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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
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)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The 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.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The 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.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The 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.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The 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.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The 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
Sorted by citations
Items 20,301–20,400 of 31,469
Association of TRB3 Q84R polymorphism with polycystic ovary syndrome in Chinese women
Zhang, X., Fu, L., Zhang, Q., Yan, L., Ma, Y., Tu, B., Liu, N., & Qiao, J. (2011) · Reproductive Biology and Endocrinology · doi:10.1186/1477-7827-9-46 · Cited by 12
The Role of Metabolic Syndrome and Related Clinical Variables in Determining CEA Levels
Esteghamati, A., Zandieh, A., Saadipoor, A., Hafezi‐Nejad, N., Noshad, S., Esteghamati, A., Seyedahmadinejad, S., & Nakhjavani, M. (2014) · Advances in Clinical and Experimental Medicine · doi:10.17219/acem/37334 · Cited by 11
Gualano, B., Ugrinowitsch, C., Artioli, G. G., Benatti, F. B., Scagliusi, F. B., Harris, R. C., & Lancha, A. H. (2008) · Journal of the International Society of Sports Nutrition · doi:10.1186/1550-2783-5-16 · Cited by 12
Objective Habitual Physical Activity and Estradiol Levels in Obese Latina Adolescents
Gyllenhammer, L. E., Vanni, A. K., Byrd-Williams, C. E., Kalan, M. J., Bernstein, L., & Davis, J. N. (2013) · Journal of Physical Activity and Health · doi:10.1123/jpah.10.5.727 · Cited by 11
POTENTIAL MARKERS OF INSULIN RESISTANCE IN HEALTHY VS OBESE AND OVERWEIGHT SUBJECTS
Horáková, D., Stejskal, D., Pastucha, D., Muchova, L., & Janout, V. (2010) · Biomedical Papers · doi:10.5507/bp.2010.037 · Cited by 11
Gelens, M. A. C. J., Christiaans, M. H. L., & van Hooff, J. P. (2007) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfm544 · Cited by 11
Rask‐Andersen, M., Philippot, G., Moschonis, G., Dedoussis, G. V., Μanios, Y., Marcus, C., Fredriksson, R., & Schiöth, H. B. (2014) · PLoS ONE · doi:10.1371/journal.pone.0093193 · Cited by 12
Vitamin D Levels in Overweight/Obese Adults With and Without Metabolic Syndrome
Karataş, S., Hekimsoy, Z., Dinç, G., et al. (2013) · Journal of Endocrinology and Metabolism · doi:10.4021/jem.v3i3.182 · Cited by 11
HOMA-AD in Assessing Insulin Resistance in Lean Noncirrhotic HCV Outpatients
Michalczuk, M. T., Kappel, C., Birkhan, O. A., Bragança, A. C., & Álvares‐da‐Silva, M. R. (2012) · International Journal of Hepatology · doi:10.1155/2012/576584 · Cited by 11
Beneficial impact of L-carnitine in liver: a study in a rat model of syndrome X
Rajasekar, P., Viswanathan, P., & Anuradha, C. V. (2007) · Amino Acids · doi:10.1007/s00726-007-0559-3 · Cited by 11
Karatela, R. A., & Sainani, G. S. (2009) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2009.08.043 · Cited by 11
van Bürck, L., Blutke, A., Kautz, S., Rathkolb, B., Klaften, M., Wagner, S., Kemter, E., de Angelis, M. H., Wolf, E., Aigner, B., et al. (2009) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00465.2009 · Cited by 12
Asymmetric dimethylarginine level in hyperglycemic gestation
Sertkaya, A., Kafkaslı, A., Türkçüoğlu, İ., et al. (2011) · Endocrine · doi:10.1007/s12020-011-9461-6 · Cited by 11
Paquet, C., Propsting, S. L., & Daniel, M. (2013) · Public Health Nutrition · doi:10.1017/s1368980013000542 · Cited by 13
Matthews, D. R., Zinman, B., Tong, C., et al. (2015) · Diabetic Medicine · doi:10.1111/dme.13033 · Cited by 11
Self-citationde Luis, D. A., Sagrado, M. G., Conde, R., Aller, R., Izaola, O., Mj, C., & Romero, E. (2010) · PubMed · Cited by 11
Insulin resistance in type 2 diabetic Nigerians.
A.G., A. G. B., & Onyemelukwe, G. C. (2019) · International Journal of Diabetes and Metabolism · doi:10.1159/000497570 · Cited by 11
Berstein, L. M., Евгеньевна, П. Т., Turkevich, E. A., Vasilyev, D. A., Baltrukova, A. N., Коваленко, И. М., & Берлев, И. В. (2015) · Future Science OA · doi:10.4155/fso.15.68 · Cited by 11
Disease Progression Analysis: Towards Mechanism-Based Models
Schmidt, S., Post, T. M., Boroujerdi, M. A., van Kesteren, C., Ploeger, B. A., Pasqua, O. E. D., & Danhof, M. (2010) · AAPS advances in the pharmaceutical sciences series · doi:10.1007/978-1-4419-7415-0_19 · Cited by 11
Acculturation and Insulin Resistance Among US Chinese Immigrant Women
Tseng, M., & Fang, C. Y. (2015) · Ethnicity & Disease · doi:10.18865/ed.25.4.443 · Cited by 11
Measurement and Correlation of Indices of Insulin Resistance in Patients on Peritoneal Dialysis
King-Morris, K., Değer, S. M., Hung, A. M., Egbert, P., Ellis, C. D., Graves, A. J., Shintani, A., & Ikizler, T. A. (2015) · Peritoneal Dialysis International · doi:10.3747/pdi.2013.00296 · Cited by 11
Plasma catecholamines in Nigerians with primary hypertension.
Adebiyi, A. A., Akinosun, O. M., Nwafor, C. E., & Falase, A. O. (2011) · PubMed · Cited by 10
Myocardial and metabolic dysfunction in type 2 diabetic rats: impact of ghrelin
Hussein, A. M., Abdel‐Aziz, A., Gabr, M., & Hemmaid, K. Z. (2012) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/y11-103 · Cited by 11
Effect of oral glucose on acylated and total ghrelin secretion in acromegalic patients.
Isidro, M. L., Nemiña, R., García‐Buela, J., et al. (2007) · PubMed · Cited by 11
Korkmaz, H., Ünler, G. K., Göktürk, H. S., et al. (2015) · European Journal of Gastroenterology & Hepatology · doi:10.1097/meg.0000000000000407 · Cited by 11
Özkan, E. A., Khosroshahi, H. E., Serin, H. İ., et al. (2015) · PubMed · Cited by 11
Tura, A., bl, C. G. O., Moro, E., & Pacini, G. (2016) · Endocrine Journal · doi:10.1507/endocrj.ej16-0298 · Cited by 11
Gastric bypass surgery reveals independency of obesity and diabetes melitus type 2
Fenger, M., Hansen, D. L., Worm, D., Hvolris, L., Kristiansen, V. B., Carlsson, E. R., & Madsbad, S. (2016) · BMC Endocrine Disorders · doi:10.1186/s12902-016-0140-8 · Cited by 11
Hu, X., Ma, X., Luo, Y., Xu, Y., Xiong, Q., Pan, X., Bao, Y., & Jia, W. (2016) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2016.11.009 · Cited by 11
Heggen, E., Svendsen, M., & Tonstad, S. (2017) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2016.12.011 · Cited by 11
Li, Y., Ran, W., Zhang, J., Chen, S., Li, Y., Luo, D., Wang, C., & Jia, W. (2017) · IUBMB Life · doi:10.1002/iub.1592 · Cited by 11
Ha, J., Jo, K., Lim, D., et al. (2017) · PLoS ONE · doi:10.1371/journal.pone.0175132 · Cited by 11
Qiao, F., Longley, K. R., Feng, S., Schnack, S., Gao, H., Li, Y., Schlenker, E. H., & Wang, H. (2017) · Physiological Reports · doi:10.14814/phy2.13260 · Cited by 10
Fujii, C., Kawai, T., Azuma, K., Oguma, Y., Katsukawa, F., Hirose, H., Tanaka, K., Meguro, S., Matsumoto, H., & Itoh, H. (2017) · Journal of Diabetes Research · doi:10.1155/2017/1567467 · Cited by 11
Madeira, M. S. M. D. S., Rolo, E. A., Lopes, P. A., Ramos, D. A., Alfaia, C. M., Pires, V. M. R., Martins, S. V., Pinto, R. M. A., & Prates, J. A. M. (2017) · Journal of the Science of Food and Agriculture · doi:10.1002/jsfa.8504 · Cited by 11
Billeter, A. T., Vittas, S., Israel, B., Scheurlen, K. M., Hidmark, A. S., Fleming, T., Kopf, S., Büchler, M. W., & Müller-Stich, B. P. (2017) · Langenbeck s Archives of Surgery · doi:10.1007/s00423-017-1601-x · Cited by 11
Silva, M. D., Chartrand, D. J., Vohl, M., Barbier, O., & Rudkowska, I. (2017) · Journal of Personalized Medicine · doi:10.3390/jpm7030008 · Cited by 11
Micić, D., Lalic, N. M., Djukić, V., et al. (2017) · Journal of Medical Biochemistry · doi:10.1515/jomb-2017-0043 · Cited by 11
Hu, X., He, X., Ma, X., Su, H., Ying, L., Peng, J., Wang, Y., Bao, Y., Zhou, J., & Jia, W. (2017) · Diabetic Medicine · doi:10.1111/dme.13534 · Cited by 11
Low serum uric acid concentration augments insulin effects on the prevalence of metabolic syndrome
Porchia, L. M., González-Mejía, M. E., Torres‐Rasgado, E., Ruiz‐Vivanco, G., & Pérez-Fuentes, R. (2017) · Diabetes & Metabolic Syndrome Clinical Research & Reviews · doi:10.1016/j.dsx.2017.12.012 · Cited by 10
Kim, J. K., Lee, A., Kang, J., Yu, B.-Y., & Kim, S.-J. (2018) · Korean Journal of Family Medicine · doi:10.4082/kjfm.2018.39.1.42 · Cited by 11
Lipid accumulation product index in HIV-infected patients: a marker of cardiovascular risk
Guimarães, M. M., Greco, D., Moreira, A., Guimarães, N., Freire, C. V., Rohlfs, B. G., & Machado, L. J. D. C. (2018) · Brazilian Journal of Infectious Diseases · doi:10.1016/j.bjid.2018.03.006 · Cited by 9
Philippe, M., Gatterer, H., Eder, E. M., Dzien, A., Somavilla, M., Melmer, A., Ebenbichler, C. F., Müller, T., & Burtscher, M. (2017) · PubMed · Cited by 11
Serum adiponectin level in osteoporotic postmenopausal women with type 2 diabetes mellitus
Alosami, M. H., & Hameed, E. K. (2018) · Diabetes & Metabolic Syndrome Clinical Research & Reviews · doi:10.1016/j.dsx.2018.05.019 · Cited by 11
Alissa, E. M. (2018) · Journal of Family Medicine and Primary Care · doi:10.4103/jfmpc.jfmpc_194_17 · Cited by 11
The Relationship between Aortic Knob Width and Metabolic Syndrome
Lee, E., Han, J. H., Kwon, K.-Y., et al. (2018) · Korean Journal of Family Medicine · doi:10.4082/kjfm.17.0038 · Cited by 11
Pellegrin, M. C., Michelon, D., Faleschini, E., Germani, C., Barbi, E., & Tornese, G. (2019) · Journal of Clinical Research in Pediatric Endocrinology · doi:10.4274/jcrpe.galenos.2019.2019.0281 · Cited by 11
N-acetylcysteine with low-dose estrogen reduces cardiac ischemia-reperfusion injury
Sivasinprasasn, S., Palee, S., Chattipakorn, K., Jaiwongkum, T., Apaijai, N., Pratchayasakul, W., Chattipakorn, S. C., & Chattipakorn, N. (2019) · Journal of Endocrinology · doi:10.1530/joe-19-0108 · Cited by 11
Stavnsbo, M., Skrede, T., Aadland, E., Aadland, K. N., Chinapaw, M. J. M., Anderssen, S. A., Andersen, L. B., & Resaland, G. K. (2019) · PLoS ONE · doi:10.1371/journal.pone.0220239 · Cited by 11
Rafferty, A. R., Geraghty, A. A., Kennelly, M. A., O’Brien, E. C., Reji, R. M., Mehegan, J., Segurado, R., Smith, T., Maguire, O., Cronin, M., et al. (2020) · Reproductive Sciences · doi:10.1007/s43032-019-00045-0 · Cited by 11
Joung, K. H., Kim, J. M., Choung, S., Lee, J. H., Kim, H. J., & Ku, B. J. (2020) · Annals of Translational Medicine · doi:10.21037/atm.2020.01.17 · Cited by 10
Heeba, G. H., El-Deen, R. M., Abdellatif, R., & Khalifa, M. M. A. (2020) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2019-0487 · Cited by 12
Causal Association of Haptoglobin With Obesity in Mexican Children: A Mendelian Randomization Study
Vázquez‐Moreno, M. A., Locia‐Morales, D., Pérez‐Herrera, A., Gómez-Díaz, R. A., González‐Dzib, R., Valdez-González, A. L., Flores‐Alfaro, E., Corona-Salazar, P., Suárez‐Sánchez, F., Gómez-Zamudio, J. H., et al. (2020) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaa213 · Cited by 11
Lim, J., Park, H. S., Lee, S. K., Jang, Y. J., Lee, Y. J., & Heo, Y. (2015) · Obesity Surgery · doi:10.1007/s11695-015-1808-2 · Cited by 10
Joo, E., Muraoka, A., Hamasaki, A., Harada, N., Yamane, S., Kondo, Y., Suzuki, K., Nasteska, D., Shibue, K., Harada, T., et al. (2014) · Journal of Diabetes Investigation · doi:10.1111/jdi.12289 · Cited by 12
Nemes, A., Lengyel, C., Forster, T., Várkonyi, T. T., Takács, R., Nagy, I., Kempler, P., Lonovics, J., & Csanády, M. (2005) · Diabetic Medicine · doi:10.1111/j.1464-5491.2005.01681.x · Cited by 11
Tarsitano, C. A. B., Paffaro, V. A., Pauli, J. R., da Silva, G. H., Saad, M. J. A., Salgado, I., da Cruz‐Höfling, M. A., & Hyslop, S. (2007) · Cell and Tissue Research · doi:10.1007/s00441-007-0411-9 · Cited by 11
Mavri, A., Bastelica, D., Poggi, M., Morange, P., Peiretti, F., Verdier, M., Juhan-Vague, I., & Alessi, M. (2007) · Thrombosis and Haemostasis · doi:10.1160/th06-06-0314 · Cited by 11
Sun, X., Cao, Z., Tanisawa, K., Ito, T., Oshima, S., & Higuchi, M. (2014) · Nutrients · doi:10.3390/nu7010091 · Cited by 11
Elseweidy, M. M., Sadik, N. A. H., Malek, M. M., & Amin, R. S. (2013) · Pathology - Research and Practice · doi:10.1016/j.prp.2013.09.010 · Cited by 11
Rizzo, M. R., Ragno, E., Barbieri, M., et al. (2002) · Atherosclerosis · doi:10.1016/s0021-9150(01)00575-5 · Cited by 11
Hong, L. ‐., & Hsieh, P.-H. (2007) · American Journal of Hypertension · doi:10.1016/j.amjhyper.2006.11.004 · Cited by 11
Ezenwaka, C. E., & Kalloo, R. (2005) · PubMed · Cited by 11
Lee, M. Y., Koh, J. H., Nam, S. M., Jung, P. M., Sung, J. K., Kim, S., Shin, J. Y., Shin, Y. G., & Chung, C. H. (2008) · Yonsei Medical Journal · doi:10.3349/ymj.2008.49.6.901 · Cited by 10
Donadon, V., Balbi, M., Perciaccante, A., et al. (2009) · Clinical Medicine Insights Endocrinology and Diabetes · doi:10.4137/cmed.s3116 · Cited by 11
Mori, Y., Hoshino, K., Yokota, K., Itoh, Y., & Tajima, N. (2006) · Endocrine · doi:10.1385/endo:29:2:357 · Cited by 11
Glucose intolerance in a xenotransplantation model: studies in alpha‐gal knockout mice
Dahl, K., Buschard, K., Gram, D. X., d’Apice, A. J. F., & Hansen, A. K. (2006) · Apmis · doi:10.1111/j.1600-0463.2006.apm_393.x · Cited by 11
Smaller Hip Circumference is Associated with Dyslipidemia and the Metabolic Syndrome in Obese Women
Dixon, J. B., Strauss, B. J., Laurie, C., et al. (2007) · Obesity Surgery · doi:10.1007/s11695-007-9142-y · Cited by 11
Kamarudin, N., Hew, F. L., Christopher, M., Alford, J., Rantzau, C., Ward, G. M., & ALFORD, F. P. (1999) · Metabolism · doi:10.1016/s0026-0495(99)90148-8 · Cited by 11
Gaillard, T. R., Schuster, D., & Osei, K. (2008) · Journal of the American Society of Hypertension · doi:10.1016/j.jash.2008.07.003 · Cited by 11
Troglitazone corrects metabolic changes but not vascular dysfunction in dietary-obese rats
Naderali, E. K., Pickavance, L. C., Wilding, J. P. H., Doyle, P. J., & Williams, G. (2001) · European Journal of Pharmacology · doi:10.1016/s0014-2999(01)00866-4 · Cited by 10
Lee, W., Lee, W.-L., Tang, Y., Liang, K., Chien, Y.-H., Tsou, S. S., & Sheu, W. H. (2007) · Clinica Chimica Acta · doi:10.1016/j.cca.2007.12.013 · Cited by 11
Insulin resistance and pre-eclampsia: a role for tumor necrosis factor-α
Anim‐Nyame, N., Sooranna, S. R., Jones, J., Alaghband-Zadeh, J., Steer, P. J., & Johnson, M. R. (2004) · Gynecological Endocrinology · doi:10.1080/09513590410001667832 · Cited by 11
Effect of Growth Hormone and Oxandrolone Treatment on Glucose Metabolism in Turner Syndrome
JOSS, E. E., Zurbrügg, R. P., Tönz, O., & Mullis, P. (2000) · Hormone Research in Paediatrics · doi:10.1159/000023505 · Cited by 11
Keulen, E. T. P., Schaper, N. C., Houben, A. J. H. M., van Lin, J. M. J. P., Lutgens, I., Rijkers, K., Dallinga‐Thie, G. M., & de Bruin, T. W. (2002) · Atherosclerosis · doi:10.1016/s0021-9150(02)00021-7 · Cited by 11
Erkkilä, A. T., Schwab, U., Ågren, J. J., Hallikainen, M., Gylling, H., & Uusitupa, M. I. J. (2007) · European Journal of Clinical Nutrition · doi:10.1038/sj.ejcn.1602620 · Cited by 11
Hölzl, B., Iglseder, B., Stadlmayr, A., Hedegger, M., Morè, E., Reiter, R., Sandhofer, F., & Paulweber, B. (2003) · European Journal of Clinical Investigation · doi:10.1046/j.1365-2362.2003.01113.x · Cited by 11
Katsuki, A., Urakawa, H., Gabazza, E. C., Murashima, S., Nakatani, K., TOGASHI, K., Yano, Y., Adachi, Y., & Sumida, Y. (2005) · Endocrine Journal · doi:10.1507/endocrj.52.253 · Cited by 11
Emergence of Cardiovascular Risk Factors From Mild Obesity in Japanese Elementary School Children
Yoshinaga, M., Sameshima, K., Jougasaki, M., et al. (2006) · Diabetes Care · doi:10.2337/dc06-2538 · Cited by 11
Liu, H., Chen, S., Zhang, S., et al. (2007) · Journal of genetics and genomics/Journal of Genetics and Genomics · doi:10.1016/s1673-8527(07)60099-x · Cited by 11
Aguilar-Salinas, C. A., Rojas, R., Gomez-Perez, F. J., Valles, V., Franco, A., Oláiz, G., TAPIA-CONYER, R. C., Sepúlveda, J., & Rull, J. A. (2002) · Salud Pública de México · doi:10.1590/s0036-36342002000600007 · Cited by 13
Falchi, M., Wilson, S. G., Paximadas, D., Swaminathan, R., & Spector, T. D. (2008) · Diabetes · doi:10.2337/db07-0708 · Cited by 11
Metabolic implications of GH treatment in small for gestational age
Delemarre, E. M., Rotteveel, J., & de Waal, H. A. D. (2007) · European Journal of Endocrinology · doi:10.1530/eje-07-0163 · Cited by 11
Masuo, K., Katsuya, T., Fu, Y., et al. (2005) · Hypertension · doi:10.1161/01.hyp.0000170464.41776.98 · Cited by 11
Effect of Weight Loss on the Pulsatile Insulin Secretion
Zˇarković, M., Ćirić, J., Penezić, Z., Trbojević, B., & Drezgić, M. (2000) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.85.10.6919 · Cited by 11
Protective effects of SP600125 in a diet-induced rat model of non-alcoholic steatohepatitis
Hu, Y., & Liu, X. (2009) · Scandinavian Journal of Gastroenterology · doi:10.3109/00365520903312441 · Cited by 11
Population-based modeling to demonstrate extrapancreatic effects of tolbutamide
Rostami‐Hodjegan, A., Peacey, S. R., George, E., Heller, S. R., & Tucker, G. T. (1998) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1998.274.4.e758 · Cited by 11
Kowalska, I., Strączkowski, M., Nikołajuk, A., Kinalska, I., Górska, M., Prokop, J., Bachórzewska-Gajewska, H., & Musial, W. J. (2006) · PubMed · Cited by 11
Waist circumference, metabolic syndrome and coronary artery disease in a Pakistani cohort
Wierzbicki, A. S., Nishtar, S., Lumb, P. J., et al. (2007) · International Journal of Cardiology · doi:10.1016/j.ijcard.2007.05.036 · Cited by 11
Proinsulin in Girls: Relationship to Obesity, Hyperinsulinemia, and Puberty
Chin, D., Oberfield, S. E., Silfen, M. E., McMahon, D. J., Manibo, A. M., Accili, D., & Levine, L. S. (2002) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2001-011535 · Cited by 11
Impaired Glucose and Insulin Metabolism in Borderline Hypertension
Lemne, C. E., Efendić, S., Hamsten, A., & Fairé, U. D. (1994) · Blood Pressure · doi:10.3109/08037059409102276 · Cited by 11
Correction of Hypothyroidism Leads to Change in Lean Body Mass without Altering Insulin Resistance
Sirigiri, S., Vaikkakara, S., Sachan, A., Srinivasarao, P., Epuri, S., Anantarapu, S., Mukka, A., Chokkapu, S. R., Venkatanarasu, A., & Poojari, R. (2016) · European Thyroid Journal · doi:10.1159/000448889 · Cited by 11
Szewieczek, J., Dulawa, J., Strzałkowska, D., Batko-Szwaczka, A., & Hornik, B. (2009) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2008.02.006 · Cited by 10
Madjd, A., Taylor, M. A., Delavari, A., Malekzadeh, R., Macdonald, I. A., & Farshchi, H. R. (2019) · Obesity · doi:10.1002/oby.22416 · Cited by 10
Rhaiem, T. B., Owczarek, A. J., Wójtowicz, M., Ciura, D., Madej, P., Chudek, J. T., & Olszanecka‐Glinianowicz, M. (2025) · Life · doi:10.3390/life15050691 · Cited by 11
Hjorth, T., Schadow, A. M., Revheim, I., Spielau, U., Meyer, K., Rieder, A., Varela, P., Ballance, S., Koerner, A., Landberg, R., et al. (2025) · American Journal of Clinical Nutrition · doi:10.1016/j.ajcnut.2025.06.018 · Cited by 12
Harray, A. J., Lucas, A. D., Herrmann, S., Vlaskovsky, P., Elagali, A. E. M., Seewoo, B. J., Chan, D. C., Chiarugi, D., Kulkarni, R., Trevenen, M., et al. (2026) · Nature Medicine · doi:10.1038/s41591-026-04324-7 · Cited by 10
Mogul, H. R., Freeman, R., & Nguyen, K. (2016) · Endocrine Practice · doi:10.4158/ep151087.or · Cited by 11
Calzada, M. J., López, N., Velasco, J. A. N., Mendiola, J., & Torres-Cantero, A. M. (2018) · Journal of Endocrinological Investigation · doi:10.1007/s40618-018-0888-y · Cited by 10
Yun, J., Jung, Y. H., Shin, S. H., et al. (2021) · BMC Pediatrics · doi:10.1186/s12887-021-02851-5 · Cited by 10
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 ›
Are you an author, or do you see a problem with this page? Request a review
