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 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
“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]
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 25,401–25,500 of 31,469
Kondratyeva, L. V., Попкова, Т. В., & Nasonov, E. L. (2019) · Rheumatology Science and Practice · doi:10.14412/1995-4484-2019-280-283 · Cited by 4
Machado, T. Q., Pereira‐Silva, D. C., Gonçalves, L. F., et al. (2019) · Integrative Diabetes and Cardiovascular Diseases · doi:10.18314/idcd.v3i1.1817 · Cited by 4
Doi, Y., Kubo, M., Ninomiya, T., Yonemoto, K., Iwase, M., Arima, H., Hata, J., Tanizaki, Y., Iida, M., & Kiyohara, Y. (2007) · Diabetes · doi:10.2337/db07-1709 · Cited by 5
Doghaither, H. A. A., Alshaikh, E. M., Omar, U. M., Alsufiani, H. M., Mansouri, R. A., Tarbiah, N. I., Alshaikh, A. A., & Alshaikh, A. M. (2019) · Europe PMC (PubMed Central) · Cited by 4
Arterial stiffness in young women with Turner syndrome using cardio-ankle vascular index
Heo, Y. J., Jung, H. W., Lee, Y. A., Shin, C. H., & Yang, S. W. (2019) · Annals of Pediatric Endocrinology & Metabolism · doi:10.6065/apem.2019.24.3.158 · Cited by 4
Léniz, A., Fernández‐Quintela, A., del Hoyo, M., López, I. D., & Portillo, M. P. (2020) · Journal of Physiology and Biochemistry · doi:10.1007/s13105-020-00750-4 · Cited by 4
Jovanović, G. K., Mrakovčić-Šutić, I., Udović, I. Š., & Majanović, S. K. (2020) · European Journal of Integrative Medicine · doi:10.1016/j.eujim.2020.101165 · Cited by 4
Zanetti, H. R., Mendes, E. L., Gonçalves, A., Lopes, L. T. P., Roever, L., Silva-Vergara, M. L., Neves, F. F., & Resende, E. S. (2020) · The Journal of Sports Medicine and Physical Fitness · doi:10.23736/s0022-4707.20.10838-7 · Cited by 4
Polycystic Ovary Syndrome and Hyperandrogenic States
Chang, R. J. (2009) · Elsevier eBooks · doi:10.1016/b978-1-4160-4907-4.00020-6 · Cited by 5
Wasenius, N., Isomaa, B., Östman, B., Söderström, J., Forsén, B., Lahti, K., Hakaste, L., Eriksson, J. G., Groop, L., Hansson, O., et al. (2020) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2020-001377 · Cited by 4
Bobrus‐Chociej, A., Wasilewska, N., Harasim‐Symbor, E., Flisiak‐Jackiewicz, M., Wojtkowska, M., Chabowski, A., & Lebensztejn, D. M. (2020) · Advances in Medical Sciences · doi:10.1016/j.advms.2020.11.004 · Cited by 4
Abdelhaffez, A., El-Aziz, E. A. A., Tohamy, M. B., & Ahmed, A. M. (2021) · Archives of Physiology and Biochemistry · doi:10.1080/13813455.2021.1876735 · Cited by 4
Zhao, L., Lü, A., Shen, W., Liu, H., Xiao-ye, M. A., Fan, X., & Zhang, Q. (2010) · Chinese Medical Journal · doi:10.3760/cma.j.issn.0366-6999.2010.06.003 · Cited by 4
Saito, H. (2015) · Journal of Food and Nutrition Sciences · doi:10.11648/j.jfns.20150304.11 · Cited by 4
Wakatsuki, A., Ogawa, Y., Saibara, T., Okatani, Y., & Fukaya, T. (2002) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.87.8.3676 · Cited by 4
Hallikainen, M., Vidgren, H. M., Ågren, J. J., Kiviniemi, V. V., Miettinen, T. A., & Gylling, H. (2006) · Clinica Chimica Acta · doi:10.1016/j.cca.2006.05.028 · Cited by 4
Is there any use for the oral glucose tolerance test?
Vaccaro, O., Ruffa, G., & Riccardi, G. (2000) · Diabetes Care · doi:10.2337/diacare.23.5.714a · Cited by 4
Body fatness, insulin sensitivity and muscle oxygen supply in adolescents
Arrowsmith, F., Ward, J. A., Rooney, K. B., Kriketos, A. D., Baur, L. A., & Thompson, C. H. (2002) · Clinical Science · doi:10.1042/cs1030391 · Cited by 4
Warensjö, E. (2007) · Uppsala University Publications (Uppsala University) · Cited by 4
Assessment of Insulin Sensitivity
Szendroedi, J., Phielix, E., & Roden, M. (2011) · Wiley eBooks · doi:10.1002/9781444347319.ch6 · Cited by 4
Homeostasis Model Assessment (HOMA) en Pacientes Diabéticos Tipo 2
Bermúdez, V., Cano-Ponce, C., Souki, R., Mayerlim Medina, R., Lemus, M. A., Elliuz Leal, G., Arias, N., Merlyn Ambard de las, S., Maryluz Núñez, P., John Andrade, G., et al. (2000) · AVFT – Archivos Venezolanos de Farmacología y Terapéutica · Cited by 4
Bartnik, M. (2005) · Figshare · Cited by 4
Treatment of type 2 diabetes: the sooner, the better
Yamada, T., Komatsu, M., Sato, A., et al. (2001) · Journal of Internal Medicine · doi:10.1046/j.1365-2796.2001.00873.x · Cited by 4
Non-radioisotopic glucose turnover in children with falciparum malaria and enteric fever
Singh, B. B., Choo, K. E., Ibrahim, J., et al. (1998) · Transactions of the Royal Society of Tropical Medicine and Hygiene · doi:10.1016/s0035-9203(98)90903-8 · Cited by 4
Do Resistin and Tumor Necrosis Factor-α Relate to Changes in Insulin Resistance in Normal Pregnancy?
Zarei, S. (2010) · American journal of biochemistry & biotechnology/American journal of biochemistry and biotechnology · doi:10.3844/ajbbsp.2010.19.24 · Cited by 4
Kishimoto, H., Taniguchi, A., Sakai, M., et al. (2001) · Diabetic Medicine · doi:10.1046/j.1464-5491.2001.00526-4.x · Cited by 4
Kanauchi, M. (2003) · European Journal of Clinical Investigation · doi:10.1046/j.1365-2362.2003.01249.x · Cited by 4
Kamei, N., Yamane, K., Nakanishi, S., Ishida, K., Ohtaki, M., Okubo, M., & Kohno, N. (2005) · Metabolism · doi:10.1016/j.metabol.2004.12.016 · Cited by 4
Fernandes, A. C., Gazzinelli, A., & Velásquez-Meléndez, G. (2009) · PubMed · Cited by 4
Mastroeni, S. S. D. B. S. (2009) · doi:10.11606/t.6.2009.tde-29092009-101158 · Cited by 4
Índice glicêmico da dieta habitual e alteração da homeostase glicêmica em nipo-brasileiros de Bauru
Sartorelli, D. S. (2005) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.6.2005.tde-15042008-102623 · Cited by 4
Alonso, M. Á. M., & González‐Jiménez, E. (2014) · PubMed · doi:10.3305/nh.2013.28.3.6437 · Cited by 4
Adipocyte insulin action in hypogonadotrophic hypogonadism
Marsden, P. J. (2000) · Human Reproduction · doi:10.1093/humrep/15.8.1672 · Cited by 4
Hockaday, T. D. R. (2005) · Diabetologia · doi:10.1007/s00125-004-1656-4 · Cited by 4
Treiber, K. H. (2006) · VTechWorks (Virginia Tech) · Cited by 4
Genetic disorders in the growth hormone-IGF-I axis
Walenkamp, M. J. (2007) · Leiden Repository (Leiden University) · Cited by 4
de Araújo, C., Fitz, R. C., Nogara, D. A., Schestatsky, P., & Gerchman, F. (2018) · Trials · doi:10.1186/s13063-018-2776-3 · Cited by 5
Does insulin signalling decide glucose levels in the fasting steady state?Preprint
Diwekar-Joshi, M., & Watve, M. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/553016 · Cited by 4
Index of Cardiac Age Index and Cardiometabolic Biomarkers in Adults with Metabolic Syndrome
Choi, E. J., & Lee, S. Y. (2021) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2020.0095 · Cited by 4
Eisenstein, E. L., Peterson, E. D., Jollis, J. G., Tardiff, B. E., Califf, R. M., Knight, J. D., & Mark, D. B. (1997) · Europe PMC (PubMed Central) · Cited by 4
Kruszyńska, E., Kozakova, M., Loboz Rudnicka, M., Morizzo, C., Palombo, C., Loboz Grudzien, K., & Jaroch, J. (2019) · Journal of Metabolic Syndrome · doi:10.4172/2167-0943 · Cited by 4
Elkind-Hirsch, K. E., Chappell, N. R., Shaler, D., Storment, J. M., & Bellanger, D. E. (2021) · Research Square · doi:10.21203/rs.3.rs-799341/v1 · Cited by 4
Being Born Large for Gestational Age : Metabolic and Epidemiological Studies
Ahlsson, F. (2008) · Uppsala University Publications (Uppsala University) · Cited by 4
Amirkhizi, F., Taghizadeh, M., Hamedi-Shahraki, S., & Asghari, S. (2025) · Nutrition & Metabolism · doi:10.1186/s12986-025-00932-1 · Cited by 3
“Insulin resistance was evaluated by calculating Homeo-static Model Assessment for Insulin Resistance (HOMA-IR) according to the formula developed by Matthews et al. as following formula: fasting insulin (U/l) × fasting glucose (mg/dl)/405 [33].”
Mesri Alamdari, N., Namazi Shabestari, A., Najafipour, F., & Mirmazhari, A. (2024) · Biomedicine Advances · doi:10.34172/bma.05 · Cited by 4
“The homeostatic model assessment for IR (HOMA-IR) was used as follows 23 : HOMA-IR = [fasting insulin (µIU/ mL) × fasting glucose (mg/dL)] /405.”
Adelmeyer, J., Schauer, C. M., & Kann, P. H. (2024) · Hormones · doi:10.1007/s42000-024-00542-1 · Cited by 3
“These data were used to calculate homeostasis model assessment for insulin resis - tance (HOMA IR) [17], insulin sensitivity Matsuda Index (ISI-M) [ 18 ], and area under the curve (AUC 0-300 min) of insulin using Simpsons rule to evaluate insulin secretion and resistance.”
Zakrzewski-Fruer, J. K., Morari, V., Champion, R. B., Bailey, D. P., Ferrandino, L., & Jones, R. L. (2023) · Nutrients · doi:10.3390/nu15143210 · Cited by 3
Genovesi, S., Tassistro, E., Lieti, G., Patti, I., Giussani, M., Antolini, L., Orlando, A., Salvi, P., & Parati, G. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12216919 · Cited by 3
Mievis, V., Minschart, C., Myngheer, N., Maes, T., Block, C. E. M. D., Bochanen, N., Pottelbergh, I. V., Abrams, P. J., Vinck, W. J., Leuridan, L., et al. (2024) · Diabetic Medicine · doi:10.1111/dme.15400 · Cited by 4
Sundaram, R., muthu, K., Almansour, A. I., et al. (2024) · Revista Brasileira de Farmacognosia · doi:10.1007/s43450-024-00600-0 · Cited by 3
Singhal, S., CHAUHAN, K., Tripathi, A., & CHOUDHARY, R. (2024) · MAEDICA – a Journal of Clinical Medicine · doi:10.26574/maedica.2024.19.3.494 · Cited by 3
Wang, G. (2024) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2024.108037 · Cited by 4
Simon, A. B., Yackobovitch‐Gavan, M., Uretzky, A., Segev‐Becker, A., Perl, L., Midlij, E., Borger, O., Brener, A., & Lebenthal, Y. (2024) · Pediatric Research · doi:10.1038/s41390-024-03776-2 · Cited by 3
Tanaka, N. I., Kitagawa, F., & Akima, H. (2024) · Clinical Physiology and Functional Imaging · doi:10.1111/cpf.12922 · Cited by 3
Schroeder, H. T., Muller, C. H. D. L., Rodrigues, M. I. L., de Azevedo, M. A., Heck, T. G., Krause, M. D. S., & de Bittencourt, P. I. H. (2024) · Clinical Science · doi:10.1042/cs20243515 · Cited by 4
Thomas, J. V., Davy, B. M., Winett, R. A., Depner, C. M., Drummond, M. J., Estabrooks, P. A., Hardikar, S. S., Ou, Z., Shen, J., & Halliday, T. M. (2025) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00507.2024 · Cited by 4
Hazaimeh, R. A., Shackelford, L. A., & Boateng, J. A. (2025) · Journal of Functional Foods · doi:10.1016/j.jff.2025.106693 · Cited by 3
Polycystic Ovary Syndrome and Sex Hormones in Bariatric Surgery Candidates
Dong, S., Law, S., Ou, C., Wu, B., Dong, Z., Yang, W., & Zhang, X. (2025) · Obesity Surgery · doi:10.1007/s11695-025-07740-9 · Cited by 4
van der Sluijs, K. M., Vloet, J. I. A., Thijssen, D. H. J., Eijsvogels, T. M. H., & Bakker, E. A. (2025) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000003705 · Cited by 3
Kamani, L., Siddiqui, M., & Rahat, A. (2025) · BMC Gastroenterology · doi:10.1186/s12876-025-03790-6 · Cited by 4
Variations in Human Milk Metabolites After Gestational Diabetes: Associations with Infant Growth
Fradet, A., Berthiaume, L., Laroche, L.-A., Dugas, C., Perron, J., Doyen, A., Audet‐Walsh, É., & Robitaille, J. (2025) · Nutrients · doi:10.3390/nu17091466 · Cited by 5
Zhang, Q., Zhang, Q., Dong, S.-Q., Liu, X., Wei, J., Li, K., & Yu, L. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1486197 · Cited by 3
Pancreatic Fat Infiltration: A Key Marker in the Metabolic Continuum
Marín‐Serrano, E., de Villar, N. G. P., Manuel, M. P. J., Fernández-Martos, R., Cano, A. B., & Martín‐Arranz, M. D. (2025) · Pancreas · doi:10.1097/mpa.0000000000002505 · Cited by 3
Intranasal insulin enhances resting-state functional connectivity in Type 2 Diabetes
Zhang, Z., Novak, V., Novák, P., Mantzoros, C. S., Ngo, L. H., Lioutas, V., & Dai, W. (2025) · PLoS ONE · doi:10.1371/journal.pone.0324029 · Cited by 3
Ouyang, Y., Xiang, X., Hu, X., Chu, X., Tang, W., & Feng, W. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1580159 · Cited by 3
Microbial metabolism mediates the deteriorative effects of sedentary behaviour on insulin resistance
Ju, J., He, J., Ye, B., Li, S., Zhao, J., Chen, W., Zhang, Q., Zhao, W., Yang, J., Liu, L., et al. (2025) · Clinical and Translational Medicine · doi:10.1002/ctm2.70348 · Cited by 4
Bock, P. M., Kowalewski, L. S., Ayres, L. R., Russo, M. K. B., Dornelles, L. I., Leites, G. T., Martins, A. F., de Oliveira, Á. R., & Krause, M. D. S. (2025) · Sao Paulo Medical Journal · doi:10.1590/1516-3180-2024.0040.r1.13082024 · Cited by 3
Hofmann, K., Singer, S., Theis, S., Hasenburg, A., Schwab, R. M., & Skala, C. (2025) · Minerva Endocrinology · doi:10.23736/s2724-6507.25.04245-9 · Cited by 3
Cai, M., Hou, G., Guo, S., Liu, Y., Zhao, C., Zhao, L., Su, L., Li, K., Yue, Q., & Zhang, S. (2025) · Scientific Reports · doi:10.1038/s41598-025-06935-5 · Cited by 3
Wang, H., Wei, X., Ba, Y., Liu, H., Zhou, Y., Wang, W., & Zheng, L. (2025) · Endocrine Connections · doi:10.1530/ec-25-0191 · Cited by 3
Iman, A. E. H., Onel, C., Furău, G. O., Furau, C. G., Furau, R., Lucan, M., Şandor, M. I., Sachelarie, L., & Huniadi, A. C. (2025) · Diagnostics · doi:10.3390/diagnostics15131704 · Cited by 3
Žák, A., Vecka, M., Szitányi, P., Floriánková, M., Staňková, B., Uhlíková, P., Dostálová, V., & Burda, M. (2025) · Nutrients · doi:10.3390/nu17142347 · Cited by 3
Pagano, R., Ostolin, T. L. V. D. P., Fonseca, D. C., Marcadenti, A., Carvalho, A. P. P. F., Weber, B., Daltro, C., Lara, E. M. D. S., Nolêto, F. C. M., Bressan, J., et al. (2025) · Nutrients · doi:10.3390/nu17152518 · Cited by 4
de Deus, I. J., de Abreu, A. R. D., Fagundes, M. M. D. A., Silva, J. L., Breguez, G. S., Silva, Â. A., Siqueira, É. C. D. S. O., Carneiro, C. M., Costa, D. C., Paula-Gomes, S., et al. (2025) · Journal of Developmental Origins of Health and Disease · doi:10.1017/s2040174425100123 · Cited by 3
Pastore, M. N., Bonfiglio, C., Tatoli, R., Donghia, R., Pesole, P. L., & Giannelli, G. (2025) · Nutrients · doi:10.3390/nu17152477 · Cited by 4
Hernández-García, M. Á., Orzaiz, B. A., Fernández-García, C. E., Fuertes-Yebra, E., Rey, E., Berlana, Á., Farré, R., García‐Monzón, C., Almendros, I., Landete, P., et al. (2025) · Antioxidants · doi:10.3390/antiox14080971 · Cited by 6
Cheng, G., Zhou, Y., Wang, Y., Tao, L., & Xu, J. (2025) · Journal of Clinical & Translational Endocrinology · doi:10.1016/j.jcte.2025.100414 · Cited by 3
Berbrier, D. E., Huckins, W., Berkel, E. K. V., Delage, S. I., Hannaian, S. J., Myara, R., Okafor, O. N., Chung, T. H., Tulandi, T., Reinblatt, S. L., et al. (2025) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00286.2025 · Cited by 3
Rubino, M., Massimino, M., Mancuso, E., Averta, C., Palummo, A., Perticone, M., Succurro, E., Sciacqua, A., Mannino, G. C., & Andreozzi, F. (2025) · Acta Diabetologica · doi:10.1007/s00592-025-02576-2 · Cited by 4
Azar, M. M., Shirazinia, M., Nematy, M., Rahimi, V. B., Bateni, M., Gheibi, F. T. P., Rajabzadeh, F., Goshayeshi, L., Honari, S., Mottahedi, M., et al. (2025) · Inflammopharmacology · doi:10.1007/s10787-025-01919-3 · Cited by 4
Khoudary, S. R. E., Matuk, J., Brooks, M. M., McConnell, D. S., Crawford, S. L., Wang, Z., Janssen, İ., & Rader, D. J. (2025) · JACC Advances · doi:10.1016/j.jacadv.2025.102131 · Cited by 4
Açmaz, B., Bahçebaşı, S., Aydın, E., Yıldız, Ş., & Biçer, İ. (2025) · Journal of Diabetes Research · doi:10.1155/jdr/9933219 · Cited by 5
Kusano, K., Uno, K., Tamahara, T., Asano, N., Sudo, K., Tanabe, M., Ogasawara, K., Kanno, T., Koike, T., Shimizu, R., et al. (2025) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2025.101629 · Cited by 4
Xin, G., Li, H., & Ji, J. (2025) · PeerJ · doi:10.7717/peerj.19994 · Cited by 3
Murugavel, S., Retnakaran, R. R., Feig, D. S., Zinman, B., & Kramer, C. K. (2025) · Diabetes Obesity and Metabolism · doi:10.1111/dom.70146 · Cited by 3
Ozkaya, D. Y., Haymana, C., Demirci, İ., Duman, U. G., Küpçük, E., Koç, G. E., Taşçı, İ., & Sonmez, Y. A. (2025) · Archives of Endocrinology and Metabolism · doi:10.20945/2359-4292-2025-0063 · Cited by 5
Liu, H., Tang, G., Yuan, Y., et al. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1643360 · Cited by 3
Chen, Y., Zhou, Q., Ju, H., et al. (2025) · Diabetology & Metabolic Syndrome · doi:10.1186/s13098-025-01944-w · Cited by 3
Burns, K. A., Stuckey, A. W., Wilson, S. G., Watts, G. F., & Stuckey, B. G. A. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1572427 · Cited by 6
Memetoglu, O., Du, F., Chouinard, V., & Öngür, D. (2025) · Biological Psychiatry · doi:10.1016/j.biopsych.2025.10.008 · Cited by 4
Ewell, T. R., Bomar, M. C., Abbotts, K. S. S., et al. (2025) · Cannabis and Cannabinoid Research · doi:10.1177/25785125251391085 · Cited by 3
Gut Microbiota, Intestinal Barrier Function, and Metabolism Across Adiposity and Glucose Tolerance
Lopes, K. G., de Souza, M. D. G. C., Lopes, F. D. A. M., Júnior, V. L. D. S., Carvalho, A. T. P., Rapozo, D. C. M., Barbosa, C. M. D. L., Bouskela, E., Castiglione, R. C., Albano, R. M., et al. (2025) · Nutrients · doi:10.3390/nu17213380 · Cited by 4
Lee, H. J., Lee, Y. H., Kim, J. S., et al. (2025) · Kidney Research and Clinical Practice · doi:10.23876/j.krcp.25.095 · Cited by 3
Kishimoto, M., Tamaru, S., & Odawara, M. (2025) · Scientific Reports · doi:10.1038/s41598-025-23404-1 · Cited by 5
de Luis, D. A., Izaola, O., Primo, D., Rico, D., & Gómez, J. J. L. (2025) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2025.109209 · Cited by 3
Jia, X., Wang, S., Wang, J., Ding, Y., Li, M., Lin, Y., Zheng, R., Huang, F., Wei, H., Hu, C., et al. (2025) · Cardiovascular Diabetology · doi:10.1186/s12933-025-03008-9 · Cited by 5
Mensah, D. O., Everett, A. B., Fouts, A. E., Hoelscher, G. L., Martin, S. L., Bahorski, J. S., Mensah, P. H., Callahan, M. L., Garvey, W. T., & Chandler-Laney, P. C. (2025) · Pediatric Obesity · doi:10.1111/ijpo.70066 · Cited by 4
Belfort-DeAguiar, R., Yeckel, C., Elshafie, A., Comarella, A. P., & Hwang, J. J. (2025) · Diabetes Care · doi:10.2337/dc25-1395 · Cited by 5
Updated Review of HOMA-IR (Homeostatic Model Assessment for Insulin Resistance)
Ambalavanan, J. (2025) · Evidence to Action Official Journal of MDCalc · doi:10.65357/001c.154184 · Cited by 5
Kondamudi, S., Sadu, S., Deva, S., Yalamanchi, A., & Yalamanchi, A. (2025) · Food & Nutrition Research · doi:10.29219/fnr.v69.13244 · Cited by 4
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
