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.
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Claims the paper makes
15 Own result · 7 Own interpretation · 3 No full text of the sources · 1 Partly supported · 1 No basis given · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The fasting plasma insulin concentration is largely determined by the glucose concentration [3]”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
What the sources say
- Partly supportedcites [3] McCarthy ST, Harris F, Turner RC (1977) Glucose control of basal insulin secretion in diabetes. Diabetologia 13: 93?97 sourceExperimental — accuracy not yet measured
The Results and Discussion (page unavailable in our copy) show that changing plasma glucose affects basal insulin secretion. But they also report markedly impaired responses in diabetic subjects, including cases where insulin remained nearly constant despite a substantial glucose decrease. The paper therefore supports glucose as an influence, but not the unqualified claim that it largely determines fasting insulin concentration. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The estimate of deficient/3cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (R~ = 0.61, p< 0.01)”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (R~=0.88,p<0.0001)”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There was no correlation with any aspect of insulin-receptor binding.”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the fasting insulin concentration (P~ = 0.81, p < 0.0001)”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mean coefficient of variation over the two studies was 32%.”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Reproducibility of estimate of /3-cell function by HOMA
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“in both groups together (1% 0.61, p < 0.01 : Fig. 3).”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Comparisons of methods of assessing ~3-cell function
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and with the estimate from the intravenous glucose tolerance test (R~ = 0.64, p < 0.05).”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and in both groups together: 1% = 0.64, p< 0.05; Fig. 3).”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > HOMA compared with intravenous glucose tolerance test.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Neither receptor numbers or any aspect of high or low affinity binding correlated with other measures of insulin resistance (HOMA, clamp, basal insulin or CIGMA: ~ all < 0.55; NS).”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > HOMA compared with the hyperglycaemic clamp. The
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
- It may state two separate claims as one. 2
- The quote only partly states this claim. 1
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for/3-cell deficit) limits its use”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Summary.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mean coefficient of variation over the two studies was 31%.”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Hyperglycaemic clamp : ~-cell function (%)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The degree of the hyperglycaemia does not correlate significantly with either the degrees of abnormal fl-cell function or insulin resistance.”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Discussion
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- The authors state this as an assumption: Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
- Rests on an assumption: The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
The authors state this as an assumption.
Normal-weight normal subjects aged <35 years have 100% beta-cell function and an insulin resistance of 1.
“Assuming that normal-weight normal subjects aged < 35 years have 100% r-cell function, and an insulin resistance of 1, the values for a patient can be assessed from the insulin and glucose concentrations by the formulae: r-cell”
The paper relies on this without support.
The plasma glucose:insulin response for normal subjects is equivalent to the C-peptide response and is insulin = 5 (glucose-3.5).
“The plasma glucose:insulin response for normal subjects, equivalent to the C-peptide response, is insulin = 5 (glucose-3.5).”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Surrogate markers of peripheral insulin activity, such as homeostasis model assessment and whole-body insulin sensitivity indexes, could be useful as well in the early identification of patients with IR, before overt DM sets in ().”
From Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management (2017) · cites this paper as [240]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“After the unprocessed diet, fasting glucose and insulin levels tended to decrease compared to baseline and the homeostasis model assessment of insulin resistance (HOMA-IR) (Matthews et al., 1985) was significantly decreased compared to baseline.”
From Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake (2019) · cites this paper as Matthews et al., 1985
The cited source says what the claim attributes to it.
In the citing paper
“The Homeostasis Model Assessment of Insulin Resistance (HoMA-IR) was calculated according to Matthews et al. [25].”
From Chronotype: A Tool to Screen Eating Habits in Polycystic Ovary Syndrome? (2022) · cites this paper as [25]
The cited source says what the claim attributes to it.
In the citing paper
“AAV9-mTERT treated mice also showed a trend for an improved glucose uptake and a better homeostatic model assessment (HOMA (Heikkinen et al, 2007; Matthews et al, 1985)) compared to the AAV9-eGFP controls, although differences did not reach statistical significance (Supporting Information Fig S4D and E).”
From Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer (2012) · cites this paper as Matthews et al, 1985
In the citing paper
“ndirect estimates of insulin resistance, such as HOMA-IR 63 and QUICKI, 64 are derived from fasting S-insulin and glucose concentrations and have been widely used in both nondiabetic and type 2 diabetic subjects as surrogates of insulin sensitivity.65,66”
From Increased liver fat, impaired insulin clearance, and hepatic and adipose tissue insulin resistance in type 2 diabetes. (2008) · cites this paper as [63]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > Subjects and procedures
“The same 12 normal subjects and 11 Type 2 diabetic patients came to the hospital fasting on a separate day for a continuous infusion”
§ Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man > HOMA compared with the hyperglycaemic clamp. The
“HOMA compared with CIGMA.The HOMA estimate of insulin resistance from the mean of 15 stressed fasting samples before the CIGMA correlated with that measured by CIGMA in 11 normal subjects (R~ = 0.69, p < 0.02), in 12 diabetic subjects (R~ 0.97, p < 0.0001)”
Citations
Cites
Glucose clamp technique: a method for quantifying insulin secretion and resistance.
DeFronzo, R. A., Tobin, J. D., & Andres, R. (1979) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1979.237.3.e214 · Cited by 7,425
Quantitative estimation of insulin sensitivity.
Bergman, R. N., Ider, Y. Z., Bowden, C. R., & Cobelli, C. (1979) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1979.236.6.e667 · Cited by 1,874 · cited 1×
“This use of modelling to provide a reference graph contrasts with other models where an individual patient's data have to be entered into a computer to determine the relationships between rapidly changing variables, such as occur after an intravenous glucose test [19].”
Method[WHO Expert Committee on diabetes mellitus].
Reitsma, W. D., & Terpstra, J. (1981) · PubMed · Cited by 556
Turner, R. C., Holman, R. R., Matthews, D., Hockaday, T. D. R., & Peto, J. (1979) · Metabolism · doi:10.1016/0026-0495(79)90146-x · Cited by 388
Self-citationCharacteristics of Human Erythrocyte Insulin Receptors
Gambhir, K. K., Archer, J. A., & BRADLEY, C. J. (1978) · Diabetes · doi:10.2337/diab.27.7.701 · Cited by 290
The Insulin Receptor: Its Role in Insulin Resistance of Obesity and Diabetes
Olefsky, J. M. (1976) · Diabetes · doi:10.2337/diab.25.12.1154 · Cited by 289
Hosker, J. P., Matthews, D. R., Rudenski, A. S., Burnett, M. A., Darling, P., Bown, E. G., & Turner, R. C. (1985) · Diabetologia · doi:10.1007/bf00280882 · Cited by 287
Self-citationPulsatile Insulin Has Greater Hypoglycemic Effect Than Continuous Delivery
Matthews, D. R., Naylor, B. A., Jones, R., Ward, G. M., & Turner, R. C. (1983) · Diabetes · doi:10.2337/diab.32.7.617 · Cited by 256
Self-citationControl of pulsatile insulin secretion in man
Matthews, D. R., Lang, D. A., Burnett, M. A., & Turner, R. C. (1983) · Diabetologia · doi:10.1007/bf00282705 · Cited by 175
Self-citationTHE BASAL PLASMA GLUCOSE: A SIMPLE RELEVANT INDEX OF MATURITY‐ONSET DIABETES
HOLMAN, R. R., & TURNER, R. C. (1981) · Clinical Endocrinology · doi:10.1111/j.1365-2265.1981.tb00196.x · Cited by 64
Self-citation
Research works printed but not linked: 2
- Metropolitan Life Assurance Co (1959) Net weight standard for men and women. Stat Bull Metrol Life Found 40: 1?4
- Matthews DR, Hosker JP (1984) An unbiased, flexible computer programme for glucose clamping, with graphics and running statistics. Diabetologia 27: 308?309 A
Cited by
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Items 20,601–20,700 of 31,469
Larsen, B. A., Klinedinst, B. S., Wolf, T., McLimans, K. E., Wang, Q., Pollpeter, A., Li, T., Mohammadiarvejeh, P., Fili, M., Grundy, J. G., et al. (2023) · Physiology & Behavior · doi:10.1016/j.physbeh.2023.114321 · Cited by 14
Chang, Y., Hsu, C., Chong, K., Yang, P., Ser, K., Lee, P., Chen, S., Hsuan, C., Lee, Y.-C., Hsu, C., et al. (2023) · Obesity Surgery · doi:10.1007/s11695-023-06656-6 · Cited by 11
Ruíz-Herrera, V. V., Navarro-Lara, S. A., Andrade-Villanueva, J. F., Álvarez-Zavala, M., Sánchez-Reyes, K., Toscano-Piña, M., Méndez-Clemente, A. S., Martínez-Ayala, P., Valle-Rodríguez, A., & González-Hernández, L. A. (2023) · International Journal of STD & AIDS · doi:10.1177/09564624231196600 · Cited by 10
Cai, X., Sun, J., Jin, A., et al. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106268 · Cited by 10
Liu, S., Kuang, X., Song, X., Li, H., Shao, X., Gao, T., Guo, X., Li, S., Liu, R., Li, K., et al. (2023) · Food & Function · doi:10.1039/d3fo01491f · Cited by 12
Evans, A. T., Brink, H. V., Lim, J. S. W., Jarrett, B. Y., Lin, A., Lujan, M. E., & Hoeger, K. M. (2023) · Biomedicines · doi:10.3390/biomedicines11102763 · Cited by 12
Accelerometry‐assessed sleep clusters and cardiometabolic risk factors in adolescents
Wang, M., Flexeder, C., Harris, C. P., Thiering, E., Koletzko, S., Bauer, C., Schulte‐Körne, G., Berg, A. V., Berdel, D., Heinrich, J., et al. (2023) · Obesity · doi:10.1002/oby.23918 · Cited by 10
Ruiz-Ponce, M., Cuesta-López, L., López-Montilla, M. D., et al. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115779 · Cited by 10
Cruz, K. J. C., de Oliveira, A. R. S., Fontenelle, L. C., Morais, J. B. S., Melo, S. R. D. S., dos Santos, L. R., de Sousa, T. G. V., de Freitas, S. T., Henriques, G. S., Bordin, S. A., et al. (2023) · Biological Trace Element Research · doi:10.1007/s12011-023-03938-z · Cited by 10
Ly, H. T., Pham, K. D., Le, P., Do, T. H. T., Nguyen, T. T. H., & Le, V. M. (2023) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2023.117427 · Cited by 10
Ratajczak, M., Krzywicka, M., Szulińska, M., Musiałowska, D., Kusy, K., & Karolkiewicz, J. (2024) · Diabetes Metabolic Syndrome and Obesity · doi:10.2147/dmso.s432954 · Cited by 14
Zhang, Y., Sun, J., Wasserman, H. D., Adams, J. A., Higgins, C. B., Kelly, S. C., Lantier, L., & DeBosch, B. J. (2024) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2024.01.016 · Cited by 10
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MacDonald-Ramos, K., Monroy, A., Bobadilla‐Bravo, M., & Cerbón, M. A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25042050 · Cited by 10
Calza, L., Giglia, M., Colangeli, V., et al. (2024) · HIV Medicine · doi:10.1111/hiv.13644 · Cited by 10
Li, J., Xie, R., Tian, H., Wang, D., Mo, M., Yang, J., & Guo, W. (2024) · Lipids in Health and Disease · doi:10.1186/s12944-024-02306-7 · Cited by 10
Ito, R., Fukui, T., Hayashi, T., et al. (2015) · Drugs in R&D · doi:10.1007/s40268-015-0096-6 · Cited by 10
Mita, M., Miyake, K., Zenibayashi, M., Hirota, Y., Teranishi, T., Kouyama, K., Sakaguchi, K., & Kasuga, M. (2008) · PubMed · doi:10.24546/81000869 · Cited by 10
Ruiz, N., Rangel, A., Rodríguez, C., Rodríguez, L., & Rodríguez, V. (2014) · Archivos Argentinos de Pediatria · doi:10.5546/aap.2014.511 · Cited by 15
Okyay, G. U., Okyay, K., Solak, E. P., Şahinarslan, A., Paşaoğlu, Ö. T., Ebinç, F. A., Paşaoğlu, H., Derici, Ü., Sindel, Ş., & Arınsoy, T. (2015) · Hemodialysis International · doi:10.1111/hdi.12276 · Cited by 10
Hsieh, C., Chung, R.-H., Lee, W., et al. (2015) · PLoS ONE · doi:10.1371/journal.pone.0135681 · Cited by 10
Kim, K., Ahn, N., Park, J.-S., Koh, J., Jung, S., Kim, S. H., & Moon, S. (2015) · Obesity Research & Clinical Practice · doi:10.1016/j.orcp.2015.09.008 · Cited by 10
Petta, S., Bellia, C., Mazzola, A., et al. (2011) · Journal of Viral Hepatitis · doi:10.1111/j.1365-2893.2011.01557.x · Cited by 10
Associations between aggressive behaviour scores and cardiovascular risk factors in childhood
Louise, S., Warrington, N. M., McCaskie, P. A., Oddy, W. H., Zubrick, S. R., Hands, B. P., Mori, T. A., Briollais, L., Silburn, S., Palmer, L. J., et al. (2012) · Pediatric Obesity · doi:10.1111/j.2047-6310.2012.00047.x · Cited by 10
Nanni, L., Quagliarini, F., Megiorni, F., Montali, A., Minicocci, I., Campagna, F., Pizzuti, A., & Arca, M. (2010) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2010.08.055 · Cited by 10
Chen, G., Li, M., Xu, Y., Chen, N., Huang, H., Liang, J., Li, L., Wen, J., Lin, L., & Yao, J. Y. (2012) · Diabetes Technology & Therapeutics · doi:10.1089/dia.2011.0245 · Cited by 10
Alharbi, K. K., Khan, I. A., Al‐Sheikh, Y. A., et al. (2014) · Acta Biochimica Polonica · doi:10.18388/abp.2014_1844 · Cited by 10
Hamarneh, S. R., Murphy, C. A., Shih, C. W., Frontera, W. R., Torriani, M., Irazoqui, J. E., & Makimura, H. (2014) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2014-2711 · Cited by 10
The role of adiponectin gene variants in glycemic control in patients with Type 2 diabetes
Al-Azzam, S. I., Khabour, O. F., Alzoubi, K. H., Mukattash, T. L., Ghanma, M. W., & Saleh, H. (2013) · Endocrine Research · doi:10.3109/07435800.2013.794427 · Cited by 10
Gambino, R., Bo, S., Musso, G., et al. (2007) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2007.07.005 · Cited by 10
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Li, H., Heilbronn, L. K., Da-chun, H., Poynten, A. M., Blackburn, M. A., Shirkhedkar, D. P., Kaplan, W. H., Kriketos, A. D., Ye, J., & Chisholm, D. J. (2008) · Obesity · doi:10.1038/oby.2007.76 · Cited by 10
Igaki, N., Takashima, M., Ohyama, M., et al. (2004) · Clinical and Experimental Nephrology · doi:10.1007/s10157-004-0278-y · Cited by 10
Matsuyama‐Yokono, A., Tahara, A., Nakano, R., Someya, Y., Hayakawa, M., & Shibasaki, M. (2008) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-008-0348-x · Cited by 10
Indicadores do perfil lipídico plasmático relacionados à resistência à insulina
Vasques, A. C. J., Rosado, L. E. F. P. L., Rosado, G. P., Ribeiro, R. D. C. L., Franceschini, S. D. C. C., Priore, S. E., Geloneze, B., & de Oliveira, D. R. (2009) · Revista da Associação Médica Brasileira · doi:10.1590/s0104-42302009000300030 · Cited by 10
Walton, T. A., Nishtar, S., Lumb, P. J., Crook, M. A., Marber, M. S., Gill, J. S., & Wierzbicki, A. S. (2015) · International Journal of Clinical Practice · doi:10.1111/ijcp.12615 · Cited by 10
Assessment of atrial conduction time in patients with polycystic ovary syndrome
Zehi̇r, R., Karabay, C. Y., Kocabay, G., Kalaycı, A., Kaymaz, Ö., Aykan, A. Ç., Karabay, E., & Kırma, C. (2014) · Journal of Interventional Cardiac Electrophysiology · doi:10.1007/s10840-014-9925-8 · Cited by 10
Uma exploração multidimensional dos componentes da síndrome metabólica
de Freitas, E. D., Haddad, J. P. A., & Velásquez-Meléndez, G. (2009) · Cadernos de Saúde Pública · doi:10.1590/s0102-311x2009000500014 · Cited by 10
Çalışkan, M., Çiftçi, Ö., Güllü, H., et al. (2012) · Clinical and Experimental Hypertension · doi:10.3109/10641963.2012.712176 · Cited by 10
Plasma coenzyme Q10 is increased during gestational diabetes
Giannubilo, S. R., Tiano, L., Cecchi, S., Principi, F., Tranquilli, A. L., & Littarru, G. P. (2011) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2011.07.007 · Cited by 10
Lu, H.-J., Tzeng, T., Liou, S., Chang, C. J., Yang, C. Z., Wu, M., & Liu, I.-M. (2014) · BioMed Research International · doi:10.1155/2014/652680 · Cited by 10
Chang, H.-R., Hsieh, J., Chen, M. Y., Wang, J.-H., Hsu, B., Chang, H.-R., Chen, M. Y., Hsu, B., Wang, J., & Wang, L.-Y. (2014) · The American Journal of the Medical Sciences · doi:10.1097/maj.0000000000000234 · Cited by 10
Wolfson, N., Garish, D., Goldberg, Y., Boaz, M., Matas, Z., & Shargorodsky, M. (2010) · Annals of Nutrition and Metabolism · doi:10.1159/000313453 · Cited by 10
Lima-Filho, M. O., de Figueiredo, G. L., Foss‐Freitas, M. C., Foss, M. C., & Marin‐Neto, J. A. (2010) · Brazilian Journal of Medical and Biological Research · doi:10.1590/s0100-879x2010007500051 · Cited by 10
Dorkhan, M., Tripathy, D., Malm, G., Asgharian, H., Tuomilehto, J., & Groop, L. (2008) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2008.01921.x · Cited by 10
Shape of glucose curve can be used as a predictor for screening prediabetes in obese children
Yin, C., Zhang, H.-A., Xiao, Y., & Liu, W. (2014) · Acta Paediatrica · doi:10.1111/apa.12572 · Cited by 10
Chan‐Cua, S. (2012) · Journal of the ASEAN Federation of Endocrine Societies · doi:10.15605/jafes.027.01.13 · Cited by 11
Pereira, M. A. D. G., Galvão, R. D. O., & Zanella, M. T. (2005) · Revista de Nutrição · doi:10.1590/s1415-52732005000100001 · Cited by 10
Munch‐Andersen, T., Olsen, D. B., Søndergaard, H., et al. (2012) · International Journal of Circumpolar Health · doi:10.3402/ijch.v71i0.17342 · Cited by 10
Celık, T., Iyısoy, A., Açıkel, C., et al. (2008) · Blood Pressure Monitoring · doi:10.1097/mbp.0b013e3282fed786 · Cited by 10
MTHFR C677T polymorphism, folate status and colon cancer risk in acromegalic patients
Torre, M. L., Russo, G. T., Ragonese, M., Giandalia, A., Menis, E. D., Arnaldi, G., Alibrandi, A., Buda, C. A., Romanello, G., Romeo, E. L., et al. (2013) · Pituitary · doi:10.1007/s11102-013-0499-8 · Cited by 10
Mogul, H. R., Freeman, R., Nguyen, K., Frey, M., Klein, L.-A., Jozak, S., & Tanenbaum, K. (2014) · PLoS ONE · doi:10.1371/journal.pone.0108264 · Cited by 10
Abiko, A., Makita, S., Naganuma, Y., Nagai, M., & Nakamura, M. (2011) · Internal Medicine · doi:10.2169/internalmedicine.50.4476 · Cited by 10
Inoue, T., Uchida, T., Kamishirado, H., Sakuma, M., Sakai, Y., Takayanagi, K., Hayashi, T., & Morooka, S. (2002) · Clinical Cardiology · doi:10.1002/clc.4960251110 · Cited by 10
Rijpert, M., Evers, I. M., de Valk, H. W., Vroede, M. D., Tersteeg-Kamperman, M. D. J., Heijnen, C. J., & Visser, G. H. A. (2010) · Early Human Development · doi:10.1016/j.earlhumdev.2010.10.002 · Cited by 10
Kim, H. Y., Kim, C. W., Lee, C. D., Choi, J. Y., Park, C.-H., Bae, S. H., Yoon, S. K., Han, K., & Park, Y. (2014) · Digestive Diseases and Sciences · doi:10.1007/s10620-013-2995-0 · Cited by 11
Riesco, É., Roussel, M., Lemoine, S., Garnier, S., Sanguignol, F., & Mauriège, P. (2008) · Applied Physiology Nutrition and Metabolism · doi:10.1139/h08-063 · Cited by 10
Effect of Meglitinides on Postprandial Ghrelin Secretion Pattern in Type 2 Diabetes Mellitus
Rudovich, N. N., Möhlig, M., Otto, B., Pivovarova‐Ramich, O., Spranger, J., Weickert, M. O., & Pfeiffer, A. F. H. (2010) · Diabetes Technology & Therapeutics · doi:10.1089/dia.2009.0129 · Cited by 10
Aortic elastic properties in nonalcoholic fatty liver disease
Fotbolcu, H., Yakar, T., Duman, D., Özden, K., Karaahmet, T., Tigen, K., Kurtoğlu, Ü., & Dindar, İ. (2010) · Blood Pressure Monitoring · doi:10.1097/mbp.0b013e328339e2c8 · Cited by 10
Inoue, T., Matsunaga, R., Morooka, S., et al. (2000) · Atherosclerosis · doi:10.1016/s0021-9150(99)00293-2 · Cited by 10
Vassy, J. L., Shrader, P. J., Yang, Q., Liu, T., Yesupriya, A., Chang, M., Dowling, N. F., Ned, R. M., Dupuis, J., Florez, J. C., et al. (2011) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2011.0021 · Cited by 10
Boscaini, C., & Pellanda, L. C. (2015) · Journal of Obesity · doi:10.1155/2015/846376 · Cited by 10
Hung, Y., Lee, N., Lin, S., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0049102 · Cited by 10
Ybarra, J., Fernández, S., Sánchez-Hernández, J., et al. (2014) · European Journal of Gastroenterology & Hepatology · doi:10.1097/meg.0000000000000086 · Cited by 10
A New Diabetic Mouse Model Derived from the ddY Strain
Noge, I., Kagawa, Y., & Maeda, T. (2010) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.33.988 · Cited by 10
Jermendy, Á., Körner, A., Kovács, M., et al. (2011) · Journal of Pediatric Endocrinology and Metabolism · doi:10.1515/jpem.2011.111 · Cited by 10
Association of FTO, KCNJ11, SLC30A8, and CDKN2B polymorphisms with type 2 diabetes mellitus
Nikitin, A. G., Potapov, V. A., Бровкин, А. Н., Лаврикова, Е. Ю., Ходырев, Д. С., Шамхалова, М. Ш., Андреевна, С. С., Суплотова, Л. А., Shestakova, M. V., Nosikov, V. V., et al. (2015) · Molecular Biology · doi:10.1134/s0026893315010112 · Cited by 10
Funada, J., Dennis, A., Roberts, R., Karpe, F., & Frayn, K. N. (2010) · Clinical Science · doi:10.1042/cs20100066 · Cited by 10
Gijón‐Conde, T., Graciani, A., Guallar‐Castillón, P., Aguilera, M. T., Rodríguez‐Artalejo, F., & Banegas, J. R. (2015) · Revista Española de Cardiología · doi:10.1016/j.recesp.2014.08.015 · Cited by 10
Lim, K., & Shin, Y. (2014) · Aging Clinical and Experimental Research · doi:10.1007/s40520-014-0213-3 · Cited by 10
Branchi, A., Torri, A., Berra, C., Colombo, E., & Sommariva, D. (2012) · Journal of Nutrition and Metabolism · doi:10.1155/2012/215052 · Cited by 10
Magalhães, G. C. B., Feitoza, F., Moreira, S., Carmo, A. V., Souto, F. J. D., Reis, S. R. L., Martins, M. S. F., & da Silva, M. H. G. G. (2013) · Journal of Human Nutrition and Dietetics · doi:10.1111/jhn.12110 · Cited by 10
Tsuzaki, K., Kotani, K., Fujiwara, S., et al. (2007) · Metabolism · doi:10.1016/j.metabol.2007.07.012 · Cited by 10
Ardiansyah, Shirakawa, H., Giriwono, P. E., et al. (2015) · Bioscience Biotechnology and Biochemistry · doi:10.1080/09168451.2015.1052772 · Cited by 10
Azuma, K., Curb, J. D., Kadowaki, T., Edmundowicz, D., Kadowaki, S., Masaki, K., El‐Saed, A., Nishio, Y., Seto, T. B., Okamura, T., et al. (2011) · Obesity Research & Clinical Practice · doi:10.1016/j.orcp.2011.11.007 · Cited by 10
Mäkelä, J., Lagström, H., Kaljonen, A., Simell, O., & Niinikoski, H. (2013) · Early Human Development · doi:10.1016/j.earlhumdev.2013.01.007 · Cited by 10
Exposure to Racial Discrimination and Ambulatory Blood Pressure in Women with Type 2 Diabetes
Wagner, J. A., Tennen, H. A., Finan, P. H., Feinn, R., Burg, M. M., Seawell, A. H., & White, W. B. (2015) · Stress and Health · doi:10.1002/smi.2622 · Cited by 10
Aral, C., Akkіprіk, M., Çağlayan, S., ATABEY, Z., Özışık, G., Bekiroglu, N., & Özer, A. (2011) · HORMONES · doi:10.14310/horm.2002.1321 · Cited by 10
Muldoon, M. F., Erickson, K. I., Goodpaster, B. H., Jakicic, J. M., Conklin, S. M., Sekikawa, A. M., Yao, J. K., & Manuck, S. B. (2013) · Journal of Nutrition · doi:10.3945/jn.113.174078 · Cited by 10
Sinha, A., Hollingsworth, K. G., Ball, S. G., & Cheetham, T. D. (2013) · Clinical Endocrinology · doi:10.1111/cen.12252 · Cited by 10
Huisman, E. J., van Hoek, B., van Soest, H., van Nieuwkerk, K. M., Arends, J. E., Siersema, P. D., & van Erpecum, K. J. (2012) · Journal of Hepatology · doi:10.1016/j.jhep.2012.06.029 · Cited by 10
Granulocyte-colony stimulating factor prevents the development of hepatic steatosis in rats
Song, Y.-S., Joo, H.-W., Park, I.-H., Shen, G.-Y., Lee, Y., Shin, J., Kim, H., & Kim, K.-S. (2015) · Annals of Hepatology · doi:10.1016/s1665-2681(19)30787-2 · Cited by 10
Effect of Exercise on Insulin Sensitivity in Healthy Postmenopausal Women: The SHAPE Study
van Gemert, W. A., Monninkhof, E. M., May, A. M., Peeters, P. H. M., & Schuit, A. J. (2014) · Cancer Epidemiology Biomarkers & Prevention · doi:10.1158/1055-9965.epi-14-0722 · Cited by 11
Ishitobi, T., Hyogo, H., Kan, H., Hiramatsu, A., Arihiro, K., Aikata, H., & Chayama, K. (2014) · Hepatology Research · doi:10.1111/hepr.12382 · Cited by 10
Unrecognized Diabetes and Myocardial Necrosis: Predictors of Hyperglycemia in Myocardial Infarction
Ladeira, R. T., Baracioli, L. M., Faulin, T. D. E. S., Abdalla, D. S. P., Seydell, T. M., Maranhão, R. C., Mendonca, B. B., Strunz, C. M. C., de Castro, I., & Nicolau, J. C. (2013) · Arquivos Brasileiros de Cardiologia · doi:10.5935/abc.20130087 · Cited by 10
Barbosa, K. B. F., Volp, A. C. P., Marques-Rocha, J. L., Ribeiro, S. M. R., Navarro-Blasco, Í., Zulet, M. Á., Martínez, J. A., & Bressan, J. (2014) · Nutrition · doi:10.1016/j.nut.2014.03.031 · Cited by 10
Park, H. W., Kwon, T., Kim, K., et al. (2010) · Korean Circulation Journal · doi:10.4070/kcj.2010.40.2.62 · Cited by 10
Vasques, A. C. J., Pareja, J. C., de Oliveira, M. D. S., Novaes, F. S., Lima, M. M. D. O., Chaim, É. A., Piccinini, F., Man, C. D., Cobelli, C., & Geloneze, B. (2013) · Diabetes Care · doi:10.2337/dc13-0530 · Cited by 10
Lee, W., Rhee, E., Choi, E. S., Kim, J., Won, J. C., Park, C., Lee, W., Oh, K. W., Park, S. W., & Kim, S. W. (2008) · Korean Diabetes Journal · doi:10.4093/kdj.2008.32.4.317 · Cited by 10
Pizzi, O. L., Brandão, A. A., Pozzan, R., Magalhães, M. E. C., Campana, É. M. G., Fonseca, F. L., de Freitas, E. V., & Brandão, A. P. (2012) · Arquivos Brasileiros de Cardiologia · doi:10.1590/s0066-782x2012005000116 · Cited by 10
Solera-Martínez, M., López-Martínez, S., Sánchez‐López, M., Martínez, P. M., Notario‐Pacheco, B., Arias-Palencia, N. M., Morales, P. F., & Martínez‐Vizcaíno, V. (2011) · Revista Española de Cardiología (English Edition) · doi:10.1016/j.rec.2010.11.009 · Cited by 10
Derosa, G., Cicero, A. F. G., Carbone, A., Querci, F., Fogari, E., D’Angelo, A., & Maffioli, P. (2013) · Expert Opinion on Drug Safety · doi:10.1517/14740338.2013.816674 · Cited by 10
Retracted[Residual effect of muscle strength exercise in secondary prevention of children obesity].
Vásquez, F., Díaz-Bautista, E., Lera, L., Meza, J. S., Salas, I., Rojas, P., Atalah, E., & Burrows, R. A. (2013) · PubMed · doi:10.3305/nh.2013.28.2.6159 · Cited by 10
Solera-Martínez, M., López-Martínez, S., Sánchez‐López, M., Martínez, P. M., Notario‐Pacheco, B., Arias-Palencia, N. M., Morales, P. F., & Martínez‐Vizcaíno, V. (2011) · Revista Española de Cardiología · doi:10.1016/j.recesp.2010.11.010 · Cited by 10
Liu, K., Chen, P.-Y., Wang, C.-M., Chen, W., Chen, C.-W., Owaga, E., & Chang, J. (2015) · Food & Function · doi:10.1039/c5fo01252j · Cited by 10
Koiou, E., Τζιόμαλος, Κ., Katsikis, I., Dinas, K. D., Tsourdi, E. A., Kandaraki, E., Delkos, D., Papadakis, E. P., & Panidis, D. (2012) · HORMONES · doi:10.1007/bf03401540 · Cited by 10
Zhang, Y., Jin, H., Qin, Z., Ma, J., Zhao, H., Zhang, L., & Chen, Z. (2015) · Gynecologic and Obstetric Investigation · doi:10.1159/000440618 · Cited by 10
Circulating serum chemerin levels are elevated in lipodystrophy
Miehle, K., Ebert, T., Kralisch, S., Hoffmann, A., Kratzsch, J., Schlögl, H., Stümvoll, M., & Faßhauer, M. (2015) · Clinical Endocrinology · doi:10.1111/cen.12976 · Cited by 10
Metabolomics: On the way to an integration of biochemistry, analytical chemistry, and informatics
Goncharov, N. V., Уколов, А. И., Orlova, T. I., Migalovskaia, E. D., & Войтенко, Н. Г. (2015) · Biology Bulletin Reviews · doi:10.1134/s2079086415040027 · Cited by 10
Nuthalapati, R. K., & Indukuri, B. R. (2016) · Indian Journal of Endocrinology and Metabolism · doi:10.4103/2230-8210.176349 · Cited by 10
Risk related cardiovascular changes in metabolically healthy obese adolescents
Chaychenko, T. (2016) · Polish Annals of Medicine · doi:10.1016/j.poamed.2016.01.006 · Cited by 10
Baldasseroni, S., Pratesi, A., Orso, F., Serio, C. D., Foschini, A., Marella, A. G., Bartoli, N., Bari, M. D., Fumagalli, S., Marchionni, N., et al. (2013) · Monaldi Archives for Chest Disease · doi:10.4081/monaldi.2013.5233 · Cited by 10
Metadata
- Authors
- Matthews, D. R., Hosker, J. P., Rudenski, A. S., Naylor, B. A., Treacher, D. F., & Turner, R. C.
- Affiliations
- University of Oxford (GB)
- ORCID
- Matthews, D. R.
- Venue
- Diabetologia
- Published
- 1985-07
- Volume
- 28
- Issue
- 7
- Pages
- 412-419
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2160234571
- Cited by
- 31,502
- References
- 21
- Citations by year
- 2026: 933 · 2025: 1060 · 2024: 1240 · 2023: 1291 · 2022: 1489 · 2021: 1528 · 2020: 1424 · 2019: 1427 · 2018: 1456 · 2017: 1440 · 2016: 1481 · 2015: 1682 · 2014: 1693 · 2013: 1621 · 2012: 1518
- FWCI
- 7.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- HOMA, insulin resistance, beta-cell function, fasting blood glucose, fasting insulin, hyperglycaemic clamp, euglycaemic clamp, intravenous glucose tolerance test, insulin receptor binding, type 2 diabetes
- MeSH terms
- Adult, Blood Glucose, Computers, Diabetes Mellitus, Type 2, Erythrocytes, Fasting, Homeostasis, Humans, Insulin, Insulin Resistance, Islets of Langerhans, Middle Aged, Monocytes, Receptor, Insulin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-14, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-14 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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