The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index; 1 of the 6 sources its claims cite were checked for support.
Homeostasis model assessment: insulin resistance and ?-cell function from fasting plasma glucose and insulin concentrations in man
Open accessAbstract
The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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Claims the paper makes
15 Own result · 7 Own interpretation · 3 No full text of the sources · 1 Partly supported · 1 No basis given · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The fasting plasma insulin concentration is largely determined by the glucose concentration [3]”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
What the sources say
- Partly supportedcites [3] McCarthy ST, Harris F, Turner RC (1977) Glucose control of basal insulin secretion in diabetes. Diabetologia 13: 93?97 sourceExperimental — accuracy not yet measured
The Results and Discussion (page unavailable in our copy) show that changing plasma glucose affects basal insulin secretion. But they also report markedly impaired responses in diabetic subjects, including cases where insulin remained nearly constant despite a substantial glucose decrease. The paper therefore supports glucose as an influence, but not the unqualified claim that it largely determines fasting insulin concentration. (LLM, conf=0.84)
plainstates a cause- 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.
- 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
“The estimate of deficient/3cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (R~ = 0.61, p< 0.01)”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plainstates an association- 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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 estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (R~=0.88,p<0.0001)”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plainstates an association- 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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 no correlation with any aspect of insulin-receptor binding.”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plain- 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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 insulin concentration (P~ = 0.81, p < 0.0001)”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plainstates an association- 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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 mean coefficient of variation over the two studies was 32%.”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Reproducibility of estimate of /3-cell function by HOMA
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.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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 both groups together (1% 0.61, p < 0.01 : Fig. 3).”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Comparisons of methods of assessing ~3-cell function
plainstates an association- 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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 with the estimate from the intravenous glucose tolerance test (R~ = 0.64, p < 0.05).”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plainstates an association- 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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 in both groups together: 1% = 0.64, p< 0.05; Fig. 3).”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > HOMA compared with intravenous glucose tolerance test.
plainstates an association- 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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
“Neither receptor numbers or any aspect of high or low affinity binding correlated with other measures of insulin resistance (HOMA, clamp, basal insulin or CIGMA: ~ all < 0.55; NS).”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > HOMA compared with the hyperglycaemic clamp. The
plain- 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
- It may state two separate claims as one. 2
- The quote only partly states this claim. 1
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 low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for/3-cell deficit) limits its use”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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 mean coefficient of variation over the two studies was 31%.”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Hyperglycaemic clamp : ~-cell function (%)
plain- 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.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
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
“The degree of the hyperglycaemia does not correlate significantly with either the degrees of abnormal fl-cell function or insulin resistance.”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > 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 authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
The authors state this as an assumption.
Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
“Assuming that normal-weight normal subjects aged < 35 years have 100% r-cell function, and an insulin resistance of 1, the values for a patient can be assessed from the insulin and glucose concentrations by the formulae: r-cell”
The paper relies on this without support.
The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
“The plasma glucose:insulin response for normal subjects, equivalent to the C-peptide response, is insulin = 5 (glucose-3.5).”
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Surrogate markers of peripheral insulin activity, such as homeostasis model assessment and whole-body insulin sensitivity indexes, could be useful as well in the early identification of patients with IR, before overt DM sets in ().”
From Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management (2017) · cites this paper as [240]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“After the unprocessed diet, fasting glucose and insulin levels tended to decrease compared to baseline and the homeostasis model assessment of insulin resistance (HOMA-IR) (Matthews et al., 1985) was significantly decreased compared to baseline.”
From Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake (2019) · cites this paper as Matthews et al., 1985
The cited source says what the claim attributes to it.
In the citing paper
“The Homeostasis Model Assessment of Insulin Resistance (HoMA-IR) was calculated according to Matthews et al. [25].”
From Chronotype: A Tool to Screen Eating Habits in Polycystic Ovary Syndrome? (2022) · cites this paper as [25]
The cited source says what the claim attributes to it.
In the citing paper
“AAV9-mTERT treated mice also showed a trend for an improved glucose uptake and a better homeostatic model assessment (HOMA (Heikkinen et al, 2007; Matthews et al, 1985)) compared to the AAV9-eGFP controls, although differences did not reach statistical significance (Supporting Information Fig S4D and E).”
From Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer (2012) · cites this paper as Matthews et al, 1985
In the citing paper
“ndirect estimates of insulin resistance, such as HOMA-IR 63 and QUICKI, 64 are derived from fasting S-insulin and glucose concentrations and have been widely used in both nondiabetic and type 2 diabetic subjects as surrogates of insulin sensitivity.65,66”
From Increased liver fat, impaired insulin clearance, and hepatic and adipose tissue insulin resistance in type 2 diabetes. (2008) · cites this paper as [63]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Subjects and procedures
“The same 12 normal subjects and 11 Type 2 diabetic patients came to the hospital fasting on a separate day for a continuous infusion”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > HOMA compared with the hyperglycaemic clamp. The
“HOMA compared with CIGMA.The HOMA estimate of insulin resistance from the mean of 15 stressed fasting samples before the CIGMA correlated with that measured by CIGMA in 11 normal subjects (R~ = 0.69, p < 0.02), in 12 diabetic subjects (R~ 0.97, p < 0.0001)”
Citations
Cites
Glucose clamp technique: a method for quantifying insulin secretion and resistance.
DeFronzo, R. A., Tobin, J. D., & Andres, R. (1979) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1979.237.3.e214 · Cited by 7,425
Quantitative estimation of insulin sensitivity.
Bergman, R. N., Ider, Y. Z., Bowden, C. R., & Cobelli, C. (1979) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1979.236.6.e667 · Cited by 1,874 · cited 1×
“This use of modelling to provide a reference graph contrasts with other models where an individual patient's data have to be entered into a computer to determine the relationships between rapidly changing variables, such as occur after an intravenous glucose test [19].”
Method[WHO Expert Committee on diabetes mellitus].
Reitsma, W. D., & Terpstra, J. (1981) · PubMed · Cited by 556
Turner, R. C., Holman, R. R., Matthews, D., Hockaday, T. D. R., & Peto, J. (1979) · Metabolism · doi:10.1016/0026-0495(79)90146-x · Cited by 388
Self-citationCharacteristics of Human Erythrocyte Insulin Receptors
Gambhir, K. K., Archer, J. A., & BRADLEY, C. J. (1978) · Diabetes · doi:10.2337/diab.27.7.701 · Cited by 290
The Insulin Receptor: Its Role in Insulin Resistance of Obesity and Diabetes
Olefsky, J. M. (1976) · Diabetes · doi:10.2337/diab.25.12.1154 · Cited by 289
Hosker, J. P., Matthews, D. R., Rudenski, A. S., Burnett, M. A., Darling, P., Bown, E. G., & Turner, R. C. (1985) · Diabetologia · doi:10.1007/bf00280882 · Cited by 287
Self-citationPulsatile Insulin Has Greater Hypoglycemic Effect Than Continuous Delivery
Matthews, D. R., Naylor, B. A., Jones, R., Ward, G. M., & Turner, R. C. (1983) · Diabetes · doi:10.2337/diab.32.7.617 · Cited by 256
Self-citationControl of pulsatile insulin secretion in man
Matthews, D. R., Lang, D. A., Burnett, M. A., & Turner, R. C. (1983) · Diabetologia · doi:10.1007/bf00282705 · Cited by 175
Self-citationTHE BASAL PLASMA GLUCOSE: A SIMPLE RELEVANT INDEX OF MATURITY‐ONSET DIABETES
HOLMAN, R. R., & TURNER, R. C. (1981) · Clinical Endocrinology · doi:10.1111/j.1365-2265.1981.tb00196.x · Cited by 64
Self-citation
Research works printed but not linked: 2
- Metropolitan Life Assurance Co (1959) Net weight standard for men and women. Stat Bull Metrol Life Found 40: 1?4
- Matthews DR, Hosker JP (1984) An unbiased, flexible computer programme for glucose clamping, with graphics and running statistics. Diabetologia 27: 308?309 A
Cited by
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Items 11,701–11,800 of 31,469
Pérez‐Martínez, P., Delgado‐Lista, J., García‐Ríos, A., Ferguson, J. F., Gulseth, H. L., Williams, C. M., Karlström, B., Kieć‐Wilk, B., Blaak, E. E., Helal, O., et al. (2011) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.110.010512 · Cited by 29
Rosendahl-Riise, H., Nielsen, H. J., Mellgren, G., & Gudbrandsen, O. A. (2013) · SpringerPlus · doi:10.1186/2193-1801-2-352 · Cited by 30
Optimal waist:height ratio cut-off point for cardiometabolic risk factors in Turkish adults
Can, A. S., Yıldız, E. A., Samur, G., Rakıcıoğlu, N., Pekcan, A. G., Özbayrakçı, S., Palaoğlu, K. E., Gönen, M., & Bersot, T. P. (2009) · Public Health Nutrition · doi:10.1017/s1368980009991637 · Cited by 30
Diniz, J. M. M., & da Costa, T. H. M. (2004) · British Journal Of Nutrition · doi:10.1079/bjn20041288 · Cited by 30
Birth order progressively affects childhood height
Savage, T., Derraik, J. G. B., Miles, H. L., Mouat, F., Cutfield, W. S., & Hofman, P. L. (2013) · Clinical Endocrinology · doi:10.1111/cen.12156 · Cited by 30
Cherneva, R. V., Georgiev, O. B., Petrova, D. S., Mondeshki, T., Ruseva, S., Cakova, A., & Mitev, V. (2013) · Journal of Diabetes & Metabolic Disorders · doi:10.1186/2251-6581-12-5 · Cited by 30
Qi, Q., Xu, M., Wu, H., Liang, L., Champagne, C. M., Bray, G. A., Sacks, F. M., & Qi, L. (2013) · Diabetes Care · doi:10.2337/dc13-0018 · Cited by 32
Endogenous sex hormones and C‐reactive protein in healthy chinese men
Zhang, Y., Gao, Y., Tan, A., Yang, X., Zhang, H., Zhang, S., Wu, C., Lu, Z., Wang, M., Liao, M., et al. (2012) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2012.04359.x · Cited by 30
Lowndes, J., Sinnett, S., & Rippe, J. M. (2015) · Nutrients · doi:10.3390/nu7105430 · Cited by 36
Alkhouri, N., Eng, K., López, R., & Nobili, V. (2014) · SpringerPlus · doi:10.1186/2193-1801-3-407 · Cited by 33
Determination of insulin resistance in surgery: The choice of method is crucial
Baban, B., Thorell, A., Nygren, J., Bratt, A., & Ljungqvist, O. H. (2014) · Clinical Nutrition · doi:10.1016/j.clnu.2014.02.002 · Cited by 29
OBESITY, HYPERTENSION AND INSULIN RESISTANCE IN CHILDHOOD - A PILOT STUDY
Pastucha, D., Talafa, V., Malinčíková, J., Cíhalík, C., Hyjánek, J., Horáková, D., & Janout, V. (2010) · Biomedical Papers · doi:10.5507/bp.2010.013 · Cited by 30
Pathology of Congenital Generalized Lipodystrophy in Agpat2 –/– Mice
Vogel, P., Read, R. W., Hansen, G. M., Wingert, J., DaCosta, C. M., Buhring, L., & Shadoan, M. K. (2010) · Veterinary Pathology · doi:10.1177/0300985810383870 · Cited by 32
Sun, K., Lin, D., Li, F., Huang, C., Qi, Y., Xue, S., Tang, J., Yang, C. H., Yan, L., Ren, M., et al. (2015) · Lipids in Health and Disease · doi:10.1186/s12944-015-0153-8 · Cited by 31
Maxel, T., Smidt, K., Larsen, A., Bennetzen, M., Cullberg, K. B., Fjeldborg, K., Lund, S. A., Pedersen, S. B., & Rungby, J. (2015) · BMC Obesity · doi:10.1186/s40608-015-0076-y · Cited by 30
Glucose Metabolism in Primary Aldosteronism
Remde, H., Hanslik, G., Rayes, N., & Quinkler, M. O. (2015) · Hormone and Metabolic Research · doi:10.1055/s-0035-1565208 · Cited by 30
Wang, S., Yang, Q., Yu, S., Pan, R., Jiang, D., Liu, Y., Hu, H., Sun, W., Hong, X., Xue, H., et al. (2016) · Endocrine Journal · doi:10.1507/endocrj.ej15-0627 · Cited by 31
Hui, P., Zhao, L., Xie, Y., Wei, X., Ma, W., Wang, J., Hou, Y., Ning, J., Zhou, L., Guo, Q., et al. (2016) · The American Journal of the Medical Sciences · doi:10.1016/j.amjms.2015.12.002 · Cited by 31
Cacoub, P., Carrat, F., Bédossa, P., Lambert, J., Pénaranda, G., Pol, S., & Halfon, P. (2009) · Antiviral Therapy · doi:10.3851/imp1298 · Cited by 30
de Luis, D. A., Aller, R., Conde, R., Izaola, O., Sagrado, M. G., & Castrodeza, J. (2013) · Journal of Investigative Medicine · doi:10.2310/jim.0b013e318276161d · Cited by 30
Factors related to increased resting energy expenditure in men with liver cirrhosis
de Frías, C. P., Conchillo, M., Payeras, M., Iñarrairaegui, M., D’Avola, D., Frühbeck, G., Salvador, J., Rodríguez‐Fraile, M., Richter, J. Á., Mugueta, C., et al. (2015) · European Journal of Gastroenterology & Hepatology · doi:10.1097/meg.0000000000000516 · Cited by 32
Sadek, K. M., Beltagy, D. M., Saleh, E. A., et al. (2016) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2015-0596 · Cited by 30
Insulin resistance in a rural Maori community.
Tipene‐Leach, D., Pahau, H., Joseph, N., Coppell, K. J., McAuley, K. A., Booker, C. S., Williams, S., & Mann, J. I. (2004) · PubMed · Cited by 29
YANG, Z. K., Zhang, H., Niu, Y., Zhang, W., Zhu, L., Li, X., Lü, S., Fan, J., Li, X., Ning, G., et al. (2016) · Scientific Reports · doi:10.1038/srep37886 · Cited by 30
Silva, T. R., & Spritzer, P. (2017) · Menopause · doi:10.1097/gme.0000000000000793 · Cited by 32
A prospective study of the association between total sleep duration and incident hypertension
Yadav, D., Hyun, D.-S., Ahn, S. V., Koh, S. B., & Kim, J. (2016) · Journal of Clinical Hypertension · doi:10.1111/jch.12960 · Cited by 30
Djelti, F., Dhénain, M., Terrien, J., Picq, J., Hardy, I., Champeval, D., Perret, M., Schenker, E., Epelbaum, J., & Aujard, F. (2016) · Aging · doi:10.18632/aging.101148 · Cited by 33
Borel, A., Nazare, J., Baillot, A., Alméras, N., Tremblay, A., Bergeron, J., Poirier, P., & Després, J. (2016) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00278.2016 · Cited by 33
Nikitin, A. G., Potapov, V. Y., Brovkina, O., Koksharova, E., Ходырев, Д. С., Philippov, Y. I., Michurova, M. S., Шамхалова, М. Ш., Vikulova, O. K., Андреевна, С. С., et al. (2017) · PeerJ · doi:10.7717/peerj.3414 · Cited by 31
Cazzo, E., Jimenez, L. S., Gestic, M. A., Utrini, M. P., Chaim, F. H. M., Chaim, F. D. M., Pareja, J. C., & Chaim, É. A. (2017) · Obesity Surgery · doi:10.1007/s11695-017-2829-9 · Cited by 30
Vauzour, D., Rodríguez‐Ramiro, I., Rushbrook, S., Ipharraguerre, I. R., Bevan, D., Davies, S. E., Tejera, N., Mena, P. R., de Pascual‐Teresa, S., Rio, D. D., et al. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2017.10.002 · Cited by 30
Alam, S., Hasan, S. N., Mustafa, G., et al. (2017) · Journal of Translational Internal Medicine · doi:10.1515/jtim-2017-0021 · Cited by 30
Kearney, M., Perron, J., Marc, I., Weisnagel, S. J., Tchernof, A., & Robitaille, J. (2017) · Clinical Obesity · doi:10.1111/cob.12237 · Cited by 29
Cebeci, E., Çakan, C., Gürsu, M., Uzun, S., Karadağ, S., Koldaş, M., Çalhan, T., Helvacı, Ş. A., & Öztürk, S. (2018) · Experimental and Clinical Endocrinology & Diabetes · doi:10.1055/s-0043-121262 · Cited by 30
Carreras, N. L., Martorell, P., Chenoll, E., Genovés, S., Ramón, D., & Aleixandre, A. (2018) · Beneficial Microbes · doi:10.3920/bm2017.0141 · Cited by 32
Klakk, H., Kristensen, P. L., Andersen, L. B., Froberg, K., Møller, N. C., & Grøntved, A. (2018) · Preventive Medicine Reports · doi:10.1016/j.pmedr.2018.05.017 · Cited by 33
Travier, N., Buckland, G., Vendrell, J. J., Fernández‐Veledo, S., Peiró, I., Barco, S. D., Pernas, S., Zamora, E., Bellet, M., Vila, M. M., et al. (2018) · European Journal of Cancer Care · doi:10.1111/ecc.12861 · Cited by 31
Yang, J. W., Hong, N., Shim, J., Rhee, Y., & Kim, H. C. (2018) · Journal of Bone Metabolism · doi:10.11005/jbm.2018.25.2.123 · Cited by 30
Elevated RBP4 plasma levels were associated with diabetic retinopathy in type 2 diabetes
Li, J., Chen, X., Lu, X.-H., Zhang, C., Shi, Q., & Feng, L. (2018) · Bioscience Reports · doi:10.1042/bsr20181100 · Cited by 31
İmga, N. N., Karcı, A. Ç., Öztaş, D., Berker, D. S., & Güler, S. (2018) · Archives of Medical Science · doi:10.5114/aoms.2018.75864 · Cited by 31
Santos‐Parker, J. R., Santos-Parker, K. S., McQueen, M. B., Martens, C. R., & Seals, D. R. (2018) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00458.2018 · Cited by 31
Eshima, H., Tamura, Y., Kakehi, S., Nakamura, K., Kurebayashi, N., Murayama, T., Kakigi, R., Sakurai, T., Kawamori, R., & Watada, H. (2018) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00048.2018 · Cited by 29
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Ali, H., Zmuda, J. M., Cvejkus, R., Kershaw, E. E., Kuipers, A. L., Oczypok, E. A., Wheeler, V. W., Bunker, C. H., & Miljkovic, I. (2019) · Journal of the Endocrine Society · doi:10.1210/js.2018-00325 · Cited by 30
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Prevalence of Advanced Liver Fibrosis in Patients With Severe Psoriasis
Maybury, C. M., Porter, H. F., Kloczko, E., et al. (2019) · JAMA Dermatology · doi:10.1001/jamadermatol.2019.0721 · Cited by 30
Stoker, C., Andreoli, M. F., Kass, L., Bosquiazzo, V. L., Rossetti, M. F., Canesini, G., Luque, E. H., & Ramos, J. G. (2019) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2019.110614 · Cited by 30
Morrison, S. A., Fazeli, P. L., Gower, B. A., Willig, A. L., Younger, J., Sneed, N. M., & Vance, D. E. (2019) · Journal of the Association of Nurses in AIDS Care · doi:10.1097/jnc.0000000000000110 · Cited by 30
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NESBITT, S., Julius, S., LEONARD, D., Egan, B. M., & Grozinski, M. (2005) · American Journal of Hypertension · doi:10.1016/j.amjhyper.2005.01.021 · Cited by 30
Goldenberg, N., Glueck, C. J., Loftspring, M. C., Sherman, A., & Wang, P. (2004) · Metabolism · doi:10.1016/j.metabol.2004.08.007 · Cited by 30
Wybrańska, I., Malczewska-Malec, M., Niedbał, S., Naskalski, J. W., & Dembinska-Kiec, A. (2003) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm.2003.076 · Cited by 30
Ho, R. C., Davy, K. P., Davy, B. M., & Melby, C. L. (2002) · Metabolism · doi:10.1053/meta.2002.35577 · Cited by 30
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Piecha, G., Adamczak, M., Chudek, J. T., et al. (2007) · Kidney & Blood Pressure Research · doi:10.1159/000103279 · Cited by 30
Limone, P. P. (2003) · Journal of Infection · doi:10.1016/s0163-4453(03)00055-0 · Cited by 30
Falhammar, H., Thoren, M., & Hagenfeldt, K. (2008) · Journal of Endocrinological Investigation · doi:10.1007/bf03345586 · Cited by 30
Undiagnosed dysglycaemia and inflammation in cardiovascular disease
Johansen, O. E., Birkeland, K., Brustad, E., Aaser, E., Lindahl, A. K., Midha, R., Ueland, T., Aukrust, P., & Gullestad, L. L. (2006) · European Journal of Clinical Investigation · doi:10.1111/j.1365-2362.2006.01679.x · Cited by 30
Gómez, J. M., Sahún, M. J. S., Vila, R., Domènech, P., Catalina, P. F., Soler, J., & Badimón, L. (2006) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2006.02518.x · Cited by 30
Park, H., Kyeong-Ho, Park, D., Lee, H., Chang, H. W., Kim, Y.-S., & Cho, K. H. (2008) · Journal of Stroke and Cerebrovascular Diseases · doi:10.1016/j.jstrokecerebrovasdis.2008.06.004 · Cited by 30
Reinehr, T., de Sousa, G., & Roth, C. L. (2007) · Journal of Pediatric Gastroenterology and Nutrition · doi:10.1097/mpg.0b013e3180406a24 · Cited by 30
Weigensberg, M. J., Cruz, M. L., & Goran, M. I. (2003) · Diabetes Care · doi:10.2337/diacare.26.7.2094 · Cited by 31
Kanauchi, M., Tsujimoto, N., & Hashimoto, T. (2002) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(01)00313-8 · Cited by 31
Matteucci, E., Rosada, J., Pinelli, M., et al. (2006) · Journal of Hypertension · doi:10.1097/01.hjh.0000242398.60838.5d · Cited by 30
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Herbert, A. G., Liu, C., Karamohamed, S., Liu, J., Manning, A. K., Fox, C. S., Meigs, J. B., & Cupples, L. A. (2006) · Obesity · doi:10.1038/oby.2006.165 · Cited by 30
Kawada, T., Otsuka, T., Inagaki, H., Wakayama, Y., Li, Q., Li, Y. J., & Katsumata, M. (2010) · Obesity Research & Clinical Practice · doi:10.1016/j.orcp.2009.12.004 · Cited by 30
Sir‐Petermann, T., Bárbara Angel, B., Maliqueo, M. A., Santos, J. L., Riesco, M. D., Toloza, H., & Pérez‐Bravo, F. (2004) · Nutrition · doi:10.1016/j.nut.2004.08.017 · Cited by 30
Glucose homoeostasis in rats exposed to acute intermittent hypoxia
Rafacho, A., Gonçalves-Neto, L. M., Ferreira, F. B. D., Protzek, A. O. P., Boschero, A. C., Nunes, E. A., & Zoccal, D. B. (2013) · Acta Physiologica · doi:10.1111/apha.12118 · Cited by 31
Usta, M., Turan, E., Aral, H., et al. (2011) · Journal of Clinical Laboratory Analysis · doi:10.1002/jcla.20471 · Cited by 30
Crinò, A., Giorgio, G. D., Manco, M., Grugni, G., & Maggioni, A. (2007) · Hormone Research in Paediatrics · doi:10.1159/000100371 · Cited by 30
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Reeds, D. N., Cade, W. T., Patterson, B. W., Powderly, W. G., Klein, S., & Yarasheski, K. E. (2006) · Diabetes · doi:10.2337/db06-0255 · Cited by 30
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Tan, C., Chew, L. S., Chio, L. F., Tai, E. S., Lim, H., Lim, S. C., Jayakumar, L., Eng, H. K., & Packard, C. J. (2001) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(00)00211-4 · Cited by 30
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Unnikrishnan, A. G., Singh, S., & Sanjeevi, C. B. (2004) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1337.018 · Cited by 30
Lawlor, D. A., Timpson, N. J., Ebrahim, S. B. J., Day, I. N. M., & Smith, G. D. (2006) · European Heart Journal · doi:10.1093/eurheartj/ehi833 · Cited by 30
Use of glimepiride and insulin sensitizers in the treatment of type 2 diabetes--a study in Indians.
Ramachandran, A., Snehalatha, C., Salini, J., & Vijay, V. (2004) · PubMed · Cited by 30
Lewis, J. G., Shand, B. I., Elder, P. A., & Scott, R. S. (2004) · Diabetes Obesity and Metabolism · doi:10.1111/j.1462-8902.2004.00343.x · Cited by 30
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Gibson, F., Herçberg, S., & Froguel, P. (2005) · Diabetes · doi:10.2337/diabetes.54.10.3040 · Cited by 30
Carotid hemodynamic alterations in hypertensive patients with insulin resistance
Watanabe, S. (2002) · American Journal of Hypertension · doi:10.1016/s0895-7061(02)02988-6 · Cited by 30
An Acyl-CoA Synthetase Gene Family in Chromosome 16p12 May Contribute to Multiple Risk Factors
Iwai, N., Mannami, T., Tomoike, H., Ono, K., & Iwanaga, Y. (2003) · Hypertension · doi:10.1161/01.hyp.0000064944.60569.87 · Cited by 30
Wagner, J. A., Larson, P., Weiss, S., Miller, J., Doebber, T. W., Wu, M., Moller, D. E., & Gottesdiener, K. M. (2005) · The Journal of Clinical Pharmacology · doi:10.1177/0091270004273136 · Cited by 30
Adiponectin receptors gene expression in lymphocytes of obese and anorexic patients
Alberti, L., Gilardini, L., Girola, A., Moro, M., Cavagnini, F., & Invitti, C. (2006) · Diabetes Obesity and Metabolism · doi:10.1111/j.1463-1326.2006.00614.x · Cited by 30
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Ruige, J. B., Mertens, I. L., Bartholomeeusen, E., Dirinck, E. L., Ferrannini, E., & Gaal, L. F. V. (2006) · Obesity · doi:10.1038/oby.2006.142 · Cited by 29
Lemne, C. E., & Brismar, K. (1998) · PubMed · Cited by 31
Misra, A., Chaudhary, D., Vikram, N. K., Mittal, V., Devi, J. R., Pandey, R. M., Khanna, N., Sharma, R., & Peshin, S. (2002) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(01)00364-3 · Cited by 30
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Malacara, J. M., Fajardo, M. E., & Nava, L. E. (2001) · Steroids · doi:10.1016/s0039-128x(00)00223-3 · Cited by 30
Furutani, M., Nakashima, T., Sumida, Y., Hirohama, A., Yoh, T., Kakisaka, Y., Mitsuyoshi, H., Senmaru, H., & Okanoue, T. (2003) · Liver International · doi:10.1034/j.1600-0676.2003.00841.x · Cited by 30
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Phillips, M. L., Lewis, M., Chew, V., Kow, L., Slavotinek, J., Daniels, L., Valentine, R., Toouli, J., & Thompson, C. H. (2005) · Obesity Surgery · doi:10.1381/096089205774859353 · Cited by 30
Gloyn, A. L., Ellard, S., Shepherd, M. H., Howell, R. T., Parry, E. M., Jefferson, A., Levy, E. R., & Hattersley, A. T. (2002) · Diabetes · doi:10.2337/diabetes.51.7.2329 · Cited by 30
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Vague, P., & Nguyen, L. T. K. (2002) · Diabetes · doi:10.2337/diabetes.51.2007.s240 · Cited by 30
Araújo, D. A. C., Farias, M. L. F., & Andrade, A. T. L. (2002) · Climacteric · doi:10.1080/cmt.5.3.286.292 · Cited by 30
Dubé, M. P., Edmondson‐Melançon, H., Qian, D., Aqeel, R., Johnson, D. L., & Buchanan, T. A. (2001) · JAIDS Journal of Acquired Immune Deficiency Syndromes · doi:10.1097/00042560-200106010-00006 · Cited by 30
Morrison, J., Gruppo, R., Glueck, C., Stroop, D., Fontaine, R., Wang, P., & Smith, K. L. (2004) · Metabolism: Clinical and Experimental · doi:10.1016/j.metabol.2003.10.029 · Cited by 32
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Comlekci, A., Akpınar, H., Yeşil, Ş., Okan, İ., Ellidokuz, E., Okan, A., Ersöz, G., Tankurt, E., & Batur, Y. (2003) · Scandinavian Journal of Gastroenterology · doi:10.1080/00365520310003877 · Cited by 29
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Martín‐Martín, A., Orduña‐Malea, E., Ayllón, J. M., & López‐Cózar, E. D. (2014) · arXiv (Cornell University) · doi:10.48550/arxiv.1410.8464 · Cited by 48
Kim, K.-S., Oh, H.-J., Kim, J.-W., Lee, Y.-K., Kim, S.-K., Park, S.-W., Kim, Y.-L., Park, W.-K., & Cho, Y.-W. (2010) · Korean Diabetes Journal · doi:10.4093/kdj.2010.34.2.119 · Cited by 28
Metabolic syndrome and endothelial fibrinolytic capacity in obese adults
Van Guilder, G. P., Hoetzer, G. L., Greiner, J. J., Stauffer, B. L., & DeSouza, C. A. (2008) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00564.2007 · Cited by 29
Suman, R. K., Ray, I., Maheshwari, U., Borde, M. K., & Deshmukh, Y. (2016) · Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy · doi:10.2147/dmso.s109599 · Cited by 34
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Associations of healthy dietary patterns with mortality among people with prediabetes
Li, L., Wan, Z., Geng, T., Lu, Q., Zhu, K., Qiu, Z., Zhang, X., Liu, Y., Tian, Q., Liu, L., et al. (2022) · European Journal of Nutrition · doi:10.1007/s00394-022-03078-5 · Cited by 32
Al‐Rawaf, H. A., Gabr, S. A., Iqbal, A., & Alghadir, A. H. (2023) · Medicina · doi:10.3390/medicina59071320 · Cited by 34
Petrelli, A., Cugnata, F., Carnovale, D., Bosi, E., Libman, I. M., Piemonti, L., Cuthbertson, D. D., & Sosenko, J. M. (2023) · Diabetologia · doi:10.1007/s00125-023-06034-y · Cited by 37
Soares, J. M., Hayashida, S. A. Y., Marcondes, J. A. M., Maciel, G. A. R., Barcellos, C. R. G., Maffazioli, G. D. N., Monteiro, K. K. A. C., Turri, J. A. O., Azziz, R., & Baracat, E. C. (2023) · Biomedicines · doi:10.3390/biomedicines11123262 · Cited by 29
Metadata
- Authors
- Matthews, D. R., Hosker, J. P., Rudenski, A. S., Naylor, B. A., Treacher, D. F., & Turner, R. C.
- Affiliations
- University of Oxford (GB)
- ORCID
- Matthews, D. R.
- Venue
- Diabetologia
- Published
- 1985-07
- Volume
- 28
- Issue
- 7
- Pages
- 412-419
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2160234571
- Cited by
- 31,502
- References
- 21
- Citations by year
- 2026: 933 · 2025: 1060 · 2024: 1240 · 2023: 1291 · 2022: 1489 · 2021: 1528 · 2020: 1424 · 2019: 1427 · 2018: 1456 · 2017: 1440 · 2016: 1481 · 2015: 1682 · 2014: 1693 · 2013: 1621 · 2012: 1518
- FWCI
- 7.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- HOMA, insulin resistance, beta-cell function, fasting blood glucose, fasting insulin, hyperglycaemic clamp, euglycaemic clamp, intravenous glucose tolerance test, insulin receptor binding, type 2 diabetes
- MeSH terms
- Adult, Blood Glucose, Computers, Diabetes Mellitus, Type 2, Erythrocytes, Fasting, Homeostasis, Humans, Insulin, Insulin Resistance, Islets of Langerhans, Middle Aged, Monocytes, Receptor, Insulin
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 2026-10-14, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-14 (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 ›
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