglyceride (IHTG) content and in subjects matched on IHTG content who had either low or high VAT volume.”
- Also stated in: § ACKNOWLEDGMENTS. · plain
“*, value is significantly different from corresponding value in the normal IHTG group, P Ͻ 0.05.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > ACKNOWLEDGMENTS.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- Also stated in: § ACKNOWLEDGMENTS. · plain
In the paper
“The importance of CD36 in FFA transport and ectopic triglyceride accumulation has been demonstrated by observations in human subjects indicating that increased skeletal muscle plasmalemma CD36 content is associated with increased muscle FFA uptake and intramyocellular triglyceride accumulation (25).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Discussion
What the sources say
- Not checked yetcites [25] source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Subjects in each group were matched on age, sex, body mass index (BMI), and percentage of body fat, but differed in either IHTG content or VAT volume (Table 1).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Body Composition.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, it is possible that excessive IHTG is not only a marker of metabolic dysfunction, but also contributes to the increase in VLDL-TG secretion rate and plasma triglyceride concentration observed in obese persons with NAFLD.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The mechanism(s) responsible for the interrelationship among IHTG content, insulin resistance, and hypertriglyceridemia is not known.
None of the sources cited for this claim have been checked yet.
In the paper
“Adiponectin administration decreases IHTG (35), increases hepatic insulin sensitivity (36), and reverses obesity-related skeletal muscle insulin resistance (37).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Discussion
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“data from metabolic studies conducted on human subjects (3,4) indicate that an increase in VAT is associated with impaired glucose tolerance, insulin resistance, and increased very-low-density lipoproteintriglyceride (VLDL-TG) secretion.”
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These data demonstrate that IHTG content, not VAT volume, is a marker of obesity-related metabolic dysfunction.”
- Also stated in: § Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity · boosted
“These data demonstrate that IHTG, not VAT, is a better marker of the metabolic derangements associated with obesity.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Discussion
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: A causal link between VAT and metabolic dysfunction has not been demonstrated in humans.
- Also stated in: § Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity · boosted
In the paper
“In addition, fatty acids released from lipolysis of IHTG might stimulate hepatic VLDL-TG production, demonstrating that IHTG in itself could be directly involved in the pathogenesis of dyslipidemia associated with NAFLD (11).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Discussion
What the sources say
- Not checked yetcites [11] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The mechanism(s) responsible for the interrelationship among IHTG content, insulin resistance, and hypertriglyceridemia is not known.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, increased IHTG is an independent indicator of multiorgan insulin resistance and increased hepatic secretion of VLDL-TG.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Discussion
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Each subject with normal IHTG and a given VAT volume was matched with a subject from the high IHTG group on VAT (within Ϸ20% of VAT volume of the normal IHTG group).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Subjects.
plainSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We did not have knowledge of any outcome measures when the matches were performed.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Subjects.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Isotopic steady-state conditions were achieved during the final 30 min of the basal period and stages 1 and 2 of the clamp procedure, so Steele's equation for steady-state conditions was used to calculate substrate kinetics (49).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Calculations.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Subjects within groups were matched on age, sex, BMI, and percentage of body fat.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Subjects.
plainn = 31- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, the majority of adipokines in the portal vein are derived from s.c.fat, which releases adipokines into the systemic circulation that enter the portal vein through the splanchnic bed.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All data sets were normally distributed according to the Kolmogorov-Smirnov test, so comparisons between subjects within each group-ing (i.e., between subjects who had the same VAT volume but either normal or high IHTG content and subjects who had the same IHTG content but different VAT volume) were performed by using parametric procedures.”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Statistical Analyses.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Group 2 subjects (n ϭ 20) were matched on IHTG content and had either low (n ϭ 10) or high (n ϭ 10) VAT volume (Table 1).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Subjects.
plainn = 2- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“In fact, only Ϸ20% of portal vein FFA delivered to the liver and 14% of systemic FFA delivered to skeletal muscle are derived from lipolysis of VAT in obese subjects (20,21).”
§ Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity > Discussion
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
A causal link between VAT and metabolic dysfunction has not been demonstrated in humans.
“Although VAT is associated with metabolic disease, a causal link between VAT and metabolic dysfunction has not been demonstrated in humans.”
The paper relies on this without support.
The mechanism(s) responsible for the interrelationship among IHTG content, insulin resistance, and hypertriglyceridemia is not known.
“The mechanism(s) responsible for the interrelationship among IHTG content, insulin resistance, and hypertriglyceridemia is not known, but could involve redirecting plasma FFA uptake and intracellular triglyceride production from adipose tissue depots to other tissues, such as liver and skeletal muscle, which can impair insulin signaling (13,14) and stimulate VLDL-TG secretion (11).”
The paper relies on this without support.
The mechanism responsible for excessive triglyceride accumulation in nonadipose tissues (i.e., ectopic fat) is not known.
“The mechanism responsible for excessive triglyceride accumulation in nonadipose tissues (i.e., ectopic fat) is not known.”
The paper relies on this without support.
The mechanism responsible for differences in tissue CD36 content is not known.
“The mechanism responsible for differences in tissue CD36 content is not known, but could be related to circulating insulin, because plasma insulin concentration was inversely correlated with adipose tissue CD36 expression and directly correlated with muscle insoluble CD36 content in our subjects.”
The paper relies on this without support.
It is not known whether IHTG or VAT is independently associated with metabolic risk.
“However, it is not known whether IHTG or VAT is independently associated with metabolic risk because both are strongly correlated with each other (8-10).”
The authors state this as an assumption.
Glucose rate of disappearance from plasma was equal to glucose rate of appearance during basal conditions.
“It was assumed that glucose rate of disappearance (Rd) from plasma was equal to glucose rate of appearance (Ra) during basal conditions”
The authors state this as an assumption.
During the clamp procedure, glucose rate of disappearance was equal to the sum of endogenous glucose rate of appearance and the rate of infused glucose.
“during the clamp procedure glucose Rd was assumed to be equal to the sum of endogenous glucose Ra and the rate of infused glucose.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Fabbrini and colleagues91 similarly reported that intrahepatic triglyceride content, not visceral adiposity, was associated with insulin resistance and increased triglyceride secretion.”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [91]
Citations
Cites
Matsuda, M., & DeFronzo, R. A. (1999) · Diabetes Care · doi:10.2337/diacare.22.9.1462 · Cited by 5,621
Yamauchi, T., Kamon, J., Waki, H., Terauchi, Y., Kubota, N., Hara, K., Mori, Y., Ide, T., Murakami, K., Tsuboyama-Kasaoka, N., et al. (2001) · Nature Medicine · doi:10.1038/90984 · Cited by 4,915
Abdominal obesity and metabolic syndrome
Després, J.-P., & Lemieux, I. (2006) · Nature · doi:10.1038/nature05488 · Cited by 4,354
Donnelly, K. L., Smith, C. I., Schwarzenberg, S. J., Jessurun, J., Boldt, M. D., & Parks, E. J. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23621 · Cited by 3,604
Cellular mechanisms of insulin resistance
Shulman, G. I. (2000) · Journal of Clinical Investigation · doi:10.1172/jci10583 · Cited by 2,714
Nonalcoholic Fatty Liver Disease
Marchesini, G., Brizi, M., Bianchi, G., Tomassetti, S., Bugianesi, E., Lenzi, M., McCullough, A. J., Natale, S., Forlani, G., & Melchionda, N. (2001) · Diabetes · doi:10.2337/diabetes.50.8.1844 · Cited by 2,581
The adipocyte-secreted protein Acrp30 enhances hepatic insulin action
Berg, A. H., Combs, T. P., Du, X., Brownlee, M., & Scherer, P. E. (2001) · Nature Medicine · doi:10.1038/90992 · Cited by 2,526
A placebo-controlled trial of pioglitazone in subjects with nonalcoholic steatohepatitis
Belfort, R., Harrison, S. A., Brown, K., Darland, C., Finch, J., Hardies, J., Balas, B., Gastaldelli, A., Tio, F., Pulcini, J., et al. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa060326 · Cited by 1,827
Molecular mediators of hepatic steatosis and liver injury
Browning, J. D., & Horton, J. D. (2004) · Journal of Clinical Investigation · doi:10.1172/jci200422422 · Cited by 1,772
INFLUENCES OF GLUCOSE LOADING AND OF INJECTED INSULIN ON HEPATIC GLUCOSE OUTPUT*
Steele, R. D. (1959) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1959.tb44923.x · Cited by 1,680
Cited by
Sorted by citations
Items 401–500 of 969
Wang, D. Q. ‐., Portincasa, P., & Neuschwander‐Tetri, B. A. (2013) · Comprehensive physiology · doi:10.1002/cphy.c130001 · Cited by 41
Carli, F., Sabatini, S., Gaggini, M., Sironi, A. M., Bedogni, G., & Gastaldelli, A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241914651 · Cited by 37
Al‐Dwairi, A., Brown, A. R., Pabona, J. M. P., Van, T. H., Hamdan, H., Mercado, C. P., Quick, C. M., Wight, P. A., Simmen, R. C. M., & Simmen, F. A. (2014) · PLoS ONE · doi:10.1371/journal.pone.0113058 · Cited by 38
Driuchina, A., Hintikka, J. E., Lehtonen, M., Keski‐Rahkonen, P., O’Connell, T. M., Juvonen, R. O., Kuula, J., Hakkarainen, A., Laukkanen, J. A., Mäkinen, E., et al. (2023) · mBio · doi:10.1128/mbio.02663-22 · Cited by 39
Smith, G. I., Reeds, D. N., Okunade, A. L., Patterson, B. W., & Mittendorfer, B. (2014) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2013-4470 · Cited by 37
Self-citationKrüppel-like factor 2 promotes liver steatosis through upregulation of CD36
Chen, J., Lu, X., Zou, K., & Ye, K. (2013) · Journal of Lipid Research · doi:10.1194/jlr.m039453 · Cited by 37
Fabbrini, E., Magkos, F., Conte, C., Mittendorfer, B., Patterson, B. W., Okunade, A. L., & Klein, S. (2011) · Journal of Lipid Research · doi:10.1194/jlr.d020321 · Cited by 37
Self-citationLi, L., Zhang, Y., Luo, Y., Meng, X., Pan, G., Zhang, H., Li, Y., & Zhang, B. (2023) · Drug Design Development and Therapy · doi:10.2147/dddt.s399423 · Cited by 36
Magkos, F., Fabbrini, E., Korenblat, K., Okunade, A. L., Patterson, B. W., & Klein, S. J. (2010) · International Journal of Obesity · doi:10.1038/ijo.2010.265 · Cited by 38
Self-citationLi, Y., Yang, M., Lin, H., Yan, W., Deng, G., Ye, H., Shi, H., Wu, C., Ma, G., Xu, S., et al. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.801730 · Cited by 36
Obesity-Related Insulin Resistance: The Central Role of Adipose Tissue Dysfunction
Mocciaro, G., & Gastaldelli, A. (2022) · Handbook of experimental pharmacology · doi:10.1007/164_2021_573 · Cited by 37
Visceral obesity modulates the impact of apolipoprotein C3 gene variants on liver fat content
Peter, A., Kantartzis, K., Machicao, F. E., Machann, J., Wagner, S., Templin, S., Königsrainer, I., Königsrainer, A., Schick, F., Fritsche, A., et al. (2011) · International Journal of Obesity · doi:10.1038/ijo.2011.154 · Cited by 37
Hunt, S. C., Davidson, L. E., Adams, T. D., Ranson, L., McKinlay, R. D., Simper, S. C., & Litwin, S. E. (2021) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2020.0008 · Cited by 35
Desmarchelier, C., Ludwig, T., Scheundel, R., Rink, N., Bader, B., Klingenspor, M., & Daniel, H. (2012) · British Journal Of Nutrition · doi:10.1017/s0007114512003340 · Cited by 35
Type 2 Diabetes is a Delayed Late Effect of Whole-Body Irradiation in Nonhuman Primates
Kavanagh, K., Dendinger, M. D., Davis, A., Register, T. C., DeBo, R. J., Dugan, G. O., & Cline, J. M. (2015) · Radiation Research · doi:10.1667/rr13916.1 · Cited by 35
Liu, Y., Liu, F., Guan, Z., Dong, F., Cheng, J., Gao, Y., Li, D., Yan, J., Liu, C.-H., Han, D., et al. (2018) · Nature Microbiology · doi:10.1038/s41564-018-0146-2 · Cited by 34
Hepatokines as a Molecular Transducer of Exercise
Seo, D. Y., Park, S.-H., Marquez, J. C., Kwak, H., Kim, T. N., Bae, J. H., Koh, J., & Han, J. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10030385 · Cited by 37
Kinetic studies to investigate lipoprotein metabolism
Borén, J., Taskinen, M., & Adiels, M. (2011) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2011.02497.x · Cited by 37
Sugizaki, T., 渡辺, 光., Horai, Y., Kaneko-Iwasaki, N., Arita, E., Miyazaki, T., Morimoto, K., Honda, A., Irie, J., & Itoh, H. (2014) · Endocrinology · doi:10.1210/en.2013-2143 · Cited by 35
Dhurandhar, E. J., Krishnapuram, R., Hegde, V. K., Dubuisson, O. S., Tao, R., Dong, X. C., Ye, J., & Dhurandhar, N. V. (2012) · PLoS ONE · doi:10.1371/journal.pone.0047813 · Cited by 35
Lee, Y., & Friedman, S. L. (2010) · Progress in molecular biology and translational science · doi:10.1016/b978-0-12-385233-5.00006-4 · Cited by 37
Gale, C., Thomas, E. L., Jeffries, S., Durighel, G., Logan, K., Parkinson, J. R. C., Uthaya, S. N., Santhakumaran, S., Bell, J. D., & Modi, N. (2014) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.113.080200 · Cited by 34
Influence of Liver Triglycerides on Suppression of Glucose Production by Insulin in Men
Jin, E. S., Szuszkiewicz-Garcia, M., Browning, J. D., Baxter, J. D., Abate, N. I., & Malloy, C. R. (2014) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2014-2404 · Cited by 34
Chen, M., Liu, B., Wilkinson, D. C., Hutchison, A. T., Thompson, C. H., Wittert, G., & Heilbronn, L. K. (2016) · Obesity Research & Clinical Practice · doi:10.1016/j.orcp.2016.07.004 · Cited by 34
Circulating sCD36 levels in patients with non-alcoholic fatty liver disease and controls
Heebøll, S., Poulsen, M. K., Ørnstrup, M. J., Kjær, T. N., Pedersen, S. B., Nielsen, S., Grønbæk, H., & Handberg, A. (2016) · International Journal of Obesity · doi:10.1038/ijo.2016.223 · Cited by 34
Hepatic Steatosis Is Associated With Adverse Molecular Signatures in Subjects Without Diabetes
Pietzner, M., Budde, K., Homuth, G., Kastenmüller, G., Henning, A., Artati, A., Krumsiek, J., Völzke, H., Adamski, J., Lerch, M. M., et al. (2018) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2018-00999 · Cited by 32
Wang, X., Smith, G. I., Patterson, B. W., Reeds, D. N., Kampelman, J., Magkos, F., & Mittendorfer, B. (2012) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00533.2011 · Cited by 34
Self-citationWhen GLP-1 hits the liver: a novel approach for insulin resistance and NASH
Kim, Y. O., & Schuppan, D. (2012) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00078.2012 · Cited by 34
Azrad, M., Gower, B. A., Hunter, G. R., & Nagy, T. R. (2012) · Obesity · doi:10.1038/oby.2011.375 · Cited by 33
Zhang, S., Ren, X., Zhang, B., Lan, T., & Liu, B. (2024) · Molecules · doi:10.3390/molecules29081859 · Cited by 37
DNA methylation and hepatic insulin resistance and steatosis
Sookoian, S. C., & Pirola, C. J. (2012) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/mco.0b013e3283546f9f · Cited by 33
Gastrointestinal metabolic surgery for the treatment of type 2 diabetes mellitus
Pok, E.-H. (2014) · World Journal of Gastroenterology · doi:10.3748/wjg.v20.i39.14315 · Cited by 35
Hessvik, N. P., Bakke, S. S., Smith, R. L., Ravna, A. W., Sylte, I., Rustan, A. C., Thoresen, G. H., & Kase, E. T. (2011) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2011.10.006 · Cited by 34
Clinical and molecular evidence of accelerated ageing following very preterm birth
Parkinson, J. R. C., Emsley, R., Tarry‐Adkins, J. L., Longford, N., Ozanne, S. E., Holmes, E. C., & Modi, N. (2019) · Pediatric Research · doi:10.1038/s41390-019-0709-9 · Cited by 32
Visceral Adipose Tissue and Non-alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes
Nobarani, S., Alaei-Shahmiri, F., Aghili, R., Malek, M., Poustchi, H., Lahouti, M., & Khamseh, M. E. (2021) · Digestive Diseases and Sciences · doi:10.1007/s10620-021-06953-z · Cited by 35
Genetic variation in human carboxylesterase CES1 confers resistance to hepatic steatosis
Lian, J., Bahitham, W., Panigrahi, R., Nelson, R., Li, L., Watts, R., Thiesen, A., Lemieux, M. J., & Lehner, R. S. (2018) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2018.04.002 · Cited by 33
Kayser, B. D., Goran, M. I., & Bouret, S. G. (2015) · PLoS ONE · doi:10.1371/journal.pone.0121954 · Cited by 35
Wang, N., Qin, L., Han, B., Chen, Y., Zhu, C., Chen, Y., Xia, F., Lu, M., Meng, Y., Guo, Y., et al. (2015) · Journal of Gastroenterology and Hepatology · doi:10.1111/jgh.13271 · Cited by 32
Baek, S. H., Kim, M., Kim, M., Kang, M., Yoo, H. J., Lee, N. H., Kim, Y. H., Song, M., & Lee, J. H. (2016) · Obesity · doi:10.1002/oby.21724 · Cited by 32
Zhong, X., Hu, P., Armstrong, T., Li, X., Lee, Y., Tsao, T., Nickel, D. M., Kannengießer, S., Dale, B. M., Deshpande, V. S., et al. (2020) · Journal of Magnetic Resonance Imaging · doi:10.1002/jmri.27205 · Cited by 35
Nonalcoholic fatty liver disease and colorectal cancer: Correlation and missing links
Chakraborty, D., & Wang, J. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.118507 · Cited by 33
Schwarz, J., Clearfield, M. B., & Mulligan, K. M. (2017) · Journal of Osteopathic Medicine · doi:10.7556/jaoa.2017.102 · Cited by 33
Dissociation between fatty liver and insulin resistance: the role of adipose triacylglycerol lipase
Stefan, N., Staiger, H., & Häring, H. (2010) · Diabetologia · doi:10.1007/s00125-010-1938-y · Cited by 34
Metabolic dysfunction following weight cycling in male mice
Schofield, S. E., Parkinson, J. R. C., Henley, A. B., Sahuri-Arisoylu, M., Sanchez-Canon, G. J., & Bell, J. D. (2016) · International Journal of Obesity · doi:10.1038/ijo.2016.193 · Cited by 31
Depot-specific adipocyte-extracellular matrix metabolic crosstalk in murine obesity
Strieder‐Barboza, C., Baker, N. A., Flesher, C. G., Karmakar, M., Patel, A., Lumeng, C. N.-K., & O’Rourke, R. W. (2020) · Adipocyte · doi:10.1080/21623945.2020.1749500 · Cited by 31
Khalafi, M., & Symonds, M. E. (2021) · Physiology & Behavior · doi:10.1016/j.physbeh.2021.113416 · Cited by 32
Insulin resistance, adipose depots and gut: Interactions and pathological implications
Gastaldelli, A., Natali, A., Vettor, R., & Corradini, S. G. (2010) · Digestive and Liver Disease · doi:10.1016/j.dld.2010.01.013 · Cited by 32
High Fat Diet-Induced Changes in Hepatic Protein Abundance in Mice
Luo, M., Mengos, A. E., Stubblefield, T. M., & Mandarino, L. J. (2012) · Journal of Proteomics & Bioinformatics · doi:10.4172/jpb.1000214 · Cited by 31
Comparison of NAFLD, MAFLD, and MASLD Prevalence and Clinical Characteristics in Asia Adults
Huang, X., Yu, R., Tan, X., Guo, M., Xia, Y., Zou, H., Liu, X., & Qin, C. (2024) · Journal of Clinical and Experimental Hepatology · doi:10.1016/j.jceh.2024.102420 · Cited by 30
Roux-en-Y Gastric Bypass Surgery Has Unique Effects on Postprandial FGF21 but Not FGF19 Secretion
Harris, L.-A. L. S., Smith, G. I., Mittendorfer, B., Eagon, J. C., Okunade, A. L., Patterson, B. W., & Klein, S. (2017) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2017-01295 · Cited by 32
Self-citationMRI measurement of liver fat content predicts the metabolic syndrome
Ducluzeau, P., Boursier, J., Bertrais, S., Dubois, S. G., Gauthier, A., Rohmer, V., Gagnadoux, F., Lefthériotis, G., Calès, P., Andriantsitohaina, R., et al. (2013) · Diabetes & Metabolism · doi:10.1016/j.diabet.2013.01.007 · Cited by 30
Fu, J., Ma, S., Li, X., An, S., Li, T., Guo, K., Lin, M., Qu, W., Wang, S., Dong, X., et al. (2015) · International Journal of Biological Sciences · doi:10.7150/ijbs.13062 · Cited by 31
Alderete, T. L., Toledo‐Corral, C. M., Desai, P., Weigensberg, M. J., & Goran, M. I. (2013) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2013-1138 · Cited by 30
β‐cell differentiation status in type 2 diabetes
Jeffery, N. M., & Harries, L. W. (2016) · Diabetes Obesity and Metabolism · doi:10.1111/dom.12778 · Cited by 30
Na, H.-N., Dubuisson, O. S., Hegde, V. K., Nam, J., & Dhurandhar, N. V. (2014) · Biochimie · doi:10.1016/j.biochi.2014.11.005 · Cited by 29
Ma, J., Karlsen, M. C., Chung, M., Jacques, P. F., Saltzman, E., Smith, C. E., Fox, C. S., & McKeown, N. M. (2016) · Nutrition Reviews · doi:10.1093/nutrit/nuv047 · Cited by 28
Early menarche and its consequence in Korean female: reducing fructose intake could be one solution
Kim, J. H., & Lim, J. S. (2020) · Korean Journal of Pediatrics · doi:10.3345/cep.2019.00353 · Cited by 30
Hu, T., Lin, M., Zhang, D., Li, M., & Zhang, J. (2018) · Analytical and Bioanalytical Chemistry · doi:10.1007/s00216-018-1350-x · Cited by 28
Kadowaki, S., Tamura, Y., Someya, Y., Takeno, K., Kaga, H., Sugimoto, D., Kakehi, S., Funayama, T., Furukawa, Y., Suzuki, R., et al. (2019) · Journal of the Endocrine Society · doi:10.1210/js.2019-00052 · Cited by 28
Visceral fat and arterial stiffness in youth with healthy weight, obesity, and type 2 diabetes
Higgins, S., Zemel, B. S., Khoury, P. R., Urbina, E. M., & Kindler, J. M. (2021) · Pediatric Obesity · doi:10.1111/ijpo.12865 · Cited by 29
Winn, N. C., Cottam, M. A., Bhanot, M., Caslin, H. L., Garcia, J. N., Drigo, R. A. E., & Hasty, A. H. (2022) · Diabetes · doi:10.2337/db22-0161 · Cited by 30
Liver fat as risk factor of hepatic and cardiometabolic diseases
Demir, M., Bornstein, S. R., Mantzoros, C. S., & Perakakis, N. (2023) · Obesity Reviews · doi:10.1111/obr.13612 · Cited by 31
Silbernagel, G., Lütjohann, D., Machann, J., Meichsner, S., Kantartzis, K., Schick, F., Häring, H., Stefan, N., & Fritsche, A. (2011) · Experimental Diabetes Research · doi:10.1155/2012/361863 · Cited by 30
The Interactions of Nonalcoholic Fatty Liver Disease and Cardiovascular Diseases
Perazzo, H., Poynard, T., & Dufour, J. (2013) · Clinics in Liver Disease · doi:10.1016/j.cld.2013.09.014 · Cited by 28
Lorenzo, C., Hanley, A. J., Rewers, M., & Haffner, S. M. (2013) · Diabetologia · doi:10.1007/s00125-012-2826-4 · Cited by 28
Lawrence, J. C., Newcomer, B. R., Buchthal, S. D., Sirikul, B., Oster, R. A., Hunter, G. R., & Gower, B. A. (2010) · Obesity · doi:10.1038/oby.2010.148 · Cited by 29
Piché, M., Vasan, S. K., Hodson, L., & Karpe, F. (2018) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000522 · Cited by 30
Sinaiko, A. R., & Caprio, S. (2012) · The Journal of Pediatrics · doi:10.1016/j.jpeds.2012.01.012 · Cited by 28
Measuring Visceral and Hepatic Fat in Clinical Practice and Clinical Research
Naboush, A., & Hamdy, O. (2013) · Endocrine Practice · doi:10.4158/ep12331.or · Cited by 27
Nobili, V., Bedogni, G., Canani, R. B., Brambilla, P., Cianfarani, S., Pietrobelli, A., & Agostoni, C. V. (2012) · Pediatric Obesity · doi:10.1111/j.2047-6310.2012.00089.x · Cited by 27
Pattern and profile of chronic liver disease in acute on chronic liver failure
Abbas, Z., & Shazi, L. (2015) · Hepatology International · doi:10.1007/s12072-015-9627-z · Cited by 27
Obesity, Metabolic Syndrome and Disorders of Energy Balance
Han, J. C., & Weiss, R. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-62520-3.00024-5 · Cited by 27
Cao, C., Koh, H. E., van Vliet, S., Patterson, B. W., Reeds, D. N., Laforest, R. A., Gropler, R. J., & Mittendorfer, B. (2022) · Metabolism · doi:10.1016/j.metabol.2022.155216 · Cited by 27
Self-citationWicklow, B. A., Wittmeier, K. D. M., Jong, G. W. ‘., McGavock, J., Robert, M., Duhamel, T. A., & Dolinsky, V. W. (2015) · Biochemistry and Cell Biology · doi:10.1139/bcb-2014-0136 · Cited by 27
Lee, Y., Shin, H., Vassy, J. L., Kim, J. T., Cho, S., Kang, S. M., Choi, S. H., Kim, K. W., Park, K. S., Jang, H. C., et al. (2012) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2012.07.013 · Cited by 27
Gianotti, T. F., Burgueño, A. L., Mansilla, N. G., Pirola, C. J., & Sookoian, S. (2013) · PLoS ONE · doi:10.1371/journal.pone.0076912 · Cited by 27
Hamley, S., Kloosterman, D., Duthie, T., Man, C. D., VISENTIN, R., Mason, S. A., Ang, T., Selathurai, A., Kaur, G., Morales-Scholz, M. G., et al. (2019) · Diabetologia · doi:10.1007/s00125-019-04990-y · Cited by 30
Machann, J., Stefan, N., Wagner, R. J., Fritsche, A., Bell, J. D., Whitcher, B. J., Häring, H., Birkenfeld, A. L., Nikolaou, K., Schick, F., et al. (2020) · Nutrients · doi:10.3390/nu12072064 · Cited by 27
Magkos, F., Bradley, D. P., Eagon, J. C., Patterson, B. W., & Klein, S. (2015) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.115.116111 · Cited by 28
Self-citationMicroRNA Expression Relating to Dietary-Induced Liver Steatosis and NASH
Zarfeshani, A., Ngo, S., & Sheppard, A. M. (2015) · Journal of Clinical Medicine · doi:10.3390/jcm4111938 · Cited by 26
Pushpakom, S. P., Kolamunnage‐Dona, R., Taylor, C., Foster, T., Spowart, C., García‐Fiñana, M., Kemp, G. J., Jaki, T., Khoo, S., Williamson, P. R., et al. (2019) · Clinical Infectious Diseases · doi:10.1093/cid/ciz589 · Cited by 26
Pregnancy and Metabolic-associated Fatty Liver Disease: A Clinical Update
Fouda, S., Vennikandam, M. M., Pappachan, J. M., & Fernandez, C. J. (2022) · Journal of Clinical and Translational Hepatology · doi:10.14218/jcth.2022.00052 · Cited by 27
Park, H. K., Hwang, J. S., Moon, J. S., Lee, J. A., Kim, D. H., & Lim, J. S. (2013) · Journal of Pediatric Gastroenterology and Nutrition · doi:10.1097/mpg.0b013e31828b4e67 · Cited by 27
Fatty liver disease in obese children – relation to other metabolic risk factors
Volovelsky, O., & Weiss, R. (2011) · International Journal of Pediatric Obesity · doi:10.3109/17477166.2011.583661 · Cited by 26
Bello, O., Mohandas, C., Shojaee‐Moradie, F., Jackson, N., Hakim, O., Alberti, K. G. M. M., Peacock, J. L., Umpleby, A. M., Amiel, S. A., & Goff, L. M. (2019) · Diabetologia · doi:10.1007/s00125-019-4820-6 · Cited by 27
Adipose Tissue CTGF Expression is Associated with Adiposity and Insulin Resistance in Humans
Yoshino, J., Patterson, B. W., & Klein, S. (2019) · Obesity · doi:10.1002/oby.22463 · Cited by 29
Self-citationAt the Crossroads of Health and Disease: Consequences of Fat in the Liver
Dukewich, M., Yuan, L., & Terrault, N. A. (2025) · Annual Review of Physiology · doi:10.1146/annurev-physiol-022724-105515 · Cited by 35
Cioffi, C. E., Narayan, K. M. V., Liu, K., Uppal, K., Jones, D. P., Tran, V., Yu, T., Alvarez, J. A., Bellissimo, M. P., Maner-Smith, K. M., et al. (2020) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2019-001126 · Cited by 28
Gagnon, É., Pelletier, W., Gobeil, É., Bourgault, J., Manikpurage, H. D., Maltais‐Payette, I., Abner, E., Taba, N., Esko, T., Mitchell, P. L., et al. (2022) · Communications Medicine · doi:10.1038/s43856-022-00196-3 · Cited by 25
Anti-Angiogenic Effects of Natural Compounds in Diet-Associated Hepatic Inflammation
Novi, S., Vestuto, V., Campiglia, P., Tecce, N., Bertamino, A., & Tecce, M. F. (2023) · Nutrients · doi:10.3390/nu15122748 · Cited by 26
Metabolic Surgery for Type 2 Diabetes with BMI <35 kg/m2
Lebovitz, H. E. (2013) · Obesity Surgery · doi:10.1007/s11695-013-0907-1 · Cited by 26
Sarmiento-Ortega, V. E., Brambila, E., Flores-Hernández, J. Á., Díaz, A., Peña‐Rosas, U., Moroni-González, D., Aburto-Luna, V., & Treviño, S. (2018) · Toxics · doi:10.3390/toxics6030055 · Cited by 25
Simões, I. C. M., Janikiewicz, J., Bauer, J., Karkucińska‐Więckowska, A., Kalinowski, P., Dobrzyń, A., Wolski, A., Pronicki, M., Zieniewicz, K., Dobrzyń, P., et al. (2019) · Nutrients · doi:10.3390/nu11122871 · Cited by 27
Carbone, F., Mach, F., Pontremoli, R., Viazzi, F. C., & Montecucco, F. (2013) · Thrombosis and Haemostasis · doi:10.1160/th13-06-0499 · Cited by 25
Drummen, M., Dorenbos, E., Vreugdenhil, A. C. E., Raben, A., Fogelholm, M., Westerterp‐Plantenga, M. S., & Adam, T. C. (2018) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00162.2018 · Cited by 26
Liu, C., Jiang, W., Zeng, Q., Wu, D., Li, H., Zhou, L., Bai, L., & Tang, H. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24021297 · Cited by 24
Innate Immune System in the Pathogenesis of Non-Alcoholic Fatty Liver Disease
Ma, D. W., Ha, J., Yoon, K., Kang, I., Choi, T. G., & Kim, S. S. (2023) · Nutrients · doi:10.3390/nu15092068 · Cited by 26
Davis, J. E., Cain, J., Banz, W. J., & Peterson, R. G. (2013) · ISRN Obesity · doi:10.1155/2013/584547 · Cited by 25
Yang, Z., Inoue, S., Taniguchi, Y., Miyahara, H., Iwasaki, Y., Takeo, J., Sakaue, H., & Nakaya, Y. (2015) · Lipids in Health and Disease · doi:10.1186/s12944-015-0161-8 · Cited by 24
Pourhassan, M., Glüer, C.-C., Pick, P., Tigges, W. P., & Müller, M. J. (2016) · European Journal of Clinical Nutrition · doi:10.1038/ejcn.2016.189 · Cited by 26
Metadata
- Authors
- Fabbrini, E., Magkos, F., Mohammed, B. S., Pietka, T., Abumrad, N. A., Patterson, B. W., Okunade, A., & Klein, S.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Klein, Samuel
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2009-09-08
- Volume
- 106
- Issue
- 36
- Pages
- 15430-15435
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2741268
- OpenAlex
- W2077963393
- Semantic Scholar
- 429377a051f8aa5819de277b1869e8f8153ad424
- Cited by
- 972
- References
- 55
- Citations by year
- 2026: 17 · 2025: 27 · 2024: 34 · 2023: 47 · 2022: 50 · 2021: 45 · 2020: 54 · 2019: 55 · 2018: 56 · 2017: 56 · 2016: 60 · 2015: 76 · 2014: 87 · 2013: 89 · 2012: 77
- FWCI
- 49.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Funders
- National Institutes of Health (5r01dk060022-19, 5p41rr000954-34, UL1TR000448)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK033301, DK33301, DK37948, DK56341, R01DK037948, DK-60022, R01-DK-060022, P30DK056341)
- National Center for Research Resources (P41-RR000954, RR 00954, UL1RR024992)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- intrahepatic triglyceride, visceral adipose tissue, obesity, insulin sensitivity, VLDL triglyceride secretion, CD36, fatty acid uptake, hepatic insulin resistance, skeletal muscle insulin sensitivity, adipose tissue insulin sensitivity, metabolic complications of obesity
- MeSH terms
- Body Composition, Female, Glucose, Humans, Lipoproteins, VLDL, Liver, Male, Metabolic Diseases, Obesity, Palmitates, Triglycerides, Glucose Clamp Technique, DNA Primers, CD36 Antigens, Reverse Transcriptase Polymerase Chain Reaction, Intra-Abdominal Fat
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-09 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
