Homeostasis model assessment: insulin resistance and ?-cell function from fasting plasma glucose and insulin concentrations in man
Open accessAbstract
The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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Claims the paper makes
1 of 6 cited sources checked · 0 supported · 0 flagged · accuracy not yet measured
- Premisecitation
Fasting plasma insulin concentration is largely determined by the glucose concentration.
“The fasting plasma insulin concentration is largely determined by the glucose concentration [3]”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [3] McCarthy ST, Harris F, Turner RC (1977) Glucose control of basal insulin secretion in diabetes. Diabetologia 13: 93?97 source
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)
Experimental — accuracy not yet measured
- Findingown data
HOMA estimate of deficient beta-cell function correlates with the hyperglycaemic clamp estimate (Rs=0.61, p<0.01).
“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)”
Quote in the paperSubstantial 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).
- Findingown data
HOMA estimate of insulin resistance correlates with the euglycaemic clamp estimate (Rs=0.88, p<0.0001).
“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)”
Quote in the paperSubstantial 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).
- Findingown data
HOMA estimate of insulin resistance does not correlate with any aspect of insulin-receptor binding.
“There was no correlation with any aspect of insulin-receptor binding.”
Quote in the paperNot a substantial 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).
- Findingown data
HOMA estimate of insulin resistance correlates with the fasting insulin concentration (Rs=0.81, p<0.0001).
“the fasting insulin concentration (P~ = 0.81, p < 0.0001)”
Quote in the paperSubstantial 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).
- Findingown data
The mean coefficient of variation of paired HOMA beta-cell function estimates over the two reproducibility studies was 32%.
“The mean coefficient of variation over the two studies was 32%.”
Quote in the paperSubstantial 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).
- Findingown data
HOMA estimate of beta-cell function from a 15-min period of sampling correlates with the hyperglycaemic clamp estimate in both groups together (Rs=0.61, p<0.01).
“in both groups together (1% 0.61, p < 0.01 : Fig. 3).”
Quote in the paperSubstantial 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).
- Findingown data
HOMA estimate of deficient beta-cell function correlates with the intravenous glucose tolerance test estimate (Rs=0.64, p<0.05).
“and with the estimate from the intravenous glucose tolerance test (R~ = 0.64, p < 0.05).”
Quote in the paperSubstantial 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).
- Findingown data
Beta-cell function from the intravenous glucose tolerance test correlates with HOMA beta-cell function in both groups together (Rs=0.64, p<0.05).
“and in both groups together: 1% = 0.64, p< 0.05; Fig. 3).”
Quote in the paperSubstantial 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).
- Findingown data
Neither receptor numbers nor 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).
“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).”
Quote in the paperNot a substantial 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).
- Findingown data
HOMA estimate of insulin resistance from the mean of 15 stressed fasting samples before the hyperglycaemic clamp correlates with the hyperglycaemic clamp estimate in both groups together (Rs=0.69, p=0.0005).
“in both groups together (R~ = 0.69, p= 0.0005, Fig. 2).”
Quote in the paperSubstantial 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).
- Findingown data
HOMA estimate of insulin resistance correlates with the hyperglycaemic clamp estimate (Rs=0.69, p<0.01).
“and the hyperglycaemic clamp, (Rs=0.69,p<0.01).”
Quote in the paperSubstantial 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).
- Findingown data
CIGMA estimates of beta-cell function correlate with HOMA estimates in both groups together (Rs=0.90, p<0.0001).
“and in both groups of subjects together (1% = 0.90, p< 0.0001).”
Quote in the paperSubstantial 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).
- Findingown data
HOMA estimate of insulin resistance from the mean of 15 stressed fasting samples before CIGMA correlates with the CIGMA estimate in both groups together (Rs=0.87, p<0.0001).
“in both groups together (Rs = 0.87, p < 0.0001).”
Quote in the paperSubstantial 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).
- Premisecitation
Basal hyperglycaemia in diabetes arises from the feedback loop between the liver and beta-cells, maintaining effective insulin action in the liver and periphery.
“the basal hyperglycaemia in diabetes appears to arise from the feedback loop between the liver and/3-cells, thereby maintaining an effective insulin action in the liver and at the periphery [1,4].”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationreasoning
Hyperglycaemia results from a combination of beta-cell dysfunction and insulin resistance, rather than from either alone.
“This is not surprising in that the hyperglycaemia results from a combination of these two factors, rather than from either alone.”
Quote in the paperSubstantial 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).
- Premisecitation
Fasting plasma glucose and insulin concentrations in each normal subject or Type 2 diabetic patient are set at a level characteristic for that individual for a given state of nutrition.
“The fasting plasma glucose and insulin concentrations in each normal subject or Type 2 (non-insulin-dependent) diabetic patient are set at a level characteristic for that individual for a given state of nutrition [1,2].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [1] Holman RR, Turner RC (1979) Maintenance of basal plasma glucose and insulin concentration in maturity-onset diabetes. Diabetes 28: 227?230 source
- cites [2] Holman RR, Turner RC (1980) The basal plasma glucose: a simple relevant index of maturity onset diabetes. Clin Endocrinol 14: 279?286 source
- Interpretationown data
The correlation of HOMA estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feedback loop.
“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.”
Quote in the paperSubstantial 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).
- Interpretationreasoning
Fasting plasma insulin and glucose concentrations found in normal and diabetic subjects were similar to those predicted by the mathematical model, given the insulin resistance and beta-cell function as measured by other tests.
“Thus, the fasting plasma insulin and glucose concentrations found in normal and diabetic subjects were similar to those which the mathematical model predicted, given the insulin resistance and fl-cell function as measured by other tests.”
Quote in the paperSubstantial 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).
- Interpretationown data
HOMA allows quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to fasting hyperglycaemia.
“Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient r-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA).”
Quote in the paperSubstantial 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).
- Interpretationreasoning
The results accord with a major role for the simple interaction of plasma glucose and insulin between the liver, beta-cells and periphery.
“it accords with a major rrle for the simple interaction of plasma glucose and insulin between the liver,/3-cells and periphery.”
Quote in the paperSubstantial 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).
- Interpretationown data
The low precision of HOMA estimates limits its use.
“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”
Quote in the paperSubstantial 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).
- Premisecitation
Predictions from the mathematical model of glucose:insulin interactions are in accord with known data in man.
“The predictions from the model are in accord with known data in man [5].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [5] Turner RC, Holman RR, Matthews DR, Hockaday TDR, Peto J (1979) Insulin deficiency and insulin resistance interaction in diabetes: estimation of their relative contribution by feedback analysis from basal insulin and glucose concentrations. Metabolism 28: 1086?1096 source
- Interpretationreasoning
The degree of basal hyperglycaemia is determined by a combination of beta-cell deficiency and insulin resistance.
“The degree of basal hyperglycaemia is thus determined by a combination of/3-cell deficiency and insulin resistance.”
Quote in the paperSubstantial claim
- May combine two claims. 2
- The quote only partly states this claim. 1
May combine two claims.
Findingown dataHOMA estimates have low precision, with coefficients of variation of 31% for insulin resistance and 32% for beta-cell deficit.
“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”
Quote in the paperSubstantial 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 quote only partly states this claim.
Findingown dataThe mean coefficient of variation of HOMA estimates of insulin resistance over the two reproducibility studies was 31%.
“The mean coefficient of variation over the two studies was 31%.”
Quote in the paperNot a substantial 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).
May combine two claims.
FindingreasoningThe degree of hyperglycaemia does not correlate significantly with either the degree of abnormal beta-cell function or insulin resistance.
“The degree of the hyperglycaemia does not correlate significantly with either the degrees of abnormal fl-cell function or insulin resistance.”
Quote in the paperSubstantial 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 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?
HOMA-IR decreased significantly after the unprocessed diet compared with baseline.
“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 Homeostasis Model Assessment of Insulin Resistance (HoMA-IR) was calculated according to Matthews et al.
“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]
Surrogate markers of peripheral insulin activity, such as homeostasis model assessment and whole-body insulin sensitivity indexes, could be useful for early identification of insulin resistance before overt diabetes.
“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]
Indirect estimates of insulin resistance, such as HOMA-IR and QUICKI, 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.
“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.
Normal and diabetic group sizes are reversed for the CIGMA comparison
MinorThe methods say the CIGMA comparison used 12 normal subjects and 11 diabetic patients, but the results report 11 normal subjects and 12 diabetic subjects.
“The same 12 normal subjects and 11 Type 2 diabetic patients came to the hospital fasting on a separate day for a continuous infusion”
“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)”
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Self-citation
- 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 › Surgery › 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.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-14.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-14.
Cited sources are checked by gpt-6-sol.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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