The DOI matches its Crossref record; 32 of the 33 references it cites were found in a registry or an index, and 1 are not checked yet; 13 of the 27 sources its claims cite were checked for support.
Leptin reverses insulin resistance and hepatic steatosis in patients with severe lipodystrophy
Open accessAbstract
Lipodystrophy is a rare disorder that is characterized by selective loss of subcutaneous and visceral fat and is associated with hypertriglyceridemia, hepatomegaly, and disordered glucose metabolism. It has recently been shown that chronic leptin treatment ameliorates these abnormalities. Here we show that chronic leptin treatment improves insulin-stimulated hepatic and peripheral glucose metabolism in severely insulin-resistant lipodystrophic patients. This improvement in insulin action was associated with a marked reduction in hepatic and muscle triglyceride content. These data suggest that leptin may represent an important new therapy to reverse the severe hepatic and muscle insulin resistance and associated hepatic steatosis in patients with lipodystrophy.
Verified 2026-10-10 · 1 reference not checked yet
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
In three patients with severe generalized lipodystrophy, chronic recombinant leptin treatment improved insulin-stimulated hepatic and peripheral glucose metabolism and reduced hepatic and muscle triglyceride content. These changes suggest leptin may reverse severe insulin resistance and hepatic steatosis in lipodystrophy.
Key findings
- Before leptin, lipodystrophic patients had severe insulin resistance: glucose infusion rate was 1.2 ± 0.2 vs. 12.7 ± 0.9 mg/kg/min in controls (P < 0.0001), insulin suppression of glucose production was 40% ± 6% vs. 92% ± 7% (P = 0.0004), and fasting glucose production was 3.6 ± 0.8 vs. 1.9 ± 0.1 mg/kg/min (P = 0.019).
- After leptin, glucose infusion rate increased approximately fourfold to 5.4 ± 0.9 mg/kg/min (P = 0.04), insulin suppression of glucose production improved to 82% ± 5% (P < 0.05), and whole-body insulin-stimulated glucose metabolism was 6.1 ± 1.0 vs. 3.5 ± 0.3 mg/kg/min before treatment (P = 0.08).
- Leptin reduced hepatic triglyceride content by 86% ± 8% (P = 0.008) and muscle triglyceride content by 33% ± 3% (P = 0.006); muscle total fatty acyl CoA concentrations decreased by approximately 30%.
- Group mean fasting plasma glucose fell from 234 ± 14 to 122 ± 21 mg/dl (P < 0.05 vs. before treatment), and triglycerides fell from 5851 ± 5079 to 1134 ± 523 mg/dl in Table 1.
Methods
- Three patients with severe generalized lipodystrophy and diabetes (fasting leptin < 4 ng/ml) were studied before and after leptin treatment for 3 months, with patient NIH-1 treated for an additional 5 months; six healthy nonsmoking women of similar age, weight, and BMI served as controls.
- Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp with [6,6-2H2]glucose turnover; lipolysis by [2H5]glycerol turnover; liver and muscle triglyceride by 1H NMR; body fat by DEXA; muscle fatty acyl CoA by biopsy in patient NIH-6; and energy intake/expenditure by monitored diet and indirect calorimetry.
- Differences between controls and lipodystrophic subjects were assessed by Student t tests, and before- vs. after-leptin differences by paired Student t tests; data are mean ± SEM.
Limitations
- The paper does not include a formal limitations section. Evident from the text: the study is very small (3 lipodystrophic patients), open-label, and uses a before-after design without a placebo control.
- Treatment duration differed across patients (3 months for all, 8 months for NIH-1), and some measurements were made in only one patient (energy intake and muscle fatty acyl CoA in NIH-6).
- The paper states that a lipolytic effect of leptin on tissues “cannot be ruled out”; it also reports non-significant changes in glycerol turnover (P = 0.23) and energy expenditure (P = 0.08), so the mechanism is not fully established.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
13 of 27 cited sources checked · 6 supported · 2 flagged · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“At the time of the postleptin treatment study, all patients had their antidiabetic medication discontinued (5).”
What the sources say
- Disputedcites [5] sourceExperimental — accuracy not yet measured
Table 1 (Patient No.; page unavailable in our copy) shows that patients 3, 7, and 8 were still receiving antidiabetic medication at four months; patient 9 had none to discontinue. The Study Design and Changes in Metabolic Control sections say treatments were tapered or discontinued as needed, not discontinued for all patients. (LLM, conf=0.95)
Checked by a reasoning model — may be wrong.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Disputed
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Energy expenditure was assessed by indirect calorimetry in all patients before and after leptin treatment and was found to be slightly, but not significantly, lower in all patients after leptin treatment (1,660 ± 108 kcal/day before treatment versus 1,403 ± 62 kcal/day after treatment, P = 0.08).”
- Also stated in: another passage · hedged
“In contrast, we found that leptin treatment tended to cause a decrease in energy expenditure, which is consistent with the observations in the entire set of lipodystrophic patients (5).”
What the sources say
- Disputedcites [5] sourceExperimental — accuracy not yet measured
In “Changes in Energy Balance” (page not provided), the paper reports a decrease in resting metabolic rate in all nine patients, but gives different values and finds it statistically significant: 1,920 ± 150 to 1,580 ± 80 kcal/day (P = 0.003). The cited claim instead gives 1,660 ± 108 to 1,403 ± 62 kcal/day and calls the decrease nonsignificant (P = 0.08). (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: another passage · hedged
Every source the paper cites for this claim was checked and supports it.
In the paper
“it is likely that a fatty acid-derived intermediate, rather than intramyocellular triglyceride, is responsible for mediating the insulin resistance (23).”
What the sources say
- Supportedcites [23] source
In “A unifying hypothesis for common forms of human insulin resistance” (page not provided), the paper says that triglycerides accumulate but intracellular fatty acid metabolites are “probably more importantly” involved in insulin-signaling defects and insulin resistance. This supports the citing sentence’s qualified comparison. (LLM, conf=0.93)
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The improved glycemic control could be attributed to a marked increase in their insulin responsiveness, as reflected by an almost fourfold increase in the rate of glucose infusion required to maintain euglycemia during the clamp”
What the sources say
- Partly supportedcites [5] sourceExperimental — accuracy not yet measured
The Changes in Metabolic Control section reports improved glycemic control and insulin sensitivity after leptin therapy. But the Procedures section describes an insulin-tolerance test, not a euglycemic clamp; the reported glucose-disappearance constant rose from 0.007 to 0.017, not an almost fourfold increase in a glucose-infusion rate. No page numbers are available in our copy. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These data support the hypothesis that a similar mechanism for insulin resistance might occur in patients with severe lipodystrophy and more common forms of insulin resistance associated with obesity and type 2 diabetes (23).”
What the sources say
- Supportedcites [23] source
The section “A unifying hypothesis for common forms of human insulin resistance” explicitly proposes a shared mechanism for insulin resistance in lipodystrophy, obesity, and type 2 diabetes. It presents this as a hypothesis, matching the citing sentence’s uncertainty. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Previous studies by our group (9, 17-20) and others (7, 21, 22) have demonstrated a strong relationship between triglyceride content in liver and muscle and insulin resistance in these tissues.”
What the sources say
- Supportedcites [9] source
The Discussion (page not available) reports that improved insulin responsiveness was associated with reduced hepatic triglyceride content, and the References list prior studies linking muscle triglyceride or lipid content with insulin resistance. The paper also notes that muscle triglyceride did not fall despite improved muscle insulin sensitivity in its own trial; this does not negate the cited claim about relationships demonstrated in previous studies. (LLM, conf=0.83)
- Could not verifycites [17] sourceExperimental — accuracy not yet measured
The Introduction and Discussion report that elevated plasma free fatty acids induce insulin resistance in human skeletal muscle. They do not report a relationship between triglyceride content in liver or muscle and insulin resistance in those tissues (searched: triglyceride content, intramuscular triglyceride, liver triglyceride). (LLM, conf=0.72)
- Not checked — no full text of the sourcecites [18] source
- Not checked — no full text of the sourcecites [19] source
- Not checked — no full text of the sourcecites [20] source
- Not checked — no full text of the sourcecites [7] Szczepaniak, 1999, Am J Physiol source
- Not checked — no full text of the sourcecites [21] source
- Partly supportedcites [22] sourceExperimental — accuracy not yet measured
The Discussion reports a strong correlation between liver fat percentage and hepatic insulin sensitivity, supporting the liver portion of the claim. Our copy does not report a relationship between muscle triglyceride content and muscle insulin resistance; its mention of skeletal-muscle insulin resistance does not establish that relationship. The indexed passages provide section labels but no page numbers. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Energy intake was monitored in patient NIH-6, and leptin treatment caused an approximately 50% reduction in energy intake, from 2,017 kcal/day before treatment to 962 kcal/day after 3 months of treatment.”
- Also stated in: another passage · hedged
“Furthermore, when energy intake was carefully monitored in an inpatient setting, we found an approximately 50% reduction in the caloric intake in one patient following leptin therapy, which is similar to the self-reported observations by Arioglu Oral et al. (5) in the entire set of nine lipodystrophic patients and by Farooqi et al. (27) in a child with congenital leptin deficiency who was treated”
What the sources say
- Partly supportedcites [5] sourceExperimental — accuracy not yet measured
The Changes in Energy Balance section reports that mean self-reported intake fell during leptin therapy, from 2,680 to 1,600 kcal/day after four months. It does not report the claimed 2,017-to-962 kcal/day change for patient NIH-6 after three months; the Procedures section says food intake was reported at baseline and four months. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [27] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: another passage · hedged
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“While there were no appreciable differences in intramyocellular triglyceride content between the control and lipodystrophic patients”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA 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
“Consistent with the former possibility, all patients reported a marked reduction in appetite following leptin treatment.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“The lipodystrophic patients were severely insulin resistant, as reflected by the very low rates of glucose infusion required to maintain euglycemia during the hyperinsulinemic-euglycemic clamp (lipodystrophic, 1.2 ± 0.2 mg/kg/min versus control, 12.7 ± 0.9 mg/kg/min; P < 0.0001)”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- Probably not a substantial claim. 6
- It may state two separate claims as one. 10
- The quote only partly states this claim. 2
Every source the paper cites for this claim was checked and supports it.
In the paper
“More recently, Arioglu Oral et al. found that human recombinant leptin therapy reduced hyperglycemia and hypertriglyceridemia and increased the rate of glucose disappearance during an intravenous insulin tolerance test in nine lipodystrophic patients (5).”
What the sources say
- Supportedcites [5] source
The Abstract reports that nine patients with lipodystrophy received recombinant human leptin and that treatment improved glycemic control and reduced triglycerides. Changes in Metabolic Control reports an increased rate of glucose disappearance during the insulin-tolerance test; Figure 2 specifies intravenous insulin administration. Page numbers are not supplied in the passages. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In addition, fatty acids have been shown to increase hepatic gluconeogenesis (25, 26).”
What the sources say
- Supportedcites [25] source
The Introduction reports that gluconeogenesis rose when free fatty acids rebounded in healthy, nonobese subjects fasting for 24 hours. Table 3 in “FFA and GNG” also shows a rise in the measured gluconeogenesis rate during that rebound. The claim is a fair broad paraphrase of this finding. (LLM, conf=0.91)
- Supportedcites [26] source
The Discussion (p. 5) states that plasma free-fatty-acid elevation has been shown to increase gluconeogenesis in humans. The paper’s conclusion (p. 6) narrows its own finding: high FFA concentrations increased gluconeogenesis’s contribution to glucose production in healthy humans, while total endogenous glucose production remained unchanged. (LLM, conf=0.90)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, recent studies by our group have challenged this hypothesis and found evidence to suggest that intracellular accumulation of fatty acid-derived metabolites, such as fatty acyl CoA's, leads to activation of protein kinase Cθ , resulting in activation of a serine/threonine cascade that leads to increased serine phosphorylation of insulin receptor substrate-1 (IRS-1). IRS-1 in”
What the sources say
- Partly supportedcites [17] sourceExperimental — accuracy not yet measured
The Discussion proposes fatty acyl CoA accumulation, activation of a serine kinase (possibly PKCθ), IRS-1 serine phosphorylation, and reduced IRS-1-associated PI 3-kinase activity as a hypothesis. It does not establish the full proposed cascade or show that it reduces IRS-1 tyrosine phosphorylation or GLUT4; the Discussion presents GLUT4 effects as possibilities. Page numbers are unavailable in our copy. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [18] source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one. The quote only partly states this claim.
- Partly supported
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
“There was a marked reduction in the fasting plasma glucose concentration in patients NIH-3 and NIH-6 after 3 months of leptin treatment and in NIH-1 after 8 months of leptin treatment (Table 1).”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Prior to leptin treatment, all patients had poorly controlled diabetes (as reflected by fasting hyperglycemia and increased glycosylated hemoglobin), and hyperlipidemia (Table 1).”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one. The quote only partly states this claim.
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
“The fasting respiratory quotient was also unaffected by leptin treatment (0.85 ± 0.06 before treatment versus 0.90 ± 0.03 after treatment; P = 0.1).”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“These alterations were associated with severe hepatic steatosis in all of the patients: NIH-1, 48% liver triglyceride content, NIH-3, 4.6% liver triglyceride content, and NIH-6, 26% liver triglyceride content. In the control subjects, liver triglyceride content was less than 1%.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“there was a tendency for energy expenditure to be higher in the lipodystrophic subjects (lipodystrophic, 1,660 ± 108 kcal/day versus control subjects, 1,368 ± 96 kcal/day; P = 0.10)”
What the sources say
- Not checked — no full text of the sourcecites [16] source
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Shimomura et al. have demonstrated that leptin treatment reversed insulin resistance in a fat-specific aP2-SREBP-1c knockout mouse model of congenital generalized lipodystrophy (4).”
What the sources say
- Not checked — no full text of the sourcecites [4] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably 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
“Leptin treatment may have caused this reduction in hepatocyte and myocellular triglyceride content through decreased food intake and/or promotion of increased energy expenditure.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Lipodystrophy is a rare disorder that is characterized by selective loss of subcutaneous and visceral fat. This disease is associated with hypertriglyceridemia, hepatic steatosis, and severe insulin resistance that often results in diabetes (1-3).”
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Taken together, these data suggest that intrahepatic and intramyocellular lipid lowering effects of leptin were mediated mostly by a reduction in energy intake, as opposed to a leptininduced increase in energy expenditure, although a lipolytic effect of leptin on these tissues cannot be ruled out (4, 28).”
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Chronic leptin treatment caused a marked improvement in whole-body insulin-stimulated glucose metabolism, which could be attributed to both improved insulin sensitivity in the liver (as reflected by improved insulin suppression of glucose production) and in the muscle (as reflected by an increase in insulinstimulated peripheral glucose uptake).”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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 suggest that leptin may represent an important new therapy to reverse the severe hepatic and muscle insulin resistance and associated hepatic steatosis in patients with lipodystrophy.”
- Also stated in: another passage · hedged
“These data suggest that leptin therapy may represent an important new therapy to treat insulin resistance, hepatic steatosis, and the associated diabetes in patients with severe lipodystrophy.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: another passage · hedged
The paper relies on this without support.
The observed improvements after leptin treatment are attributable to leptin rather than to other concurrent changes or factors.
“At the time of the postleptin treatment study, all patients had their antidiabetic medication discontinued (5).”
The paper relies on this without support.
The three studied lipodystrophic patients are representative of patients with severe lipodystrophy.
“Three patients with severe, generalized lipodystrophy (fasting leptin concentration less than 4 ng/ml) associated with diabetes were studied.”
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
“The unifying model of diacylglycerol-induced insulin resistance accounts for the insulin resistance seen in obesity, and in other disorders such as congenital and acquired lipodystrophy,82 in young lean offspring of patients with type 2 diabetes mellitus, and with increase in age.66”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [82]
In the citing paper
“NAFLD is strongly linked to hepatic insulin resistance”
From The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome (2007) · cites this paper as [20]
In the citing paper
“recent studies have demonstrated that NAFLD-induced hepatic insulin resistance is a major factor responsible for the transition from normoglycemia to fasting hyperglycemia and T2DM (18–23).”
From The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome (2007) · cites this paper as [20]
In the citing paper
“Several studies have shown a strong relationship among nonalcoholic fatty liver disease, hepatic insulin resistance, and type 2 diabetes mellitus.1–3”
From Apolipoprotein C3 gene variants in nonalcoholic fatty liver disease (2010) · cites this paper as [1]
In the citing paper
“There is now strong evidence that nonalcoholic fatty liver disease has an important role in causing hepatic insulin resistance.1–3,23–27”
From Apolipoprotein C3 gene variants in nonalcoholic fatty liver disease (2010) · cites this paper as [1]
In the citing paper
“An alternate hypothesis is that the development of hepatic steatosis per se causes hepatic insulin resistance.”
From Inhibition of protein kinase Cε prevents hepatic insulin resistance in nonalcoholic fatty liver disease (2007) · cites this paper as [8]
In the citing paper
“There is increasing evidence for a causal relationship between hepatic steatosis and hepatic insulin resistance both in rodent models with hepatic steatosis and in patients with nonalcoholic fatty liver disease (4, 18-25).”
From Increased prevalence of insulin resistance and nonalcoholic fatty liver disease in Asian-Indian men (2006) · cites this paper as [18]
In the citing paper
“leptin therapy has been examined in several clinical trials in patients with lipodystrophy and these have demonstrated significant improvements in glycemia, dyslipidemia and hepatic steatosis (89, 90, 139, 142).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [142]
In the citing paper
“These parameters have been validated previously by the hyperinsulinemic-euglycemic clamp technique”
From Long-Term Efficacy of Leptin Replacement in Patients With Generalized Lipodystrophy (2005) · cites this paper as [11]
In the citing paper
“showing that r-metHuLeptin increases insulin-stimulated peripheral glucose uptake and increases insulin suppression of hepatic glucose output (11).”
From Long-Term Efficacy of Leptin Replacement in Patients With Generalized Lipodystrophy (2005) · cites this paper as [11]
In the citing paper
“Moreover, leptin dramatically improves insulin sensitivity in human lipodystrophy and in lipodystrophic mouse models which are characterized by low serum leptin levels and by severe insulin resistance (Oral et al., 2002; Petersen et al., 2002; Shimomura et al., 1999).”
From Leptin-Dependent Control of Glucose Balance and Locomotor Activity by POMC Neurons (2009) · cites this paper as Petersen et al., 2002
Citations
Cites
A RAPID METHOD OF TOTAL LIPID EXTRACTION AND PURIFICATION
Bligh, E. G., & Dyer, W. J. (1959) · Canadian Journal of Biochemistry and Physiology · doi:10.1139/o59-099 · Cited by 54,751
The metabolic phenotype in obesity: Fat mass, body fat distribution, and adipose tissue function
Goossens, G. H. (2017) · Obesity Facts · doi:10.1159/000471488 · Cited by 8,481
Randle, P. J., Garland, P. B., Hales, C. N., & Newsholme, E. A. (1963) · The Lancet · doi:10.1016/s0140-6736(63)91500-9 · Cited by 5,093
Cellular mechanisms of insulin resistance
Shulman, G. I. (2000) · Journal of Clinical Investigation · doi:10.1172/jci10583 · Cited by 2,714
Self-citationEffects of Recombinant Leptin Therapy in a Child with Congenital Leptin Deficiency
Farooqi, I. S., Jebb, S. A., Langmack, G., Lawrence, E., Cheetham, C. H., Prentice, A. M., Hughes, I. A., McCamish, M. A., & O'Rahilly, S. (1999) · New England Journal of Medicine · doi:10.1056/nejm199909163411204 · Cited by 1,998
Dresner, A., Laurent, D., Marcucci, M., Griffin, M. E., Dufour, S., Cline, G. W., Slezak, L. A., Andersen, D. K., Hundal, R. S., Rothman, D. L., et al. (1999) · Journal of Clinical Investigation · doi:10.1172/jci5001 · Cited by 1,311
Griffin, M. E., Marcucci, M. J., Cline, G. W., Bell, K., Barucci, N., Lee, D., Goodyear, L. J., Kraegen, E. W., White, M. F., & Shulman, G. I. (1999) · Diabetes · doi:10.2337/diabetes.48.6.1270 · Cited by 1,267
Self-citationLeptin-Replacement Therapy for Lipodystrophy
Oral, E. A., Simha, V., Ruiz, E., Andewelt, A., Premkumar, A., Snell, P., Wagner, A. J., DePaoli, A. M., Reitman, M. L., Taylor, S. I., et al. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa012437 · Cited by 1,247
Self-citationLeptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystrophy
Shimomura, I., Hammer, R. E., Ikemoto, S., Brown, M. S., & Goldstein, J. L. (1999) · Nature · doi:10.1038/43448 · Cited by 1,038
Perseghin, G., Scifo, P., De Cobelli, F., Pagliato, E., Battezzati, A., Arcelloni, C., Vanzulli, A., Testolin, G., Pozza, G., Del Maschio, A., et al. (1999) · Diabetes · doi:10.2337/diabetes.48.8.1600 · Cited by 877
Flagged first, then by citations
Research works printed but not linked: 1
- Szczepaniak, 1999, Am J Physiol, 276, E977
Cited by
Sorted by citations
Items 601–700 of 797
Sperling, M. A., & Garg, A. (2018) · Europe PMC (PubMed Central) · Cited by 5
Tiwari, M., & Mcilroy, G. D. (2023) · Diabetic Medicine · doi:10.1111/dme.15214 · Cited by 6
Pathogenesis of Insulin Resistance
Zaman, G. S. (2020) · IntechOpen eBooks · doi:10.5772/intechopen.92864 · Cited by 6
“Leptin treatment diminished the consumption of calorie, settled hepatic steatosis, and improved insulin activity [82].”
BackgroundLeuthardt, A. S., Bayer, J., Rodríguez, J. M. M., & Boyle, C. N. (2022) · Frontiers in Physiology · doi:10.3389/fphys.2021.772707 · Cited by 6
“Deficient leptin signaling reportedly drives lipid accumulation in the liver, as has been observed in hypoleptinemic people with lipodystrophy (Petersen et al., 2002), and in people with type 2 diabetes and leptin resistance (Cernea et al.”
BackgroundThe metabolic phenotype of pre-diabetes in obese youth
Caprio, S., & Weiss, R. (2004) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/s0939-4753(04)80054-1 · Cited by 5
Yokoyama, H., Hirose, H., Ohgo, H., & Saito, I. (2004) · Alcoholism Clinical and Experimental Research · doi:10.1097/01.alc.0000133549.77624.42 · Cited by 5
Angiopoietin-2: A Therapeutic Target for Vascular Protection in Hutchinson–Gilford Progeria Syndrome
Vakili, S., & Cao, K. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252413537 · Cited by 5
“Lipodystrophy is a disorder that is characterized by partial or total loss of the adipose tissue and has been associated with mutations in the lamin A gene [74,75].”
Ahima, R. S., Scolaro, L. M., & Park, H.-K. (2016) · Springer eBooks · doi:10.1007/978-3-319-11251-0_24 · Cited by 5
Özalkak, Ş., Demiral, M., Ünal, E., Taş, F. F., Önay, H., Demirbilek, H., & Özbek, M. N. (2022) · Journal of Clinical Research in Pediatric Endocrinology · doi:10.4274/jcrpe.galenos.2022.2022-1-25 · Cited by 4
“Metreleptin regulates appetite and also improves peripheral and hepatic insulin sensitivity, partially independent of food intake (13,14,15,16).”
BackgroundPrecision medicine: toward restoring fat with gene therapy in inherited lipodystrophy
Prieur, X., & Cao, L. (2024) · Gene Therapy · doi:10.1038/s41434-024-00489-3 · Cited by 4
da Silva, A. A., Hall, J. E., Dai, X., Wang, Z., Salgado, M. C., & do Carmo, J. M. (2021) · Diabetes · doi:10.2337/db21-0126 · Cited by 4
Chapter 14 Insulin resistance, inflammation, and the IKK/IκB/NF-κB pathway
Bhatt, B. A., & O'Doherty, R. M. (2006) · Advances in molecular and cellular endocrinology · doi:10.1016/s1569-2566(06)05014-9 · Cited by 4
Birthweight and Risk for Diabetes
Davey, R. X. (2002) · Diabetes Care · doi:10.2337/diacare.25.10.1886 · Cited by 4
Reflecting on 80 years of excellence
Neill, U. S. (2004) · Journal of Clinical Investigation · doi:10.1172/jci23290 · Cited by 4
The Central Question of Type 2 Diabetes
Rouquet, T., Bonnet, M. S., Clément, P., Dallaporta, M., Troadec, J., Roux, J., & Bariohay, B. (2013) · Pharmaceutical Patent Analyst · doi:10.4155/ppa.13.22 · Cited by 5
Adipobiology-based pharmacology
Erol, A. (2006) · Biomedical Reviews · doi:10.14748/bmr.v17.84 · Cited by 4
7 Mammalian ACAT and DGAT2 gene families
Cheng, D., Liu, J., Chang, C. C. Y., & Chang, T. (2003) · Topics in current genetics · doi:10.1007/978-3-540-40999-1_8 · Cited by 4
Garg, A., Vasandani, C., Li, X., Quittner, C., & Yokoo, T. (2025) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaf173 · Cited by 4
Periodontitis and Liver Diseases
Irie, K., Ekuni, D., Tomofuji, T., & Morita, M. (2013) · Oxidative stress in applied basic research and clinical practice · doi:10.1007/978-1-4614-9557-4_14 · Cited by 3
Leptin and insulin resistance: good, bad, or still unclear?
Oral, E. A., & Burant, C. (2009) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90914.2008 · Cited by 4
Rabson Mendenhall Syndrome; a Case Report and Review of Literature
Zamanfa, D., Mohamadi, F., & Maskopaii, S. R. (2020) · International Journal of Environmental Chemistry · doi:10.11648/j.ijec.20200401.12 · Cited by 3
“Patients with leprechaunism generally die in the first two years of life and the survival in RMS is usually less than 20 years, although there are some documented cases with longer survival [24].”
BackgroundA New Understanding of Metformin
Hardie, D. G. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-820472-6.00099-2 · Cited by 3
Kravcik, S. (2004) · HIV Clinical Trials · doi:10.1310/xp75-7vj5-hml2-yf1w · Cited by 3
La leptine, nouvelle perspective thérapeutique dans le traitement du diabète ?
Vatier, C., Capeau, J., & Vigouroux, C. (2010) · médecine/sciences · doi:10.1051/medsci/20102610803 · Cited by 3
“hépatique et musculaire avec une régression majeure de la stéatose hépatique et de l’accumulation intra- myocytaire des triglycérides chez les adultes et les enfants lipodystrophiques [5-8].”
BackgroundAssociations between abdominal adiposity, exercise, morbidity, and mortality
Kuk, J. L. (2007) · Applied Physiology, Nutrition, and Metabolism · doi:10.1139/h07-090 · Cited by 4
Bays, H. E., Mandarino, L. J., & DeFronzo, R. A. (2004) · Cited by 3
De l'obésité au diabète de type 2 : épidémiologie et physiopathologie
Fumeron, F. (2005) · Sciences des Aliments · doi:10.3166/sda.25.339-347 · Cited by 3
HOT TOPIC Adipocytokines and Insulin Resistance
Pittas, A. G., Joseph, N. A., Greenberg, A. S., & Mayer-USDA, J. (2004) · Cited by 3
Pathophysiology of Insulin Action in Humans
Prato, S. D. (2005) · Elsevier eBooks · doi:10.1016/b978-84-8174-892-5.50011-5 · Cited by 3
Evaluating the therapeutic impact of tirzepatide in people with partial lipodystrophy
Mandour, M. O., Stears, A. J., van der Klaauw, A. A., Flanagan, C., Gaff, L., Jenkins, C., & Savage, D. B. (2026) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgag126 · Cited by 3
Black, M. M., & Cunliffe, W. J. (2004) · doi:10.1002/9780470750520.ch55 · Cited by 3
Hong, L., Sun, Y., Lu, X., & Xu, X. (2025) · Biomedical Reports · doi:10.3892/br.2025.1939 · Cited by 2
“Severe forms of NAFLD and NASH can occur as complications of congenital lipodystrophy, where the absence of adipose tissue forces the liver to store excess fatty acids, leading to notable insulin resistance (24).”
Pathogenesis of Hepatic Steatosis and Fibrosis: Role of Leptin
Magkos, F., Fabbrini, E., & Klein, S. (2014) · Springer eBooks · doi:10.1007/978-3-319-09915-6_8 · Cited by 2
Ancona, G. (2025) · Current Medical Research and Opinion · doi:10.1080/03007995.2025.2475090 · Cited by 4
“Therefore, recombinant leptin has been explored as a potential lipodystrophy therapy 35–37 .”
Les lipodystrophies génétiques
Vatier, C., Bidault, G., Dour, C. L., Béréziat, V., Lascols, O., Capeau, J., & Vigouroux, C. (2011) · Médecine et Nutrition · doi:10.1051/mnut/201120005 · Cited by 2
Esteatosis hepática y resistencia a la insulina: ¿qué ocurre primero?
Esteve-Lafuente, E., & Ricart, W. (2006) · Clínica e Investigación en Arteriosclerosis · doi:10.1016/s0214-9168(06)73708-1 · Cited by 2
Soo, B., & Park, S. E. (2006) · The Journal of Korean Diabetes Association · doi:10.4093/jkda.2006.30.5.317 · Cited by 2
Metabolic Disorders in HIV-infected Children Metabolic Disorders in HIVinfected Children
Liguoro, S. M. (2014) · Journal of Metabolic Syndrome · doi:10.4172/2167-0943.1000169 · Cited by 2
“The prevalence of lipodystrophy in HIV-infected children varies from 1 to 10% in the retrospective questionnaire-based surveys [129-134] and from 12 to 33% in studies conducted using anthropometry [50-110].”
BackgroundAhima, R. S., Scolaro, L. M., & Park, H.-K. (2015) · Springer eBooks · doi:10.1007/978-3-319-12125-3_24-1 · Cited by 2
Oxidative Stress, Aging and Mitochondrial Dysfunction in Liver Pathology
Ayala‐Peña, S., & Torres‐Ramos, C. A. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-405933-7.00004-4 · Cited by 2
Pleotropic Acute and Chronic Effects of Leptin to Reverse Type 1 Diabetes
Perry, R. J. (2017) · Postdoc Journal · doi:10.14304/surya.jpr.v5n1.2 · Cited by 2
“controlled T1D patients, just as it does in lipodystrophic individuals (67).”
BackgroundLipodystrophies and Dyslipidemias
Garg, A. (2015) · Contemporary Endocrinology · doi:10.1007/978-1-60761-424-1_16 · Cited by 2
“the liver and muscle [86–88].”
Hepatic Carbohydrate Metabolism
Raddatz, D., & Ramadori, G. P. (2010) · Molecular pathology library · doi:10.1007/978-1-4419-7107-4_8 · Cited by 3
THE RELATIONSHIP THE LEPTIN HORMONE, OBESITY AND DIABETES
Sarı, A., & Sadeq, M. B. (2020) · NWSA Academic Journals · doi:10.12739/nwsa.2020.15.2.3a0095 · Cited by 2
Wang, X., Kim, S., Guan, Y., Parker, R., Rodrigues, R. M., Feng, D., Lu, S. C.-L., & Gao, B. (2022) · Hepatology Communications · doi:10.1002/hep4.2092 · Cited by 2
“In patients with lipodystrophy, leptin treatment was found to improve insulin sensitivity and reduce hepatic TG content.[41] Profibrogenic activities of leptin in liver have also been reported.”
BackgroundLeptin Is Associated with Insulin Resistance in Japanese Migrants
de Almeida-Pititto, B., Gimeno, S. G. A., Sañudo, A., Ribeiro‐Filho, F. F., Ferreira, S. R. G., & Japanese-Brazilian Diabetes Study Group (2005) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2005.3.140 · Cited by 2
“31 Such accumulation could be responsible for the lipotoxicity of non-adi-pocyte non-adi-pocyte cells that results in insulin resistance.”
The emerging clinical significance of leptin in humans with absolute or relative leptin deficiency
Moschos, S. J., & Mantzoros, C. S. (2005) · Current Opinion in Internal Medicine · doi:10.1097/01.med.0000177421.80858.74 · Cited by 2
Treatment of partial lipodystrophy: can the zebra teach us about the horse?
Hegele, R. A. (2004) · Drug Discovery Today Disease Mechanisms · doi:10.1016/j.ddmec.2004.09.009 · Cited by 2
A systems engineering approach to coronary heart disease
Mathews, M. J. (2015) · Cited by 2
Besci, Ö., Güler, M. Ç., Foss‐Freitas, M. C., & Oral, E. A. (2025) · Expert Review of Endocrinology & Metabolism · doi:10.1080/17446651.2025.2574318 · Cited by 2
Adipose tissue as a humoral–neuronal hub in metabolic regulation
Tsuji, T., & Tseng, Y. (2026) · Nature Reviews Endocrinology · doi:10.1038/s41574-026-01265-6 · Cited by 5
Molecular mechanisms and pathogenesis of MASH
Gallage, S., Govaere, O., Anstee, Q. M., Shulman, G. I., Tacke, F., & Heikenwälder, M. F. (2026) · Nature · doi:10.1038/s41586-026-10529-0 · Cited by 3
Kim, Y. (2007) · Journal of Korean Endocrine Society · doi:10.3803/jkes.2007.22.5.311 · Cited by 2
Kozak, L. P., & Ravussin, É. (2004) · CRC Press eBooks · doi:10.1201/9780203508756.pt1 · Cited by 2
Misra, S., & Hattersley, A. T. (2016) · Wiley eBooks · doi:10.1002/9781118924853.ch18 · Cited by 2
Behind BMI: The Potential Indicative Role of Abdominal Ectopic Fat on Glucose Metabolism
Li, X., Ren, H., Xu, H. N., Han, X., Lu, J. F., & Yang, Z. (2024) · Obesity Facts · doi:10.1159/000536160 · Cited by 2
“The reason may be that as the liver is the main organ of energy metabolism in the human body, the dysfunction of adipocytes, lipodystrophy, and lack of adipose tissue will lead to changes in liver fat content [35 – 37].”
BackgroundEffect of exogenous leptin on thrombotic and metabolic profiles of FVB/B6 lipodystrophic mice
Kadouh, H. C., Yang, S. J., IglayReger, H. B., & Bodary, P. F. (2013) · The FASEB Journal · doi:10.1096/fasebj.27.1_supplement.1183.4 · Cited by 1
“This coincides with previous suggestions that leptin improves lipid metabolism in both lipodystrophic humans (11, 12, 86) and mice (55, 56).”
BackgroundAmano, S. U. (2013) · The Journal of the American Medical Association (JAMA) Network (American Medical Association) · doi:10.13028/m2bw2z · Cited by 1
Faßhauer, M., & Blüher, M. (2009) · Journal of Laboratory Medicine · doi:10.1515/jlm.2009.005 · Cited by 1
Molecular mechanisms of the alternative lipogenic function of insulin
Pankov, Y. A. (2013) · Molecular Biology · doi:10.1134/s0026893313060113 · Cited by 1
“Exogenous leptin decreases the plasma levels of glucose, glycated hemo globin, and insulin; obviates the need of glycemia lowering treatments; and suppresses the lipid accumu lation in muscles and the liver [14].”
BackgroundImprovement of Leptin Resistance
Kim, Y. W. (2013) · Journal of Yeungnam Medical Science · doi:10.12701/yujm.2013.30.1.4 · Cited by 1
Potential Therapeutic Strategies for Fat Induced Insulin Resistance
Choi, C. S. (2009) · Journal of Korean Endocrine Society · doi:10.3803/jkes.2009.24.2.65 · Cited by 1
“그러나 지방조직을 이식한 lipodystrophy 마우스 모델 연구[11]와 식이조절에 의해 식사량을 감소시 킨 비만 환자 연구에서 간과 근육의 지방축적이 감소되었고, 더불어 인슐린 저항성이 현저히 호전되었다[12].”
Lipin Deficiency Impairs Diurnal Metabolic Fuel
Xu, S., Phan, J., Saad, M. F., Reue, K., & Kurland, I. J. (2006) · Cited by 1
Müller, T. D., Clemmensen, C., Finan, B., DiMarchi, R. D., & Tschöp, M. H. (2014) · Springer eBooks · doi:10.1007/978-3-319-09915-6_21 · Cited by 1
Garg, A. (2013) · Elsevier eBooks · doi:10.1016/b978-0-12-383834-6.00095-1 · Cited by 1
Growth-Promoting Effects of Zhenqi Granules on Finishing Pigs
Luo, W., Huang, Y., Qiu, X., Zhuo, W., Tao, Y., Wang, S., Li, H., Shen, J., Zhao, L., Zhang, L., et al. (2022) · Animals · doi:10.3390/ani12243521 · Cited by 1
Obesity in the Pathophysiology of Diabetes
Paniagua, J. A., & Vidal‐Puig, A. (2023) · Springer eBooks · doi:10.1007/978-3-031-25519-9_14 · Cited by 1
Aliyev, A., Samadov, E., İbrahimli, A., et al. (2023) · Pediatric Transplantation · doi:10.1111/petr.14680 · Cited by 1
“17,18 Leptin replacement therapy improves the patients' lifestyle by giving relief from the use of large amounts of antidiabetic and antilipidemic drugs.”
BackgroundLes adipokines : état des lieux et nouveautés
Bastard, J., Bastard, C., Fellahi, S., Vatier, C., Capeau, J., & Fève, B. (2016) · Obésité · doi:10.1007/s11690-016-0537-6 · Cited by 1
Biomarkers of Insulin Resistance
Cox‐York, K. A., & Pereira, R. I. (2019) · Contemporary Endocrinology · doi:10.1007/978-3-030-25057-7_11 · Cited by 1
Péptidos anorexigénicos y su participación en la conducta alimentaria
Jaimes-Hoy, L., Cabrera‐Wrooman, A., Vilches‐Flores, A., Guzmán, C., & Arroyo, I. (2005) · Revista de Endocrinología y Nutrición · Cited by 1
Foxf2 and Foxc2, two transcription factors that regulate adipocyte metabolism
Westergren, R. (2010) · Gothenburg University Publications Electronic Archive (Gothenburg University) · Cited by 1
Characteristics of Insulin Resistance in Japanese Men Working Abroad.
Iizuka, T., Uchikoshi, A., Koga, T., et al. (2003) · Health Evaluation and Promotion · doi:10.7143/jhep.30.445 · Cited by 1
Öncül, O., Top, C., & Çavuşlu, Ş. (2002) · Diabetes Care · doi:10.2337/diacare.25.10.1901 · Cited by 1
[Leptine participation in the development of liver steatosis and biliar lithiasis].
Méndez‐Sánchez, N., Ponciano‐Rodríguez, G., Chávez-Tapia, N. C., & Uribe, M. (2005) · PubMed · Cited by 1
Savage, D. B., Watson, L. P. E., Carr, K., Adams, C., Brage, S., Chatterjee, K., Hodson, L., Boesch, C., Kemp, G. J., & Sleigh, A. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/382283 · Cited by 1
“(29) who, in 3 223 patients with generalized lipodystrophy (2 congenital, 1 acquired), found similar soleus IMCL 224 to 6 age-, BMI- and weight-matched controls.”
BackgroundLeuthardt, A. S., Bayer, J., Rodríguez, J. M. M., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.09.24.461340 · Cited by 1
Prieur, X., Cariou, B., & Magré, J. (2021) · Médecine des Maladies Métaboliques · doi:10.1016/j.mmm.2021.01.006 · Cited by 1
Ali, M., Gupta, A., Verma, R. D., Akhtar, S., & Ghosh, J. K. (2024) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2024.107919 · Cited by 1
Sarvari, M., Sharifi, Y., Sharifi, F., Khezrpour, A., Javankiani, S., Nasrollahizadeh, A., Tavakoli, H., Ayati, A., Moodi, M., Shadman, Z., et al. (2026) · Journal of Diabetes & Metabolic Disorders · doi:10.1007/s40200-026-01947-y · Cited by 1
Congenital Generalized Lipodystrophy 3 & 4 Presenting as Pancreatitis
Lingudu, B., Bongi, V., Ayyagari, M., et al. (2019) · Journal of Evidence Based Medicine and Healthcare · doi:10.18410/jebmh/2019/555 · Cited by 1
Puberty, Insulin Resistance, and Type 2 Diabetes
Caprio, S., & Gower, B. A. (2005) · CRC Press eBooks · doi:10.1201/9781420026634.ch11 · Cited by 1
Lipid metabolism and insulin sensitivity
Wu, X. (2024) · Theoretical and Natural Science · doi:10.54254/2753-8818/46/20240400 · Cited by 1
Syndromes of Extreme Insulin Resistance
Grunberger, G., Myneni, A., & Alfonso, B. (2017) · Springer eBooks · doi:10.1007/978-3-319-20797-1_17-2 · Cited by 1
Role of the Adipocyte in Metabolism and Endocrine Function
Ravussin, É., & Smith, S. R. (2010) · Elsevier eBooks · doi:10.1016/b978-1-4160-5583-9.00037-x · Cited by 1
The Liver and Insulin Resistance: The Important Convergence of Endocrinology and Hepatology
Chang, C., Whitt, K. N., Liu, Z., & Caldwell, S. H. (2009) · Humana Press eBooks · doi:10.1007/978-1-59745-192-5_13
“Indeed, recent studies have shown that leptin replacement in these patients results in improved insulin sensitivity in both muscle and liver and better glycemic and lipemic control (66 , 96 , 97) . Reduced intramyocellular and liver fat contents and reduced appetite could be part of the mechanism ( 66 , 96) .”
BackgroundInfluentialInsulin Sensitivity and the Onset of Hyperphagia in Fatty Rats
Durham, H. A. (2004)
Clinical Applications of Leptin
Oral, E. A., & DePaoli, A. M. (2006) · Springer eBooks · doi:10.1007/978-0-387-31416-7_17
Considine, R. V. (2010) · Wiley eBooks · doi:10.1002/9783527629527.ch10
Non Alcoholic Fatty Liver Disease: Correlation With Clinical Hormonal and Biochemical Parameters
Goritsas, C. P., Spanos, K. T., Stefanopoulos, D., et al. (2007) · Hospital chronicles/Hospital Chronicles · doi:10.2015/hc.v2i3.37
“(24) In conclusion, the results of the present study in a group of greek patients, indicate that beyond the well known risk factors for NAFLD as obesity and hyperlipidemia – factors important for the greek population – insulin resistance holds the major role in the progression of the disease to steatohepatitis.”
ResultAdipose Tissue and Skeletal Muscle Plasticity in Obesity and Metabolic Disease
Ukropec, J., & Ukropcov, B. (2012) · InTech eBooks · doi:10.5772/28506
“respectively (Petersen et al. 2002; Rieusset et al. 2002; Van Gaal et al. 2003).”
Henry, R. R., Phillips, S. A., Mudaliar, S. R. D., & Ciaraldi, T. P. (2006) · Advances in molecular and cellular endocrinology · doi:10.1016/s1569-2566(06)05006-x
Ashley, D. T. (2010) · Dublin City University Open Access Institutional Repository (Dublin City University)
Resistencia a la insulina durante el envejecimiento: ¿un proceso mediado por leptina?
Baeza, J. (2005) · Monografías de la Real Academia Nacional de Farmacia
Sevastianova, K. (2011) · Työväentutkimus Vuosikirja
Insulin Resistance, Diabetes and its Complications
Ng, D. S. (2006) · Wiley-VCH eBooks · doi:10.1002/3527600906.mcb.200400011
Pre‐Diabetes in Obese Adolescents: Pathophysiologic Mechanisms
Cali, A. M. G., & Caprio, S. (2011) · doi:10.1002/9781444318456.ch5
Fat mass, adipokines and clinical complications of chronic kidney disease
Axelsson, J. (2006) · Figshare
A global approach to dissecting lipid-induced impairment of liver gluconeogenesis
Hayward, B. J. (2013)
Metadata
- Authors
- Petersen, K. F., Oral, E. A., Dufour, S., Befroy, D., Ariyan, C., Yu, C., Cline, G. W., DePaoli, A. M., Taylor, S. I., Gorden, P., & Shulman, G. I.
- Affiliations
- Yale University (US)
- National Institutes of Health (US)
- Howard Hughes Medical Institute (US)
- Amgen (United States) (US)
- Corresponding author
- Petersen, Kitt Falk
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2002-05-15
- Volume
- 109
- Issue
- 10
- Pages
- 1345-1350
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC150981
- OpenAlex
- W2164714249
- Cited by
- 800
- References
- 26
- Citations by year
- 2026: 10 · 2025: 10 · 2024: 20 · 2023: 21 · 2022: 23 · 2021: 27 · 2020: 25 · 2019: 29 · 2018: 29 · 2017: 31 · 2016: 38 · 2015: 39 · 2014: 34 · 2013: 45 · 2012: 35
- FWCI
- 26.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- Yale University
- National Institutes of Health (P30 DK)
- National Institute of Diabetes and Digestive and Kidney Diseases (K-23 DK-02347, R01 DK-42930, P30DK045735)
- National Center for Research Resources (M01RR000125)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- leptin, lipodystrophy, insulin resistance, hepatic steatosis, hepatic glucose metabolism, muscle glucose metabolism, triglyceride accumulation, hypertriglyceridemia, hepatomegaly
- MeSH terms
- Adult, Diabetes Mellitus, Type 2, Fatty Liver, Female, Humans, Insulin Resistance, Lipodystrophy, Liver, Hypertriglyceridemia, Leptin
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 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
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
