HOMA-IR tool

A service tool to calculate an index of insulin resistance

What is insulin resistance?

Insulin resistance is classically defined as impaired whole-body insulin-mediated glucose disposal.1

However, defective insulin action is not confined to impaired glucose disposal; it can also be seen in protein and fat metabolism. Therefore, a more accurate definition of insulin resistance is “a state in which normal insulin levels produce an attenuated biological response.”1

Improvement of insulin sensitivity/insulin action, or reduction in insulin resistance, as a therapeutic principle may play a central role in the primary prevention and treatment of type 2 diabetes, hypertension, and atherosclerosis.2

How common is insulin resistance?

Insulin resistance is very common in the general population. The prevalence of insulin resistance has been estimated to be as high as 88% in people with lipid abnormalities, such as elevated triglycerides and low HDL.3 Considering that over half of all adults in Western populations have lipid abnormalities,4 it becomes clear that insulin resistance is not a problem confined to diabetes but a mass problem afflicting the vast majority. A surprising finding is that people with elevated triglycerides and low HDL can have a similar degree of insulin resistance as that seen in patients with type 2 diabetes.3

Importantly, in the general population insulin resistance can be found even in the absence of any major metabolic disorders,3 and 25% of apparently healthy people are severely insulin resistant.5 This can be detected by elevated fasting insulin and glucose levels6,7 – and the HOMA-IR index (explained below) - and may be an indicator of “silent” atherosclerosis.8

What is the value of assessing insulin resistance?

Insulin resistance is an independent risk factor for all-cause and cardiovascular mortality,9,10 and multiple studies have shown that insulin resistance is a strong predictor of atherosclerotic cardiovascular disease as well as adverse cardiovascular outcomes in both non-diabetic and diabetic individuals.10,11

A notable study found that insulin resistance, as estimated by HOMA-IR (explained below), was associated with incident symptomatic cardiovascular disease after a 15-year follow-up.12 Importantly, the association of insulin resistance with cardiovascular disease was independent of classic risk factors (including hyperglycemia, hypertension, high LDL cholesterol, smoking, and physical activity) and of other components of the metabolic syndrome (obesity, hypertriglyceridemia, and low HDL cholesterol). The association remained significant and virtually unchanged even after accounting for novel risk factors, including adiponectin and biomarkers indicating a prothrombotic state (high fibrinogen), increased oxidative stress (high circulating oxidized LDL), endothelial dysfunction (high VCAM-1), and chronic mild inflammation (increased hsCRP).12

Furthermore, insulin resistance causes physiological impairments such as telomere attrition and endothelial dysfunction, which contribute to premature aging.13-16 Experimental studies have shown that insulin resistance accelerates atherosclerosis.17,18 In apparently healthy people, 1 out of 3 who have insulin resistance at baseline develop either heart disease or type 2 diabetes 6 years later, while people without insulin resistance do not.19 Insulin resistance seems to be the common metabolic defect underlying both type 2 diabetes, dyslipidemia, cardiovascular disease (including high blood pressure) and obesity.20,21 With the rapidly growing body of evidence linking insulin resistance to adverse health outcomes and premature death, the interest in practical ways to assess insulin resistance is escalating.

HOMA-IR, an index of insulin resistance

Insulin sensitivity / insulin resistance can be assessed in several ways. The hyperinsulinemic euglycemic glucose clamp technique is the gold standard method for the assessment of insulin sensitivity, because it directly measures the ability of insulin to promote glucose uptake into tissues from the blood.22

During the clamp procedure, intravenous infusions of insulin and glucose are given. The principle of the test is to keep the glucose level constant while increasing insulin levels.22 This is a very resource intensive method that is only conducted in research settings.

For large scale studies and in clinical practice, several simple surrogate assessments of insulin sensitivity / insulin resistance are available, the most popular of which is the homeostatic model assessment (HOMA) of insulin resistance (IR).23,24 HOMA-IR is a simple calculation based on measurements of insulin and glucose in a fasting blood sample. The formula for HOMA-IR is:

HOMA-IR = (FPI x FPG)/22.5

Where FPI is fasting plasma insulin (mU/L or µU/mL) and FPG is fasting plasma glucose (mmol/L).

The denominator of 22.5 is a normalising factor, i.e., the product of normal fasting plasma insulin of 5 µU/mL and normal fasting plasma glucose of 4.5 mmol/L, obtained from an apparently healthy “normal” individual.23 Therefore, for an individual with normal insulin sensitivity, HOMA = 1. Surveys of representative populations confirm that lean and apparently healthy individuals have HOMA-IR values between 0.5 and 1.25,26

Why is insulin alone not a good indicator of insulin resistance?

Up to 75% of people with normal fasting glucose / glucose tolerance may have hyperinsulinemia, which is the hallmark adaptation to insulin resistance.27 In healthy populations with normal glucose levels, fasting insulin alone may be a good predictor of insulin resistance, atherosclerosis and cardiometabolic risk.28,29 However, in populations with overweight/obesity, metabolic syndrome, type 2 diabetes, cardiovascular disease and non-alcoholic fatty liver disease, HOMA-IR is a better indicator of insulin resistance and metabolic disease outcomes than insulin levels alone.30,31

HOMA-IR, by including both glucose and insulin, is more generalizable to all circumstances with variable glucose levels, including prediabetic glucose levels commonly seen in people with obesity and/or visceral fat accumulation.30,32 By accounting for a wide range of metabolic conditions, HOMA-IR is a better indicator of insulin resistance than insulin levels alone, and has a greater correlation with the gold standard clamp method among obese and type 2 diabetic subjects.30,32 The superiority of HOMA-IR over insulin alone was demonstrated in a meta-analysis which showed that insulin resistance assessed by HOMA-IR, but not fasting insulin, is independently associated with greater risk of cardiovascular and all-cause mortality.10

How to interpret HOMA-IR values

The higher the HOMA-IR value, the greater the degree of insulin resistance. Hence, individuals with type 2 diabetes have much higher HOMA-IR values (often in the range of 5-6 and above) than weight-matched individuals without type 2 diabetes (often below 2).33

Numerous studies have investigated the association between insulin resistance defined by HOMA-IR and various health outcomes, as well as identified thresholds to identify subjects at increased risk for the metabolic syndrome, prediabetes and type 2 diabetes. However, it has to be kept in mind that these HOMA-IR thresholds only apply to the population from which they were derived, and hence the thresholds that identify people at high risk vary between populations.34 It is also important to point out that direct comparisons of HOMA-IR values between studies cannot be made unless the same insulin assay was used. Nevertheless, below is a summary of notable studies that investigated the association of HOMA-IR with various outcomes. These studies provide a rough guideline about the range of HOMA-IR values that can be expected to be seen in patients encountered in clinical practice.

One study found that the optimal HOMA-IR cut-off for the identification of the metabolic syndrome (IDF- and ATPIII-defined) in individuals aged 25-64 years was 1.77.35 Similarly, another study found that HOMA-IR of 1.85 identifies men with cardiometabolic risk factors.36 Optimal cut-off points to identify men with incident type 2 diabetes was HOMA1-IR = 2.17 and HOMA-B% = 67%.37 HOMA-IR values around 2-2.5 show diagnostic value in distinguishing non-alcoholic fatty liver disease carriers from control group individuals.38

Importantly, there is a significant association between HOMA-IR and risk of cardiovascular disease even after adjustment for multiple confounders.39 For example, in the San Antonio Heart Study, the risk of a cardiovascular event increased by 2.5-fold across increasing HOMA-IR categories, even after adjustment for age, sex, and ethnicity. After additional adjustment for LDL, triglyceride, HDL, systolic blood pressure, smoking, alcohol consumption, exercise, and waist circumference, individuals with HOMA-IR = 7.3 had a 2-fold higher risk of a future cardiovascular event compared to individuals with HOMA-IR = 0.6.39

One meta-analysis found that people with the highest vs. lowest HOMA-IR category had 34% higher risk of all-cause mortality and 2.1-fold higher risk of cardiovascular mortality.10 The HOMA-IR categories that were compared in included studies in the meta-analysis were 2.5 vs. 0.6,40 >2.8 vs. ≤1.4,41 >1.5 vs. 0.85–1.07,42 and >2.67 vs. <1.29.43

The research on HOMA-IR demonstrates that the diagnostic cutoffs for conditions related to insulin resistance vary between populations and studies. Nevertheless, when used and interpreted correctly, HOMA-IR can add value in clinical practice, as will be explained next.

How to use HOMA-IR – the value of assessing HOMA-IR in routine clinical practice

Assessment of insulin resistance with the HOMA-IR tool can be used for three purposes:

  1. To evaluate baseline degree of insulin resistance.
  2. To monitor progression of insulin resistance over time.
  3. To monitor the efficacy of insulin sensitizing treatments.

Due to the variability in insulin assays,44,45 and pulsatile nature of insulin secretion (which is maintained after an overnight fast, although less insulin is secreted with every burst)46, there are no universal diagnostic thresholds for “normal” vs. “abnormal” HOMA-IR values.26 Nevertheless, as outlined below, numerous studies have compared metabolic status in subjects with high vs. low HOMA-IR values, and quantified the association of high vs. low HOMA-IR values with risk for various outcomes.

Rather than making the “diagnosis of insulin resistance”, the greatest utility of HOMA-IR in clinical practice is for monitoring progression / regression of insulin resistance in patients over time, and evaluating the response to insulin sensitizing treatments. When using HOMA-IR for this purpose, it is critical that the same insulin assay is used, and that patients do the fasting blood draw under the same conditions each time (e.g. drawing blood around the same time, overnight fasting for the same number of hours and eaten the same meals the day before the blood draw, as they did before the previous blood draw).

In a given population without type 2 diabetes, the interindividual and intraindividual variation of HOMA-IR values is relatively low.47 In contrast, in patients with type 2 diabetes there is a larger variation in HOMA-IR values. The high degree of intraindividual variability of HOMA-IR seen in individuals with type 2 diabetes means that HOMA-IR values must increase by 90% or decrease by 47% in order to conclude that a significant change in insulin resistance has occurred; smaller changes in HOMA-IR values may simply reflect intraindividual variability.47 Nevertheless, HOMA-IR was found to be a reliable indicator of insulin resistance during follow-up of patients with type 2 diabetes,48 and can be used to examine changes in insulin resistance in response to various treatments,49,50 including diet/exercise50,51 and testosterone therapy.52-57

For instance, a 1-year long lifestyle intervention reduced HOMA-IR from 1.5 to 1.0 in subjects with a modest degree of baseline insulin resistance, and from 4.6 to 2.7 in subjects with a greater degree of baseline insulin resistance.51 Men with hypogonadism commonly have HOMA-IR values in the range of 4-16, indicating a relatively severe degree of insulin resistance, which is effectively reduced by testosterone therapy.52-57 For example, one notable randomized, double-blind, placebocontrolled trial (RCT) found that testosterone therapy for 2 years in men with obesity reduced HOMA-IR from 4.27 to 2.17.52 Interestingly, this was accompanied by a significant 23% reduction in carotid intima-media thickness (CIMT), 52 a surrogate measure of atherosclerosis.58 Another RCT in men with obesity and type 2 diabetes showed that testosterone therapy for 1 year reduced HOMA-IR from 11.45 to 6.81, along with a 11% reduction in CIMT.56These studies suggest that testosterone therapy reduces both insulin resistance and the atherosclerotic burden in men with hypogonadism, regardless of type 2 diabetes status.

Implementing regular assessment of insulin resistance in clinical practice is warranted for numerous reasons, including:

  • Insulin resistance is associated with cardiovascular disease independent of classic risk factors (hyperglycemia, hypertension, high LDL, smoking, physical activity, obesity, hypertriglyceridemia, and low HDL).12
  • Insulin resistance is associated with cardiovascular disease independent of novel risk factors (adiponectin, fibrinogen, oxidized LDL, endothelial dysfunction and chronic mild inflammation).12
  • Insulin resistance may account for the majority of the cardiovascular risk not accounted for by traditional risk factors (about 30%).59

It is useful for the clinician to have an objective measure of the improvement in insulin resistance in response to diet/exercise and insulin sensitizing treatments, such as testosterone therapy. The presence of a high degree of insulin resistance - as indicated by elevated HOMA-IR values - could prompt an upward dose titration and more frequent monitoring of testosterone levels to ensure that optimal testosterone levels are achieved during testosterone therapy, and/or escalation of other insulin sensitizing treatment(s). This in turn could help reduce residual cardiovascular risk.


  • Krentz AJ, Nattrass M. Insulin resistance: a multifaceted metabolic syndrome. Insights gained using a low-dose insulin infusion technique. Diabet Med. 1996;13(1):30-39. Return to content
  • Rett K, Wicklmayr M, Mehnert H. What is the clinical significance of insulin resistance? J Cardiovasc Pharmacol. 1992;20 Suppl 11:S22-26. Return to content
  • Bonora E, Kiechl S, Willeit J, et al. Prevalence of insulin resistance in metabolic disorders: the Bruneck Study. Diabetes. 1998;47(10):1643-1649. Return to content
  • Toth PP, Potter D, Ming EE. Prevalence of lipid abnormalities in the United States: the National Health and Nutrition Examination Survey 2003-2006. Journal of clinical lipidology.2012;6(4):325-330. Return to content
  • Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988;37(12):1595-1607. Return to content
  • Standards of medical care in diabetes--2015: summary of revisions. Diabetes Care. 2015;38 Suppl:S4. Return to content
  • Hollenbeck C, Reaven GM. Variations in insulin-stimulated glucose uptake in healthy individuals with normal glucose tolerance. J Clin Endocrinol Metab. 1987;64(6):1169-1173. Return to content
  • Laakso M, Sarlund H, Salonen R, et al. Asymptomatic atherosclerosis and insulin resistance. Arterioscler Thromb. 1991;11(4):1068-1076. Return to content
  • Balkau B, Eschwege E. Insulin resistance: an independent risk factor for cardiovascular disease? Diabetes, obesity & metabolism. 1999;1 Suppl 1:S23-31. Return to content
  • Zhang X, Li J, Zheng S, Luo Q, Zhou C, Wang C. Fasting insulin, insulin resistance, and risk of cardiovascular or all-cause mortality in non-diabetic adults: a meta-analysis. BiosciRep. 2017;37(5). Return to content
  • Gast KB, Tjeerdema N, Stijnen T, Smit JW, Dekkers OM. Insulin resistance and risk of incident cardiovascular events in adults without diabetes: meta-analysis. PloS one.2012;7(12):e52036. Return to content
  • Bonora E, Kiechl S, Willeit J, et al. Insulin resistance as estimated by homeostasis model assessment predicts incident symptomatic cardiovascular disease in caucasian subjects from the general population: the Bruneck study. Diabetes Care. 2007;30(2):318-324. Return to content
  • Avogaro A, de Kreutzenberg SV, Federici M, Fadini GP. The endothelium abridges insulin resistance to premature aging. Journal of the American Heart Association.2013;2(3):e000262. Return to content
  • Avogaro A, de Kreutzenberg SV, Fadini GP. Insulin signaling and life span. Pflugers Arch. 2010;459(2):301-314. Return to content
  • Rosenbloom AL, Kappy MS, DeBusk FL, Francis GL, Philpot TJ, Maclaren NK. Progeria: insulin resistance and hyperglycemia. J Pediatr. 1983;102(3):400-402. Return to content
  • Gardner JP, Li S, Srinivasan SR, et al. Rise in insulin resistance is associated with escalated telomere attrition. Circulation. 2005;111(17):2171-2177. Return to content
  • Li Q, Park K, Li C, et al. Induction of vascular insulin resistance and endothelin-1 expression and acceleration of atherosclerosis by the overexpression of protein kinase C-beta isoform in the endothelium. Circ Res. 2013;113(4):418-427. Return to content
  • Rask-Madsen C, Li Q, Freund B, et al. Loss of insulin signaling in vascular endothelial cells accelerates atherosclerosis in apolipoprotein E null mice. Cell metabolism. 2010;11(5):379-389. Return to content
  • Facchini FS, Hua N, Abbasi F, Reaven GM. Insulin resistance as a predictor of age-related diseases. J Clin Endocrinol Metab. 2001;86(8):3574-3578. Return to content
  • Kashyap SR, Defronzo RA. The insulin resistance syndrome: physiological considerations. Diabetes & vascular disease research: official journal of the International Society ofDiabetes 10. and Vascular Disease. 2007;4(1):13-19. Return to content
  • DeFronzo RA. Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. J Cardiovasc Pharmacol. 1992;20 Suppl 11:S1-16. Return to content
  • DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: a method for quantifying insulin secretion and resistance. Am J Physiol. 1979;237(3):E214-223. Return to content
  • Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucoseand insulin concentrations in man. Diabetologia. 1985;28(7):412-419 Return to content
  • Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care. 2004;27(6):1487-1495. Return to content
  • Martinez KE, Tucker LA, Bailey BW, LeCheminant JD. Expanded Normal Weight Obesity and Insulin Resistance in US Adults of the National Health and Nutrition Examination Survey. Journal of diabetes research. 2017;2017:9502643. Return to content
  • Levy JC. Personal communication, Dr. JC Levy, Oxford Centre for Diabetes, Endocrinology and Metabolism. In. Return to content
  • Caliber M, Hackett G. Important lessons about testosterone therapy- weight loss vs. testosterone therapy for symptom resolution, classical vs. functional hypogonadism, and shortterm vs. lifelong testosterone therapy. The aging male: the official journal of the International Society for the Study of the Aging Male. 2019:1-7 Return to content
  • de Rooij SR, Dekker JM, Kozakova M, et al. Fasting insulin has a stronger association with an adverse cardiometabolic risk profile than insulin resistance: the RISC study. Eur J Endocrinol. 2009;161(2):223-230. Return to content
  • Kawada T. Preliminary report: homeostasis model assessment of insulin resistance, an indicator of insulin resistance, is strongly related to serum insulin: practical data presentation and the mathematical basis. Metabolism. 2010;59(7):1044-1046. Return to content
  • Mather KJ, Hunt AE, Steinberg HO, et al. Repeatability characteristics of simple indices of insulin resistance: implications for research applications. J Clin Endocrinol Metab. 2001;86(11):5457-5464. Return to content
  • Campanati A, Ganzetti G, Di Sario A, Benedetti A, Offidani A. Insulin resistance, serum insulin and HOMA-R. J Gastroenterol. 2013;48(5):673. Return to content
  • Ikeda Y, Suehiro T, Nakamura T, Kumon Y, Hashimoto K. Clinical significance of the insulin resistance index as assessed by homeostasis model assessment. Endocr J. 2001;48(1): 81-86. Return to content
  • Bonora E, Targher G, Alberiche M, et al. Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity: studies in subjects with various degrees of glucose tolerance and insulin sensitivity. Diabetes Care. 2000;23(1):57-63. Return to content
  • Carrillo-Larco RM, Miranda JJ, Gilman RH, et al. The HOMA-IR Performance to Identify New Diabetes Cases by Degree of Urbanization and Altitude in Peru: The CRONICAS Cohort Study. Journal of diabetes research. 2018;2018:7434918. Return to content
  • Esteghamati A, Ashraf H, Khalilzadeh O, et al. Optimal cut-off of homeostasis model assessment of insulin resistance (HOMA-IR) for the diagnosis of metabolic syndrome: third national surveillance of risk factors of non-communicable diseases in Iran (SuRFNCD-2007). Nutr Metab (Lond). 2010;7:26. Return to content
  • Gayoso-Diz P, Otero-Gonzalez A, Rodriguez-Alvarez MX, et al. Insulin resistance (HOMA-IR) cut-off values and the metabolic syndrome in a general adult population: effect of gender and age: EPIRCE cross-sectional study. BMC endocrine disorders. 2013;13:47. Return to content
  • Ghasemi A, Tohidi M, Derakhshan A, Hasheminia M, Azizi F, Hadaegh F. Cut-off points of homeostasis model assessment of insulin resistance, beta-cell function, and fasting serum insulin to identify future type 2 diabetes: Tehran Lipid and Glucose Study. Acta Diabetol. 2015;52(5):905-915. Return to content
  • Salgado AL, Carvalho L, Oliveira AC, Santos VN, Vieira JG, Parise ER. Insulin resistance index (HOMA-IR) in the differentiation of patients with non-alcoholic fatty liver disease and healthy individuals. Arq Gastroenterol. 2010;47(2):165-169. Return to content
  • Hanley AJ, Williams K, Stern MP, Haffner SM. Homeostasis model assessment of insulin resistance in relation to the incidence of cardiovascular disease: the San Antonio Heart Study. Diabetes Care. 2002;25(7):1177-1184. Return to content
  • Hedblad B, Nilsson P, Engstrom G, Berglund G, Janzon L. Insulin resistance in non-diabetic subjects is associated with increased incidence of myocardial infarction and death. Diabet Med. 2002;19(6):470-475. Return to content
  • Ausk KJ, Boyko EJ, Ioannou GN. Insulin resistance predicts mortality in nondiabetic individuals in the U.S. Diabetes Care. 2010;33(6):1179-1185. Return to content
  • Kim HJ, Ryu J, Ahn SY, et al. Association of insulin resistance with lower glomerular filtration rate and all-cause mortality in the Korean elderly population: a community-based prospective cohort study. Tohoku J Exp Med. 2013;231(4):271-279. Return to content
  • Kim KS, Lee YM, Lee IK, Kim DJ, Jacobs DR, Jr., Lee DH. Paradoxical Associations of Insulin Resistance With Total and Cardiovascular Mortality in Humans. J Gerontol A Biol Sci Med Sci. 2015;70(7):847-853. Return to content
  • Manley SE, Stratton IM, Clark PM, Luzio SD. Comparison of 11 human insulin assays: implications for clinical investigation and research. Clin Chem. 2007;53(5):922-932. Return to content
  • Staten MA, Stern MP, Miller WG, Steffes MW, Campbell SE. Insulin assay standardization: leading to measures of insulin sensitivity and secretion for practical clinical care. Diabetes Care. 2010;33(1):205-206. Return to content
  • Juhl C, Grofte T, Butler PC, Veldhuis JD, Schmitz O, Porksen N. Effects of fasting on physiologically pulsatile insulin release in healthy humans. Diabetes. 2002;51 Suppl 1:S255-257. Return to content
  • Jayagopal V, Kilpatrick ES, Jennings PE, Hepburn DA, Atkin SL. Biological variation of homeostasis model assessment-derived insulin resistance in type 2 diabetes. Diabetes Care.2002;25(11):2022-2025. Return to content
  • Katsuki A, Sumida Y, Gabazza EC, et al. Homeostasis model assessment is a reliable indicator of insulin resistance during follow-up of patients with type 2 diabetes. Diabetes Care.2001;24(2):362-365. Return to content
  • McAuley KA, Mann JI, Chase JG, Lotz TF, Shaw GM. Point: HOMA--satisfactory for the time being: HOMA: the best bet for the simple determination of insulin sensitivity, until something better comes along. Diabetes Care. 2007;30(9):2411-2413.1999;22(5):818-822. Return to content
  • Emoto M, Nishizawa Y, Maekawa K, et al. Homeostasis model assessment as a clinical index of insulin resistance in type 2 diabetic patients treated with sulfonylureas. Diabetes Care. 1999;22(5):818-822. Return to content
  • Vogeser M, Konig D, Frey I, Predel HG, Parhofer KG, Berg A. Fasting serum insulin and the homeostasis model of insulin resistance (HOMA-IR) in the monitoring of lifestyle interventions in obese persons. Clin Biochem. 2007;40(13-14):964-968. Return to content
  • Aversa A, Bruzziches R, Francomano D, et al. Effects of testosterone undecanoate on cardiovascular risk factors and atherosclerosis in middle-aged men with late-onset hypogonadism and metabolic syndrome: results from a 24-month, randomized, double-blind, placebo-controlled study. The journal of sexual medicine. 2010;7(10):3495-3503. Return to content
  • Heufelder AE, Saad F, Bunck MC, Gooren L. Fifty-two-week treatment with diet and exercise plus transdermal testosterone reverses the metabolic syndrome and improves glycemic control in men with newly diagnosed type 2 diabetes and subnormal plasma testosterone. J Androl. 2009;30(6):726-733. Return to content
  • Kalinchenko SY, Tishova YA, Mskhalaya GJ, Gooren LJ, Giltay EJ, Saad F. Effects of testosterone supplementation on markers of the metabolic syndrome and inflammation in hypogonadal men with the metabolic syndrome: the double-blinded placebo-controlled Moscow study. Clin Endocrinol (Oxf). 2010;73(5):602-612. Return to content
  • Dhindsa S, Ghanim H, Batra M, et al. Insulin Resistance and Inflammation in Hypogonadotropic Hypogonadism and Their Reduction After Testosterone Replacement in Men With Type 2 Diabetes. Diabetes Care. 2016;39(1):82-91. Return to content
  • Groti K, Zuran I, Antonic B, Forsnaric L, Pfeifer M. The impact of testosterone therapy on glycemic control, vascular function, and components of the metabolicsyndrome in obese hypogonadal men with type 2 diabetes. The aging male: the official journal of the International Society for the Study of the Aging Male. 2018;21(3):158-169. Return to content
  • Dimitriadis GK, Randeva HS, Aftab S, et al. Metabolic phenotype of male obesity-related secondary hypogonadism pre-replacement and post-replacement therapy with intramuscular testosterone undecanoate therapy. Endocrine. 2018. Return to content
  • Centurion OA. Carotid Intima-Media Thickness as a Cardiovascular Risk Factor and Imaging Pathway of Atherosclerosis. Critical pathways in cardiology. 2016;15(4):152-160. Return to content
  • Di Pino A, DeFronzo RA. Insulin Resistance and Atherosclerosis: Implications for Insulin Sensitizing Agents. Endocr Rev. 2019. Return to content