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 14,101–14,200 of 31,469
Khatun, M. A., Sato, S., & Konishi, T. (2020) · Journal of Traditional and Complementary Medicine · doi:10.1016/j.jtcme.2020.03.004 · Cited by 23
Telomere shortening associates with elevated insulin and nuchal fat accumulation
Mangge, H., Herrmann, M., Almer, G., Zelzer, S., Moeller, R., Horejsi, R., & Renner, W. (2020) · Scientific Reports · doi:10.1038/s41598-020-63916-6 · Cited by 23
Okura, T., Fujioka, Y., Nakamura, R., et al. (2020) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2019-001149 · Cited by 23
Identification of a brain fingerprint for overweight and obesity
Farruggia, M. C., van Kooten, M. J., Perszyk, E. E., Burke, M. V., Scheinost, D., Constable, R. T., & Small, D. M. (2020) · Physiology & Behavior · doi:10.1016/j.physbeh.2020.112940 · Cited by 25
Kobayashi, M., Satoh, H., Matsuo, T., Kusunoki, Y., Tokushima, M., Watada, H., Namba, M., & Kitamura, T. (2020) · Endocrine Journal · doi:10.1507/endocrj.ej20-0079 · Cited by 24
Elgenaied, I., Ansari, W. E., Elsherif, M., Abdulrazzaq, S., Qabbani, A., & Elhag, W. (2020) · Surgery for Obesity and Related Diseases · doi:10.1016/j.soard.2020.05.013 · Cited by 24
Lee, S., Min, J., & Min, K. (2020) · Nutrients · doi:10.3390/nu12061783 · Cited by 23
Ferrannini, G., Norhammar, A., Gyberg, V., Mellbin, L., & Rydén, L. (2020) · Diabetes Care · doi:10.2337/dci20-0002 · Cited by 23
Moriyama, K. (2020) · Internal Medicine · doi:10.2169/internalmedicine.4954-20 · Cited by 23
Cioffi, C. E., Narayan, K. M. V., Liu, K., Uppal, K., Jones, D. P., Tran, V., Yu, T., Alvarez, J. A., Bellissimo, M. P., Maner-Smith, K. M., et al. (2020) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2019-001126 · Cited by 28
Pavithran, N., Kumar, H., Menon, A. S., Pillai, G. K., Sundaram, K. R., & Ojo, O. (2020) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph17176232 · Cited by 25
Fetal sex and maternal insulin resistance during mid-pregnancy: a retrospective cohort study
Yamashita, H., Yasuhi, I., Koga, M., Sugimi, S., Umezaki, Y., Fukuoka, M., Suga, S., Fukuda, M., & Kusuda, N. (2020) · BMC Pregnancy and Childbirth · doi:10.1186/s12884-020-03242-x · Cited by 23
Metabolic responses to intermittent hypoxia are regulated by sex and estradiol in mice
Marcouiller, F., Jochmans‐Lemoine, A., Ganouna‐Cohen, G., Mouchiroud, M., Laplante, M., Marette, A., Bairam, A., & Joseph, V. (2020) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00272.2020 · Cited by 23
Aryl Hydrocarbon Receptor Agonist VAF347 Impedes Retinal Pathogenesis in Diabetic Mice
Zapadka, T. E., Lindstrom, S. I., Batoki, J. C., Lee, C. A., Taylor, B. E., Howell, S. J., & Taylor, P. R. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22094335 · Cited by 23
My, B. N., Talib, R. A., Ak, N., & Na, K. (2013) · PubMed · Cited by 23
Erceg, D. N., Anderson, L. J., Nickles, C. M., Lane, C. J., Weigensberg, M. J., & Schroeder, E. T. (2015) · International Journal of Medical Sciences · doi:10.7150/ijms.11364 · Cited by 24
Cardiovascular Fitness and Risk Factors of Healthy African Americans and Caucasians
Zeno, S. A., Kim-Dorner, S.-J., Deuster, P. A., Davis, J. L., Remaley, A. T., & Poth, M. (2010) · Journal of the National Medical Association · doi:10.1016/s0027-9684(15)30472-7 · Cited by 24
Obert, P., Gueugnon, C., Nottin, S., Vinet, A., Gayrard, S., Rupp, T., Dumoulin, G., Tordi, N., & Mougin, F. (2013) · Obesity · doi:10.1002/oby.20495 · Cited by 23
Aoyama‐Sasabe, S., Fukushima, M., Xin, X., Taniguchi, A., Nakai, Y., Mitsui, R., Takahashi, Y., Tsuji, H., Yabe, D., Yasuda, K., et al. (2015) · Journal of Diabetes Research · doi:10.1155/2016/1298601 · Cited by 24
Mingorance, C., de Sotomayor, M. A., Jiménez‐Palacios, F. J., Mochón, M. C., Casto, C., Marhuenda, E., & Herrera, M. D. (2009) · Obesity · doi:10.1038/oby.2009.20 · Cited by 23
Lee, B., Kang, H.-W., Heo, J., Choi, S., Kim, S. Y., Min, Y., Chung, J.-H., Lee, M., Lee, M., & Kim, K.-W. (2005) · Metabolism · doi:10.1016/j.metabol.2005.08.005 · Cited by 23
de Luis, D. A., Sagrado, M. G., Aller, R., Conde, R., & Izaola, O. (2009) · Nutrition · doi:10.1016/j.nut.2008.11.019 · Cited by 23
Korantzopoulos, P. G., Tzimas, P. G., Kalantzi, K., et al. (2009) · Archives of Medical Research · doi:10.1016/j.arcmed.2009.07.012 · Cited by 23
Evaluation of two dietary treatments in obese hyperinsulinemic adolescents
Armeno, M. L., Krochik, G., & Mazza, C. S. (2011) · Journal of Pediatric Endocrinology and Metabolism · doi:10.1515/jpem.2011.291 · Cited by 23
Ruiz, J. R., Ortega, F. B., Meusel, D., & Sjöstróm, M. (2007) · Journal of Public Health · doi:10.1007/s10389-007-0098-0 · Cited by 23
Höybye, C. (2006) · Hormone Research in Paediatrics · doi:10.1159/000093229 · Cited by 22
Carnier, J., de Piano, A., Sanches, P. D. L., Tock, L., do Nascimento, C. M. O., Oyama, L. M., Correa, F. A., Ernandes, R., Lederman, H. M., de Mello, M. T., et al. (2010) · International Journal of Clinical Practice · doi:10.1111/j.1742-1241.2009.02306.x · Cited by 23
Brooke, A. M., Kalingag, L. A., Miraki‐Moud, F., Camacho‐Hübner, C., Maher, K. T., Walker, D. M., Hinson, J. P., & Monson, J. P. (2006) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2006.02648.x · Cited by 24
Ezzat, W. M., Ragab, S. H., Ismail, N. A., Elhosary, Y. A., ElBaky, A. A., Farouk, H., & Rasheed, I. A. (2012) · Journal of Genetic Engineering and Biotechnology · doi:10.1016/j.jgeb.2012.05.006 · Cited by 23
Leptin and the metabolic syndrome in patients with myotonic dystrophy type 1
Stojanović, V. R., Perić, S., Lavrnić, D., Popović, S., Ille, T., Stević, Z., Basta, I. Z., & Apostolski, S. (2009) · Acta Neurologica Scandinavica · doi:10.1111/j.1600-0404.2009.01237.x · Cited by 23
Apostol, A. T., & Tayek, J. A. (2003) · Metabolism · doi:10.1016/s0026-0495(03)00323-8 · Cited by 23
Maternal history of diabetes is associated with increased cardiometabolic risk in Chinese
Tam, C. H. T., Wang, Y., Luan, J., Lee, H. M., Luk, A. O. Y., Tutino, G., Tong, P. C. Y., Kong, A. P. S., So, W. Y., Chan, J. C. N., et al. (2014) · Nutrition and Diabetes · doi:10.1038/nutd.2014.9 · Cited by 24
Adipose tissue compartments and insulin resistance in overweight-obese Caucasian men
Chan, D. C., Watts, G. F., Sussekov, A. V., Barrett, P. H. R., Yang, Z., Hua, J., & Song, S. J. (2003) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2003.09.005 · Cited by 23
Yang, C., Li, C.-I., Liu, C.-S., Bau, D., Lin, C., Li, T., Lin, C., & Lin, C. (2012) · Molecular Biology Reports · doi:10.1007/s11033-012-2089-7 · Cited by 22
Are girls more insulin-resistant than boys?
Hirschler, V., Maccallini, G., Karam, C., González, C. D., & Aranda, C. (2009) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2009.03.002 · Cited by 23
Paolisso, G., Manzella, Rizzo, M. R., Barbieri, Gambardella, A., & Varricchio (2000) · European Journal of Clinical Investigation · doi:10.1046/j.1365-2362.2000.00626.x · Cited by 23
Nordquist, N., Göktürk, C., Comasco, E., Eensoo, D., Merenäkk, L., Veidebaum, T., Oreland, L., & Harro, J. (2009) · Obesity · doi:10.1038/oby.2009.83 · Cited by 23
de Luis, D. A., Sagrado, M. G., Aller, R., et al. (2010) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2009.12.019 · Cited by 23
Comparison between HOMA‐IR and ISI‐gly in detecting subjects with the metabolic syndrome
Schianca, G. P. C., Sainaghi, P. P., Castello, L. M., Rapetti, R., Limoncini, A., & Bartoli, E. (2005) · Diabetes/Metabolism Research and Reviews · doi:10.1002/dmrr.560 · Cited by 25
Russo, I., Mese, P. D., Doronzo, G., Salve, A. D., Secchi, M., Trovati, M., & Anfossi, G. (2007) · Clinical Chemistry · doi:10.1373/clinchem.2006.076208 · Cited by 23
Dullaart, R. P. F., de Vries, R., Dallinga‐Thie, G. M., Sluiter, W. J., & van Tol, A. (2007) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2007.03049.x · Cited by 23
Blaauw, J., Smit, A. J., van Pampus, M. G., et al. (2006) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2006.06.086 · Cited by 23
Retnakaran, R. R., Qi, Y., Sermer, M., Connelly, P. W., Zinman, B., & Hanley, A. J. (2009) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2009.04.008 · Cited by 24
Yamamoto, T., Inokuchi, T., Ka, T., et al. (2010) · Nucleosides Nucleotides & Nucleic Acids · doi:10.1080/15257771003740986 · Cited by 23
Pfützner, A., Lorra, B., Abdollahnia, M. R., et al. (2006) · Diabetes Technology & Therapeutics · doi:10.1089/dia.2006.8.375 · Cited by 23
Hormonal Alteration in Obese Adolescents with Eating Disorder: Effects of Multidisciplinary Therapy
Carnier, J., Lofrano‐Prado, M. C., do Prado, W. L., Caranti, D. A., de Piano, A., Tock, L., do Nascimento, C. M. O., Oyama, L. M., de Mello, M. T., Tufik, S. B., et al. (2008) · Hormone Research in Paediatrics · doi:10.1159/000139148 · Cited by 23
Basal Insulin Resistance and Secretion in Nigerians With Type 2 Diabetes Mellitus
Oli, J., Adeyemo, A., Okafor, G., Ofoegbu, E., Onyenekwe, B. M., Chukwuka, C. J., Onwasigwe, C. N., Ufelle, S., Chen, G., & Rotimi, C. N. (2009) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2009.0002 · Cited by 24
CHEN, W., SRINIVASAN, S., Boerwinkle, E., & Berenson, G. S. (2007) · American Journal of Hypertension · doi:10.1016/j.amjhyper.2007.09.002 · Cited by 23
de Lima, L. M. A., Wiernsperger, N. F., Kraemer‐Aguiar, L. G., & Bouskela, E. (2009) · Clinics · doi:10.1590/s1807-59322009000500008 · Cited by 23
Liu, W., Liu, M., Fan, W., Nawata, H., & Yanase, T. (2006) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2006.02.007 · Cited by 23
Does bicarbonated mineral water rich in sodium change insulin sensitivity of postmenopausal women?
Schoppen, S., Sánchez-Muniz, F. J., Pérez-Granados, M., Gómez-Gerique, J. A., Sarriá, B., Navas‐Carretero, S., & Vaquero, M. P. (2007) · PubMed · Cited by 23
Metabolic Effects of High Altitude Trekking in Patients With Type 2 Diabetes
de Mol, P., Fokkert, M. J., de Vries, S. T., de Koning, E. J. P., Dikkeschei, B. D., Gans, R. O. B., Tack, C. J., & Bilo, H. J. G. (2012) · Diabetes Care · doi:10.2337/dc12-0204 · Cited by 24
Association between MspI polymorphism of the APO AI gene and Type 2 diabetes mellitus
Morcillo, S., Cardona, F., Rojo‐Martínez, G., Esteva, I., Ruiz-de-Adana, M. S., Tinahones, F. J., Gómez‐Zumaquero, J. M., & Soriguer, F. (2005) · Diabetic Medicine · doi:10.1111/j.1464-5491.2005.01514.x · Cited by 23
Effects of Sympatholytic Therapy with Moxonidine on Serum Adiponectin Levels in Hypertensive Women
Ebinç, H., Ozkurt, Z., Ebinç, F., UCARDAG, D., Çağlayan, O., & Yılmaz, M. (2008) · Journal of International Medical Research · doi:10.1177/147323000803600111 · Cited by 23
Tiehuis, A. M., Mali, W. P. T. M., van Raamt, A. F., Visseren, F. L. J., Biessels, G. J., van Zandvoort, M. J. E., Kappelle, L. J., & van der Graaf, Y. (2009) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2009.02.337 · Cited by 23
Effect of Vitamins A, C, and E Supplementation in the Treatment of Metabolic Syndrome in Albino Rats
Bilbis, L. S., Muhammad, S. A., Saidu, Y., et al. (2012) · Biochemistry Research International · doi:10.1155/2012/678582 · Cited by 23
Behavioral, metabolic, and molecular correlates of lower insulin sensitivity in Mexican-Americans
Ho, R. C., Davy, K. P., Hickey, M. S., Summers, S. A., & Melby, C. L. (2002) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00105.2002 · Cited by 23
Wiesli, P., Bernays, R. L., Brändle, M., Zwimpfer, C., Seiler, H., Zapf, J., Spinas, G. A., & Schmid, C. (2004) · Clinica Chimica Acta · doi:10.1016/j.cccn.2004.09.022 · Cited by 23
Wang, G., Liu, X., Christoffel, K. K., Zhang, S., Wang, B., Liu, R., Li, Z., Liu, X., Brickman, W. J., Zimmerman, D., et al. (2010) · European Journal of Endocrinology · doi:10.1530/eje-10-0145 · Cited by 23
Shams, S., Ashtıani, M. T. H., Monajemzadeh, M., Koochakzadeh, L., Irani, H., Jafari, F., & Mohseni, A. (2010) · Laboratory Medicine · doi:10.1309/lms0eoouzsii2bne · Cited by 27
Insulin Resistance and Hypertension in Non-obese Africans in Tanzania
Mgonda, Y. M., Ramaiya, K. L., Swai, A. B. M., McLarty, D. G., & Alberti, K. G. M. M. (1998) · Hypertension · doi:10.1161/01.hyp.31.1.114 · Cited by 23
Gencer, M., Gazı, E., Hacıvelioğlu, S., Binnetoğlu, E., Barutçu, A., Türkön, H., Temız, A., Altun, B., Vural, A., Cevızcı, S., et al. (2014) · European Journal of Obstetrics & Gynecology and Reproductive Biology · doi:10.1016/j.ejogrb.2014.07.032 · Cited by 23
Wu, J., Zhao, M., Zheng, H., Zhang, H., & Jiang, Y. (2010) · Acta Pharmacologica Sinica · doi:10.1038/aps.2010.110 · Cited by 24
García-Rodríguez, C. E., Olza, J., Aguilera, C. M., et al. (2012) · Journal of Nutrition · doi:10.3945/jn.112.158139 · Cited by 23
Farasat, T., Cheema, A. M., & Khan, M. N. (2012) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2012.05.017 · Cited by 24
Rhee, E., Kim, J. H., Park, H., Park, S. E., Oh, H.-G., Park, C., Lee, W., Oh, K.-W., & Park, S. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.12.010 · Cited by 22
Guthoff, M., Vosseler, D., Langanke, J., Nadalin, S., Königsrainer, A., Häring, H., Fritsche, A., & Heyne, N. (2015) · PLoS ONE · doi:10.1371/journal.pone.0134971 · Cited by 22
Correlation of Abdominal Fat Accumulation and Stiffness of the Abdominal Aorta in Obese Children
Polat, T. B., Urgancı, N., Çalışkan, K. C., & Akyıldız, B. N. (2008) · Journal of Pediatric Endocrinology and Metabolism · doi:10.1515/jpem.2008.21.11.1031 · Cited by 23
Evaluation of the relationship between insulin resistance and recurrent pregnancy loss.
Çelik, N., Evsen, M. S., Sak, M. E., Soydinç, H. E., & Gül, T. (2011) · PubMed · Cited by 23
Castaldo, G., Monaco, L., Castaldo, L., Galdo, G., & Cereda, E. (2016) · International Journal of Food Sciences and Nutrition · doi:10.1080/09637486.2016.1186157 · Cited by 26
Tull, E. S., Thurland, A., LaPorte, R. E., et al. (2003) · PubMed · Cited by 23
Nutritionists’ Health Study cohort: a web-based approach of life events, habits and health outcomes
Folchetti, L. G. D., da Silva, I. T., de Almeida-Pititto, B., & Ferreira, S. R. G. (2016) · BMJ Open · doi:10.1136/bmjopen-2016-012081 · Cited by 24
de Souza, A. L., Batista, G. A., & Alegre, S. M. (2016) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2016.10.018 · Cited by 25
Kornacewicz-Jach, Z., Kossuth, I., & Czechowska, M. (2006) · Menopause Review/Przegląd Menopauzalny · Cited by 24
Prevalence of Metabolic Syndrome in obese Children
Chang, J. H., Kim, D. H., Kim, H.-S., et al. (2004) · Korean Journal of Pediatrics · Cited by 23
The metabolic and neuroinflammatory changes induced by consuming a cafeteria diet are age-dependent
Teixeira, D., Cecconello, A. L., Partata, W. A., de Fraga, L. S., Ribeiro, M. F. M., & Guedes, R. P. (2017) · Nutritional Neuroscience · doi:10.1080/1028415x.2017.1380892 · Cited by 25
Talbot, C. P. J., Plat, J., Joris, P. J., Konings, M. C. J. M., Kusters, Y. H. A. M., Schalkwijk, C. G., Ritsch, A., & Mensink, R. P. (2018) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2018.04.029 · Cited by 23
Sawathiparnich, P., Weerakulwattana, L., Santiprabhob, J., & Likitmaskul, S. (2005) · PubMed · Cited by 23
Song, K., Nam‐Goong, I. S., HAN, S., Kim, M.-S., Lee, E.-J., Lee, Y. S., Lee, M. S., Yoon, S. H., Lee, K.-U., & Park, J. (2007) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2007.04.011 · Cited by 23
Reduced Serum Acylated Ghrelin Levels in Patients with Hyperthyroidism
Altınova, A. E., Törüner, F. B., Aktürk, M., Elbeğ, Ş., Yetkin, İ., Çakır, N., & Arslan, M. (2006) · Hormone Research in Paediatrics · doi:10.1159/000092603 · Cited by 23
The relative impact of different measures of adiposity on markers of early atherosclerosis
Stamatelopoulos, K., Lekakis, J. P., Vamvakou, G. D., Katsichti, P., Protogerou, A. D., Revela, I., Karatzi, K., Alevizaki, M. K., Zakopoulos, N., & Papamichael, C. M. (2006) · International Journal of Cardiology · doi:10.1016/j.ijcard.2006.07.098 · Cited by 23
Seasonal Variation in Insulin Sensitivity in Healthy Elderly People
Bunout, D. C., Barrera, G., de la Maza, P., Vivien Gattas, Z., & Hirsch, S. (2003) · Nutrition · doi:10.1016/s0899-9007(02)01016-x · Cited by 22
The relation between clinical manifestations of polycystic ovary syndrome and β‐cell function
Weber, R. F. A., Pache, T. D., Jacobs, M. L., Doctor, R., Loriaux, D. L., Fauser, B. C. J. M., & Birkenhäger, J. C. (1993) · Clinical Endocrinology · doi:10.1111/j.1365-2265.1993.tb01009.x · Cited by 23
Sekiguchi, M., Kurabayashi, M., Adachi, H., et al. (2004) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2003.12.036 · Cited by 23
Suh, H. S., Park, Y. W., Kang, J. H., Lee, S. H., Lee, H. S., & Shim, K. W. (2004) · International Journal of Obesity · doi:10.1038/sj.ijo.0802642 · Cited by 25
Fujii, N., Tsuchihashi, K., Sasao, H., Eguchi, M., Miurakami, H., Hase, M., Higashiura, K., Yuda, S., Hashimoto, A., Miura, T., et al. (2008) · Heart and Vessels · doi:10.1007/s00380-007-1002-0 · Cited by 23
Does physical training increase insulin sensitivity in chronic heart failure patients?
Sabelis, L. W. E., Senden, P. J., Boekhorst, B. C. M. T., Hulzebos, E. H. J., van de Wiel, A., van Haeften, T. W., Zonderland, M. L., & Mosterd, W. L. (2004) · Clinical Science · doi:10.1042/cs20030254 · Cited by 23
Insulin regulation of leptin synthesis and secretion in humans: the model of myotonic dystrophy
Gómez, J. M., Molina, A., Fernández-Castañer, M., et al. (1999) · Clinical Endocrinology · doi:10.1046/j.1365-2265.1999.00675.x · Cited by 23
Sambanis, C., Τζιόμαλος, Κ., Kountana, E., Kakavas, N., Zografou, I., Balaska, A., Koulas, G., Karagiannis, A. I., & Zamboulis, C. (2007) · Acta Diabetologica · doi:10.1007/s00592-007-0014-7 · Cited by 22
Ueno, L. M., Frazzatto, E., Batalha, L. T., et al. (2005) · International Journal of Obesity · doi:10.1038/sj.ijo.0803140 · Cited by 23
Arachidonic Acid Content in Adipose Tissue Is Associated With Insulin Resistance in Healthy Children
Aldamiz-Echevarria, L. J., Prieto, J. A., Andrade, F., Elorz, J., Sanjurjo, P., & Soriano, J. R. (2007) · Journal of Pediatric Gastroenterology and Nutrition · doi:10.1097/01.mpg.0000237931.53470.ba · Cited by 23
Sabin, M. A., Holly, J. M. P., Hamilton-Shield, J. P., Turner, S. J., Grohmann, M. J., Stewart, C. E., & Crowne, E. C. (2006) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2005-1571 · Cited by 23
Redox status and immune function in type I diabetes families
Matteucci, E., Malvaldi, G., FAGNANI, F., et al. (2004) · Clinical & Experimental Immunology · doi:10.1111/j.1365-2249.2004.02470.x · Cited by 23
Park, H., Hasegawa, G., Obayashi, H., Fujinami, A., Ohta, M., Hara, H., Adachi, T., Tamaki, S., Nakajima, Y., Kimura, F., et al. (2006) · Clinica Chimica Acta · doi:10.1016/j.cca.2006.06.004 · Cited by 22
Liou, C., Lin, T., Feng-mei, H., et al. (2004) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1293.031 · Cited by 23
Mlinar, B., Pfeifer, M., Bokal, E. V., Jensterle, M., & Marc, J. (2008) · European Journal of Endocrinology · doi:10.1530/eje-08-0387 · Cited by 23
Kim, D. M., Yoon, S. J., Ahn, C. W., Cha, B. S., Lim, S.-K., Kim, K. R., Lee, H. C., & Huh, K. B. (2004) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2003.12.008 · Cited by 23
Lethagen, Å., Ub, E., Hallengren, B., Groop, L., & Tuomi, T. (2002) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.87.3.8343 · Cited by 27
Dagre, A. G., Lekakis, J., Mihas, C. C., Protogerou, A. D., Thalassinou, L., Tryfonopoulos, D. J., Douridas, G. N., Papamichael, C. M., & Alevizaki, M. K. (2006) · European Journal of Endocrinology · doi:10.1530/eje.1.02153 · Cited by 22
Fantoni, M., Borgo, C. D., & Autore, C. (2003) · AIDS · doi:10.1097/00002030-200304001-00020 · 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
