Homeostasis Model Assessment Is a Reliable Indicator of Insulin Resistance During Follow-up of Patients With Type 2 Diabetes

Katsuki, Akira; Sumida, Yasuhiro; Gabazza, Esteban C.; Murashima, Shuichi; Fukuda, Masahiko; Araki-Sasaki, Rika; Hori, Yasuko; Yano, Yutaka; Adachi, Yukihiko

doi:10.2337/diacare.24.2.362

Cited by 357 publications

(258 citation statements)

References 27 publications

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“…45 Studies have demonstrated that overall ethnic Chinese from East Asia and Malays from Southeast Asia were genetically closer than Asian Indians. 46 More specifically, although culturally distinct, Malays in Singapore had a greater genetic similarity with Chinese than Asian Indians. 46,47 Greater general adiposity of Malays as compared with Chinese explained their greater insulin resistance in our study and targeting excess weight gain in Malays should have high priority in public health efforts for chronic disease prevention.…”

Section: Discussionmentioning

confidence: 99%

“…46 More specifically, although culturally distinct, Malays in Singapore had a greater genetic similarity with Chinese than Asian Indians. 46,47 Greater general adiposity of Malays as compared with Chinese explained their greater insulin resistance in our study and targeting excess weight gain in Malays should have high priority in public health efforts for chronic disease prevention. 45 Compared with ordinary regression analysis, path analysis has the advantage that it allows examination of the potential causal processes underlying an observed relationship and to estimate the relative importance of alternative paths of influence in a complicated system.…”

Section: Discussionmentioning

confidence: 99%

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Can body fat distribution, adiponectin levels and inflammation explain differences in insulin resistance between ethnic Chinese, Malays and Asian Indians?

et al. 2011

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OBJECTIVE: Diabetes in Asia constitutes approximately half of the global burden. Although insulin resistance and incidence of type 2 diabetes differ substantially between ethnic groups within Asia, the reasons for these differences are poorly understood.We evaluated to what extent body fatness, adiponectin levels and inflammation mediate the relationship between ethnicity and insulin resistance in an Asian setting. DESIGN: Cross-sectional population-based study. SUBJECTS: In total, 4136 adult Chinese, Malays and Asian Indians residing in Singapore. MEASUREMENTS: Insulin resistance was assessed using homeostasis model assessment (HOMA-IR) and systemic inflammation by C-reactive protein (CRP). Data were analyzed using path analysis. RESULTS: HOMA-IR was highest in Asian Indians, intermediate in Malays and lowest in Chinese (Po0.001). The difference in HOMA-IR between Malays and Chinese disappeared after adjusting for body mass index (BMI). For the comparison of Asian Indians with Chinese, the association between ethnicity and HOMA-IR was mediated by BMI (men: 32.9%; women: 48.5%), BMI-adjusted waist circumference (men: 6.1%; women: 3.5%), and CRP (men: 5.1%; women: 5.6%), and unidentified factors (men: 47.2%; women: 26.5%). Part of the mediating effects of body fatness was indirect through effects of body fatness on CRP and adiponectin concentrations. CONCLUSION: Mediators of ethnic differences in insulin resistance differed markedly depending on the ethnic groups compared. General adiposity explained the difference in insulin resistance between Chinese and Malays, whereas abdominal fat distribution, inflammation and unexplained factors contributed to excess insulin resistance in Asian Indians as compared with Chinese and Malays. These findings suggest that interventions targeting excess weight gain can reduce ethnic disparities in insulin resistance among Asian Indians, Chinese and Malays.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Can body fat distribution, adiponectin levels and inflammation explain differences in insulin resistance between ethnic Chinese, Malays and Asian Indians?

et al. 2011

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“…Fasting serum insulin level by ELISA using Diagnostic systems Laboratories (DSL), HOMA insulin resistance: The estimation of insulin resistance by homeostasis model assessment (HOMA-IR) was calculated with the formula: Fasting serum insulin (µIU/ml) X fasting glucose level (mmol/L)/22.5 (17). Normally in men → 1.66 ± 1.1 and in women → 1.57±0.8.…”

Section: Methodsmentioning

confidence: 99%

Role of Peroxisome Proliferator-Activated Receptor gamma 2 (PPAR-γ2) Gene Polymorphism in Type 2 Diabetes Mellitus

et al. 2009

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Objective: To find out the relation between Pro 12 Ala polymorphism of peroxisome proliferator-activated receptor gamma2 (PPAR-g2) gene with type 2 diabetes mellitus and the possible role of this gene polymorphism as a link between obesity and type 2 diabetes mellitus. Subjects and Methods: Subjects of this study were classified into 3 groups: (15) Apparently healthy lean individuals (Group I), (15) obese non diabetic individuals (group II) and (24) patients with type 2 diabetes mellitus (group III). This group divided into: Diabetic non obese patients (12 patients) (Group IIIa) and: Diabetic obese patients (12 patients) (Group IIIb). The subjects were subjected to clinical examination, serum insulin level and estimation of PPAR-g2 gene polymorphism by Restriction fragment length polymorphism (RFLP) polymerase chain reaction (PCR). Results: Frequency of Pro allele was significant increase in diabetic non obese patients& diabetic non obese patients when compared to control group (P= 0.048 and 0.003, respectively

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“…2E). HOMA‐IR index, an indicator of insulin sensitivity 18, was significantly higher in the HFD‐fed mice than that in the ND‐fed mice ( P < 0.05; Fig. 2G).…”

Section: Resultsmentioning

confidence: 93%

The essential function of CARD9 in diet‐induced inflammation and metabolic disorders in mice

Zeng

Zhang

et al. 2018

J Cellular Molecular Medi

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Inflammation and metabolic disorder are common pathophysiological conditions, which play a vital role in the development of obesity and type 2 diabetes. The purpose of this study was to explore the effects of caspase recruitment domain (CARD) 9 in the high fat diet (HFD)‐treated mice and attempt to find a molecular therapeutic target for obesity development and treatment. Sixteen male CARD9−/− and corresponding male WT mice were fed with normal diet or high fat diet, respectively, for 12 weeks. Glucose tolerance, insulin resistance, oxygen consumption and heat production of the mice were detected. The CARD9/MAPK pathway‐related gene and protein were determined in insulin‐responsive organs using Western blotting and quantitative PCR. The results showed that HFD‐induced insulin resistance and impairment of glucose tolerance were more severe in WT mice than that in the CARD9−/− mice. CARD9 absence significantly modified O2 consumption, CO 2 production and heat production. CARD9−/− mice displayed the lower expression of p38 MAPK, JNK and ERK when compared to the WT mice in both HFD‐ and ND‐treated groups. HFD induced the increase of p38 MAPK, JNK and ERK in WT mice but not in the CARD9−/− mice. The results indicated that CARD9 absence could be a vital protective factor in diet‐induced obesity via the CARD9/MAPK pathway, which may provide new insights into the development of gene knockout to improving diet‐induced obesity and metabolism disorder.

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Homeostasis Model Assessment Is a Reliable Indicator of Insulin Resistance During Follow-up of Patients With Type 2 Diabetes

Cited by 357 publications

References 27 publications

Can body fat distribution, adiponectin levels and inflammation explain differences in insulin resistance between ethnic Chinese, Malays and Asian Indians?

Can body fat distribution, adiponectin levels and inflammation explain differences in insulin resistance between ethnic Chinese, Malays and Asian Indians?

Role of Peroxisome Proliferator-Activated Receptor gamma 2 (PPAR-γ2) Gene Polymorphism in Type 2 Diabetes Mellitus

The essential function of CARD9 in diet‐induced inflammation and metabolic disorders in mice

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