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
16 Own result · 7 Own interpretation · 3 No full text of the sources · 1 Partly supported · 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).
A result the paper states — it cites no source for it, so there is none to check. 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 14,201–14,300 of 31,469
Kettaneh, A., Heude, B., Oppert, J., Scherer, P. E., Meyre, D., Borys, J.-M., Ducimetière, P., & Charles, M.-A. A. (2006) · Metabolism · doi:10.1016/j.metabol.2006.04.015 · Cited by 23
Vecoli, C., Andreassi, M. G., Liga, R., Colombo, M. G., Coceani, M., Carpeggiani, C., L’Abbate, A., & Neglia, D. (2012) · BMC Medical Genetics · doi:10.1186/1471-2350-13-92 · Cited by 22
Dibble, C. T., Gelfand, E. V., & Cannon, C. P. (2007) · Current Atherosclerosis Reports · doi:10.1007/s11883-007-0046-z · Cited by 22
Cole, R. M., Angelotti, A., Sparagna, G. C., Ni, A., & Belury, M. A. (2022) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.202101132 · Cited by 21
Son, M., Moon, S. Y., Koh, M., Kang, Y. W., & Lee, J. Y. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13061628 · Cited by 23
Effect of Time-Restricted Eating on β-Cell Function in Adults With Type 2 Diabetes
Kramer, C. K., Zinman, B., Feig, D. S., & Retnakaran, R. R. (2024) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgae594 · Cited by 22
Association between dynapenic obesity and risk of cardiovascular disease: The Hisayama study
Setoyama, Y., Honda, T., Tajimi, T., Sakata, S., Oishi, E., Furuta, Y., Shibata, M., Hata, J., Kitazono, T., Nakashima, Y., et al. (2024) · Journal of Cachexia Sarcopenia and Muscle · doi:10.1002/jcsm.13564 · Cited by 24
Rizvi, A. A., & Rizzo, M. (2024) · Medicina · doi:10.3390/medicina60101648 · Cited by 25
Won, K., Choi, S., Chun, E. J., Park, S. H., Sung, J., Jung, H. O., & Chang, H. (2024) · Cardiovascular Diabetology · doi:10.1186/s12933-024-02508-4 · Cited by 22
Martin, D., Bonneau, M., Orfila, L., Horeau, M., Hazon, M., Demay, R., Lecommandeur, E., Boumpoutou, R., Guillotel, A., Guillemot, P., et al. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.115448 · Cited by 22
Tobias, D. K., Pradhan, A. D., Duran, E. K., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-58721-6 · Cited by 22
Christensen, M. H. E., & Scragg, R. K. R. (2015) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2015.09.023 · Cited by 22
Influencia de la enfermedad por hígado graso no alcohólico en la enfermedad cardiovascular
Ampuero, J., & Romero‐Gómez, M. (2012) · Gastroenterología y Hepatología · doi:10.1016/j.gastrohep.2012.02.005 · Cited by 23
Valcour, V., Rubin, L. H., Tien, P. C., Anastos, K., Young, M., Mack, W. J., Cohen, M. H., Golub, E. T., Crystal, H., & Maki, P. M. (2015) · Journal of NeuroVirology · doi:10.1007/s13365-015-0330-6 · Cited by 22
Yun, C., Bezerra, H. G., Wu, T.-H., Yang, F.-S., Liu, C.-C., Wu, Y.-J., Kuo, J., Hung, C., Lee, J. J.-S., Hou, C. J., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0061997 · Cited by 22
Tastesen, H. S., Rønnevik, A. K., Borkowski, K., Madsen, L., Kristiansen, K., & Liaset, B. (2014) · PLoS ONE · doi:10.1371/journal.pone.0112859 · Cited by 22
Fructose and saturated fats predispose hyperinsulinemia in lean male rat offspring
Chen, C. O., Crott, J. W., Liu, Z., & Smith, D. E. (2009) · European Journal of Nutrition · doi:10.1007/s00394-009-0091-1 · Cited by 22
Haghani, K., & Bakhtiyari, S. (2012) · Genetic Testing and Molecular Biomarkers · doi:10.1089/gtmb.2012.0160 · Cited by 22
Morine, M. J., McMonagle, J., Toomey, S., et al. (2010) · BMC Bioinformatics · doi:10.1186/1471-2105-11-499 · Cited by 22
İdilman, İ. S., Keskın, O., Elhan, A. H., Idılman, R., & Karçaaltıncaba, M. (2014) · Scandinavian Journal of Gastroenterology · doi:10.3109/00365521.2014.894118 · Cited by 22
Silva, T. R., Alves, B. C., Maturana, M. A., & Spritzer, P. M. (2013) · Journal of the American College of Nutrition · doi:10.1080/07315724.2013.826111 · Cited by 22
Obesity Is an Independent Determinant of Ischemia-Modified Albumin
Mehmetoğlu, İ., Kurban, S., Yerlikaya, F. H., et al. (2012) · Obesity Facts · doi:10.1159/000343954 · Cited by 22
Bora, G. S., Guleria, S., Reddy, V. S. K., et al. (2010) · Transplantation Proceedings · doi:10.1016/j.transproceed.2010.10.008 · Cited by 22
Arancibia, C., Galgani, J. E., Valderas, J. P., Morales, M. J. L., Santos, J. L., & Felipe Pollak, C. (2014) · Revista médica de Chile · doi:10.4067/s0034-98872014000900003 · Cited by 22
Kusunoki, Y., Katsuno, T., Nakae, R., Watanabe, K., Ochi, F., Tokuda, M., Akagami, T., Miuchi, M., Miyagawa, J., & Namba, M. (2015) · Gynecological Endocrinology · doi:10.3109/09513590.2015.1075498 · Cited by 22
Obuchi, A., Adachi, H., Enomoto, M., Fukami, A., Kumagai, E., Nakamura, S., Yoshimura, A., Nohara, Y., Nakao, E., Umeki, Y., et al. (2014) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2014.07.002 · Cited by 22
Minor Contribution of Endogenous GLP-1 and GLP-2 to Postprandial Lipemia in Obese Men
Matikainen, N., Björnson, E., Söderlund, S., Borén, C., Eliasson, B., Pietiläinen, K. H., Bogl, L. H., Hakkarainen, A., Lundbom, N. M. I., Rivellese, A. A., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0145890 · Cited by 22
Zhou, Z., Ju, H., Sun, M., Fu, Q.-P., Chen, H., Ji, H.-B., Ji, F., & Jiang, D. (2016) · Clinica Chimica Acta · doi:10.1016/j.cca.2016.02.003 · Cited by 22
Radhakishun, N. N. E., van Vliet, M., von Rosenstiel, I. A., Weijer, O., Beijnen, J. H., Brandjes, D. P. M., & Diamant, M. (2013) · Journal of Pediatric Endocrinology and Metabolism · doi:10.1515/jpem-2012-0302 · Cited by 22
Brachs, M., Wiegand, S., Leupelt, V., Ernert, A., Kintscher, U., von Schwartzenberg, R. J., Decker, A.-M., Bobbert, T., Hübner, N., Chen, W., et al. (2016) · Metabolism · doi:10.1016/j.metabol.2016.03.013 · Cited by 22
Adiposity and Insufficient MVPA Predict Cardiometabolic Abnormalities in Adults
Peterson, M. D., Snih, S. A., STODDARD, J., McClain, J. J., & Lee, I.-M. M. (2014) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000000212 · Cited by 22
Pharyngeal collapsibility during sleep is elevated in insulin-resistant females with morbid obesity
Llanos, O. L., Galiatsatos, P., Guzmán‐Vélez, E., Patil, S. P., Smith, P. L., Magnuson, T. H., Schweitzer, M., Steele, K. E., Polotsky, V. Y., & Schwartz, A. R. (2016) · European Respiratory Journal · doi:10.1183/13993003.00918-2015 · Cited by 23
Pandey, S., & Garabadu, D. (2016) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-016-0418-4 · Cited by 22
de Almeida-Pititto, B., Ribeiro‐Filho, F. F., Santos, I. S., Lotufo, P. A., Benseñor, I. M., & Ferreira, S. R. G. (2016) · European Journal of Preventive Cardiology · doi:10.1177/2047487316665490 · Cited by 22
Prativadibhayankaram, V. S., Malhotra, S., Pandhi, P., et al. (2008) · Natural Product Communications · doi:10.1177/1934578x0800300230 · Cited by 22
Gómez, T., Bequer, L., Mollineda, Á., et al. (2017) · Biological Trace Element Research · doi:10.1007/s12011-017-0962-x · Cited by 22
Sanad, E. F., Hamdy, N. Μ., Eletriby, A., Sebak, S. A., & EL-Mesallamy, H. O. (2017) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2017.07.013 · Cited by 22
Mohandas, C., Bonadonna, R. C., Shojaee‐Moradie, F., Jackson, N., Boselli, L., Alberti, K. G. M. M., Peacock, J. L., Umpleby, A. M., Amiel, S. A., & Goff, L. M. (2018) · Diabetes Obesity and Metabolism · doi:10.1111/dom.13283 · Cited by 22
Li, Y., Li, Y.-Z., Li, R., Li, L., Li, C., Huang, M., Shi, D., Feng, R., & Sun, C. (2018) · Annals of Nutrition and Metabolism · doi:10.1159/000490194 · Cited by 22
Minor role of mature adipocyte mineralocorticoid receptor in high-fat diet-induced obesity
Feraco, A., Armani, A., Urbanet, R., Cat, A. N. D., Marzolla, V., Jaisser, F., & Caprio, M. (2018) · Journal of Endocrinology · doi:10.1530/joe-18-0314 · Cited by 22
Rijks, J. H. J., Vreugdenhil, A. C. E., Dorenbos, E., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-35279-6 · Cited by 22
Corona-Meraz, F.-I., Mercado, M. V.-D., Ortega, F. J., Ruíz-Quezada, S. L., Guzmán-Ornelas, M.-O., & Navarro-Hernández, R. E. (2018) · Diabetes and Vascular Disease Research · doi:10.1177/1479164118816659 · Cited by 22
Lu, M., Wu, B., Qiao, R., Gu, H., Din, Y., & Dong, X. (2019) · Journal of Clinical Research in Pediatric Endocrinology · doi:10.4274/jcrpe.galenos.2019.2018.0098 · Cited by 23
Aller, R., Izaola, O., Primo, D., et al. (2019) · Nutrition · doi:10.1016/j.nut.2019.02.012 · Cited by 22
García‐Carrizo, F., Picó, C., Rodríguez, A. M., & Palou, A. (2019) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.9b00296 · Cited by 22
Jung, S., Han, J., Park, H.-S., et al. (2019) · BMC Complementary and Alternative Medicine · doi:10.1186/s12906-019-2460-5 · Cited by 22
Jiang, B., Chen, Y., Zhou, K., Zheng, Y., Chen, Y., Qin, L., Zhu, C., Xia, F., Gu, T., Guo, Y., et al. (2019) · Obesity · doi:10.1002/oby.22432 · Cited by 22
Chromy, D., Mandorfer, M., Bucsics, T., Schwabl, P., Bauer, D. J. M., Scheiner, B., Schmidbauer, C., Lang, G. F., Szekeres, T., Ferenci, P., et al. (2019) · AIDS Patient Care and STDs · doi:10.1089/apc.2018.0333 · Cited by 22
Luordi, C., Maddaloni, E., Bizzarri, C., Pedicelli, S., Zampetti, S., D’Onofrio, L., Moretti, C., Cappa, M., & Buzzetti, R. (2019) · Journal of Endocrinological Investigation · doi:10.1007/s40618-019-01086-7 · Cited by 22
Social anxiety symptoms moderate the link between obesity and metabolic function
Jaremka, L. M., & Pacanowski, C. R. (2019) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2019.104425 · Cited by 22
Silva, A., Nunes, C. L., Matias, C., Jesus, F., Francisco, R., Cardoso, M., Santos, I., Carraça, E., Silva, M., Sardinha, L., et al. (2020) · Nutrients · doi:10.3390/nu12020286 · Cited by 21
Warkentin, S., Santos, A. C., & Oliveira, A. (2020) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2020.01.007 · Cited by 20
Compound 18 Improves Glucose Tolerance in a Hepatocyte TGR5-dependent Manner in Mice
Holter, M. M., Chirikjian, M. K., Briere, D. A., Maida, A., Sloop, K. W., Schoonjans, K., & Cummings, B. P. (2020) · Nutrients · doi:10.3390/nu12072124 · Cited by 23
Joo, Y. S., Lee, C., Kim, H., Jhee, J., Yun, H., Park, J., Chang, T., Yoo, T., Kang, S.-W., & Han, S. (2020) · Journal of the American Society of Nephrology · doi:10.1681/asn.2020010084 · Cited by 18
Barrón‐Cabrera, E., González‐Becerra, K., Rosales-Chávez, G., Mora-Jiménez, A., Hernández‐Cañaveral, I., & Martínez‐López, E. (2020) · Genes & Nutrition · doi:10.1186/s12263-020-00674-0 · Cited by 23
Miyagi, S., Takamura, T., Nguyen, T. T. T., Tsujiguchi, H., Hara, A., Nakamura, H., Suzuki, K., Tajima, A., Kannon, T., Toyama, T., et al. (2020) · Journal of Diabetes Investigation · doi:10.1111/jdi.13402 · Cited by 21
Maffazioli, G. D. N., Lopes, C. P., Heinrich‐Oliveira, V., Løbo, R. A., Hayashida, S. A. Y., Soares, J. M., Maciel, G. A. R., & Baracat, E. C. (2020) · International Journal of Gynecology & Obstetrics · doi:10.1002/ijgo.13374 · Cited by 23
Aadland, E., Kvalheim, O. M., Hansen, B. H., Kriemler, S., Ried‐Larsen, M., Wedderkopp, N., Sardinha, L. B., Møller, N. C., Hallal, P. C., Anderssen, S. A., et al. (2020) · Preventive Medicine · doi:10.1016/j.ypmed.2020.106266 · Cited by 25
Derbyshire, A. E., Allen, J. L., Gittins, M., Lakhiani, B., Bolton, J., Shaw, J., Pemberton, P. W., Needham, M., MacKintosh, M. L., Edmondson, R. J., et al. (2020) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-20-0248 · Cited by 23
Fernberg, U., Fernström, M., & Hurtig‐Wennlöf, A. (2021) · Vascular Health and Risk Management · doi:10.2147/vhrm.s283211 · Cited by 23
Maffeis, C., Cendon, M., Tomasselli, F., Tommasi, M., Bresadola, I., Fornari, E., Morandi, A., & Olivieri, F. (2020) · European Journal of Clinical Nutrition · doi:10.1038/s41430-020-00822-0 · Cited by 25
Chang, J. S., & Namkung, J. (2021) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph18052242 · Cited by 22
Sedky, A. A. (2021) · Fundamental and Clinical Pharmacology · doi:10.1111/fcp.12664 · Cited by 22
Insulin Action, Glucose Homeostasis and Free Fatty Acid Metabolism: Insights From a Novel Model
Stefanovski, D., Punjabi, N., Boston, R., & Watanabe, R. (2021) · Frontiers in Endocrinology · doi:10.3389/fendo.2021.625701 · Cited by 21
Lionett, S., Kiel, I. A., Røsbjørgen, R. E. N., Lydersen, S., Larsen, S., & Moholdt, T. T. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.649794 · Cited by 22
Plasma Apolipoprotein E3 and Glucose Levels Are Associated in APOE ɛ3/ɛ4 Carriers
Edlund, A. K., Chen, K., Lee, W., Protas, H. D., Su, Y., Reiman, E. M., Caselli, R. J., & Nielsen, H. M. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210065 · Cited by 22
Bettini, S., Serra, R., Fabris, R., Prà, C. D., Favaretto, F., Dassie, F., Duso, C., Vettor, R., & Busetto, L. (2021) · Eating and Weight Disorders - Studies on Anorexia Bulimia and Obesity · doi:10.1007/s40519-021-01182-9 · Cited by 23
Abbaszadeh, F., Azizi, S., Mobasseri, M., & Ebrahimi‐Mameghani, M. (2021) · Diabetology & Metabolic Syndrome · doi:10.1186/s13098-021-00669-w · Cited by 23
Lu, Q., Wan, Z., Guo, J., Liu, L., Pan, A., & Liu, G. (2021) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgab402 · Cited by 23
Chiu, Y., Tu, H.-H., Kung, M., Wu, H.-J., & Chen, Y. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111848 · Cited by 22
Karras, S. Ν., Koufakis, T., Adamidou, L., Dimakopoulos, G., Karalazou, P., Thisiadou, K., Makedou, K., Zebekakis, P. E., & Kotsa, K. (2021) · International Journal of Food Sciences and Nutrition · doi:10.1080/09637486.2021.1941803 · Cited by 22
Zhu, Y., Kim, S. Q., Zhang, Y., Liu, Q., & Kim, K. (2021) · Metabolism · doi:10.1016/j.metabol.2021.154861 · Cited by 22
Lim, S. K., Kim, Y. J., Khang, A. R., & Eckel, R. H. (2021) · Clinical Nutrition · doi:10.1016/j.clnu.2021.09.004 · Cited by 23
Buckland, G., Taylor, C. M., Emmett, P. M., Johnson, L., & Northstone, K. (2021) · European Journal of Nutrition · doi:10.1007/s00394-021-02652-7 · Cited by 24
Rondanelli, M., Perna, S., Ilyas, Z., Peroni, G., Bazire, P., Sajuox, I., Maugeri, R., Nichetti, M., & Gasparri, C. (2021) · Endocrine · doi:10.1007/s12020-021-02860-5 · Cited by 22
Xu, H., Thomas, M. J., Kaul, S., Kallinger, R., Ouweneel, A. B., Maruko, E. C., Oussaada, S. M., Jongejan, A., Cense, H. A., Nieuwdorp, M., et al. (2021) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.121.316615 · Cited by 22
Hendawy, O. M., Gomaa, H. A. M., Hussein, S., Alzarea, S. I., Qasim, S., Rahman, F. E.-Z. S. A., Ali, A. T., & Ahmed, S. R. (2021) · Saudi Pharmaceutical Journal · doi:10.1016/j.jsps.2021.09.014 · Cited by 22
Obesity Impairs Embryonic Myogenesis by Enhancing BMP Signaling within the Dermomyotome
Zhao, L., Law, N. C., Gomez, N. A., Son, J., Gao, Y., Liu, X., de Avila, J. M., Zhu, M. J., & Du, . (2021) · Advanced Science · doi:10.1002/advs.202102157 · Cited by 20
Influence of Obstructive Sleep Apnea on Systemic Inflammation in Pregnancy
Alonso‐Fernández, A., Quetglas, C. R., Herranz, A., Larrínaga, A. Á. R. D., Barón, A. S., Rodríguez, P., Gómez, A. V. G., Martínez, C. P., Marin, J. P. C., Nicolau, M. B., et al. (2021) · Frontiers in Medicine · doi:10.3389/fmed.2021.674997 · Cited by 23
Serum concentration of fatty acids in children with obesity and nonalcoholic fatty liver disease
Kopiczko, N., Bobrus‐Chociej, A., Harasim‐Symbor, E., Tarasów, E., Wojtkowska, M., Chabowski, A., & Lebensztejn, D. M. (2021) · Nutrition · doi:10.1016/j.nut.2021.111541 · Cited by 22
Noguchi‐Shinohara, M., Yuki-Nozaki, S., Abe, C., Mori, A., Horimoto, M., Yokogawa, M., Ishida, N., Suga, Y., Ishizaki, J., Ishimiya, M., et al. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-215153 · Cited by 21
Kim, H., Lee, M., Lee, Y., Lee, B., Soo, B., & Kang, E. S. (2021) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2021.775753 · Cited by 22
Yang, J., Lu, Y., Bai, Y., et al. (2022) · Journal of Environmental Sciences · doi:10.1016/j.jes.2021.10.023 · Cited by 22
Lee, J., Lee, Y. A., Lee, S. Y., Shin, C. H., & Kim, J. H. (2022) · The Tohoku Journal of Experimental Medicine · doi:10.1620/tjem.256.53 · Cited by 22
Dagogo-Jack, S. E., UMEKWE, N. A., Brewer, A., Owei, I., Mupparaju, V. K., Rosenthal, R. H., & Wan, J. Y. (2022) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2021-002748 · Cited by 23
Calcaterra, V., Biganzoli, G., Ferraro, S., Verduci, E., Rossi, V., Vizzuso, S., Bosetti, A., Borsani, B., Biganzoli, E. M., & Zuccotti, G. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11071856 · Cited by 21
Lee, M.-K., Lee, J.-H., Sohn, S.-Y., Lee, S. Y., Jeong, T.-Y., & Kim, S. C. (2022) · Diabetology & Metabolic Syndrome · doi:10.1186/s13098-022-00825-w · Cited by 22
Lembo, E., Russo, M. F., Verrastro, O., Anello, D., Angelini, G., Iaconelli, A., Guidone, C., Stefanizzi, G., Ciccoritti, L., Greco, F., et al. (2022) · Diabetes & Metabolism · doi:10.1016/j.diabet.2022.101363 · Cited by 23
Petersen, K. S., Murphy, J., Whitbread, J., Clifton, P. M., & Keogh, J. B. (2022) · Nutrients · doi:10.3390/nu14142986 · Cited by 22
Motto, A. E., Lawson-Evi, P., & Eklu‐Gadegbeku, K. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.113578 · Cited by 22
Sardeli, A. V., Gáspari, A. F., dos Santos, W. M., de Araújo, A. A., Angelis, K. D., Mariano, L. O., Cavaglieri, C. R., Fernhall, B., & Chacon‐Mikahil, M. P. T. (2022) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph191711042 · Cited by 27
Study of the Association between Thiols and Oxidative Stress Markers in Children with Obesity
D’Alessandro, A., Felice, G. D., Manco, M., Pastore, A., Pezzi, S., Mariani, M., Fintini, D., Muda, A. O., & Porzio, O. (2022) · Nutrients · doi:10.3390/nu14173637 · Cited by 22
Mathur, N., Severinsen, M. C. K., Jensen, M. E., Naver, L., Schrölkamp, M., Laye, M. J., Watt, M. J., Nielsen, S. J., Krogh‐Madsen, R., Pedersen, B. K., et al. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.983899 · Cited by 25
He, Y., Tao, Y., Qiu, L., Xu, W., Huang, X., Hua, W., & Tao, X. (2022) · Nutrients · doi:10.3390/nu14204348 · Cited by 25
Gut microbiome and stages of diabetes in middle-aged adults: CARDIA microbiome study
Hu, Y., Meyer, K. A., Lulla, A., Lewis, C. E., Carnethon, M. R., Schreiner, P. J., Sidney, S., Shikany, J. M., Meirelles, O., & Launer, L. J. (2023) · Nutrition & Metabolism · doi:10.1186/s12986-022-00721-0 · Cited by 24
Reckziegel, M. B., Nepomuceno, P., Machado, T. D., Renner, J. D. P., Pohl, H. H., Nogueira‐de‐Almeida, C. A., & de Mello, E. D. (2023) · Archives of Endocrinology and Metabolism · doi:10.20945/2359-3997000000506 · Cited by 24
Association between the Triglyceride-Glucose Index and Vitamin D Status in Type 2 Diabetes Mellitus
Xiang, Q., Xu, H., Zhan, J., et al. (2023) · Nutrients · doi:10.3390/nu15030639 · Cited by 22
Berezina, T. A., Obradovic, Z., Boxhammer, E., Berezin, A. A., Lichtenauer, M., & Berezin, A. Е. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12062231 · Cited by 22
Kianersi, S., Redline, S. S., Mongraw‐Chaffin, M., & Huang, T. (2023) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgad229 · Cited by 21
Félix‐Soriano, E., Sáinź, N., Gil‐Iturbe, E., Castilla‐Madrigal, R., Celay, J., Fernández‐Galilea, M., Pejenaute, Á., Lostao, M. P., Martinez-Climent, J. A., & Moreno-Aliaga, M. J. (2023) · Journal of Physiology and Biochemistry · doi:10.1007/s13105-023-00964-2 · Cited by 23
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
