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OBJECTIVE -- The objectives of this study were to determine age- and sex-specific concentrations of adiponectin in Asian Indian teenagers and adults and to assess whether its blood levels correlated with insulin resistance and other cardiometabolic parameters. RESEARCH DESIGN AND METHODS-- We studied 196 teenagers (94 boys, 102 girls) 12-18 years of age, selected from a cohort of 2,640 individuals from a cross-sectional school-based survey in Chennai, India. For comparison, adiponectin and plasma insulin were measured in 84 healthy adults. Correlation of adiponectin with plasma levels of insulin, proinsulin, insulin resistance, anthropometry, and family history of diabetes were studied. RESULTS-- Adiponectin showed a sex dimorphism, with girls having higher values (in micro;g/ml) (10.3 ± 5.0) than boys (8.4 ± 3.5) (P < 0.0001), and it showed a positive correlation with HDL cholesterol in boys only and not with other lipid parameters, insulin resistance, proinsulin, anthropometry, and family history of diabetes. In the adults, adiponectin correlated with fasting glucose and inversely with triglycerides. CONCLUSIONS-- In Asian Indian adults and teenagers, adiponectin did not correlate directly with measures of insulin sensitivity, overweight, and other cardiometabolic variables. This was at variance with several reports in other populations showing an inverse association of adiponectin with insulin resistance, proinsulin, and BMI, suggesting ethnic differences in the relationship of adiponectin with insulin sensitivity. The role of adiponectin in relation to action of insulin needs more detailed studies in Asian Indians. [ABSTRACT FROM AUTHOR]

OBJECTIVE--Type 2 diabetes has become a global epidemic, and Asian Indians have a higher susceptibility to diabetes than Europeans. We investigated whether Indians had any metabolic differences compared with Northern European Americans that may render them more susceptible to diabetes. RESEARCH DESIGN AND METHODS--We studied 13 diabetic Indians, 13 nondiabetic Indians, and 13 nondiabetic Northern European Americans who were matched for age, BMI, and sex. The primary comparisons were insulin sensitivity by hyper-insulinemic-euglycemic clamp and skeletal muscle mitochondrial capacity for Oxidative phosphorylation (OXPHOS) by measuring mitochondrial DNA copy number (mtDNA), OXPHOS gene transcripts, citrate synthase activity, and maximal mitochondrial ATP production rate (MAPR). Other factors that may cause insulin resistance were also measured. RESULTS--The glucose infusion rates required to maintain identical glucose levels during the similar insulin infusion rates were substantially lower in diabetic Indians than in the nondiabetic participants (P < 0.001), and they were lower in nondiabetic Indians than in nondiabetic Northern European Americans (P < 0.002). mtDNA (P < 0.02), OXPHOS gene transcripts (P < 0.01), citrate synthase, and MAPR (P < 0.03) were higher in Indians irrespective of their diabetic status. Intramuscular triglyceride, C-reactive protein, interleukin-6, and tumor necrosis factor-α concentrations were higher, whereas adiponectin concentrations were lower in diabetic Indians. CONCLUSIONS--Despite being more insulin resistant, diabetic Indians had similar muscle OXPHOS capacity as nondiabetic Indians, demonstrating that diabetes per se does not cause mitochondrial dysfunction. Indians irrespective of their diabetic status had higher OXPHOS capacity than Northern European Americans, although Indians were substantially more insulin resistant, indicating a dissociation between mitochondrial dysfunction and insulin resistance. Diabetes 57:1166-1175, 2008 [ABSTRACT FROM AUTHOR]

Asian Indians are highly susceptible to Type 2 Diabetes (T2D) and constitute the largest diabetic population in the world. The underlying etiology for this increased susceptibility for T2D among Asian Indians remains to be defined. To determine whether Asian Indians are more insulin resistant and whether their insulin resistance is associated with any differences in muscle gene transcript levels, we studied 13 non-diabetic (fasting glucose < 100 mg/dl) Asian Indians (Age=47.2±2.4 y, BMI=23.8±0.5 kg/m²) and 13 gender-matched Americans of North European origin (European Americans; Age=46.6±2.2 y, BMI=24.5±0.8 kg/m2). Insulin sensitivity was measured by hyperinsulinemic (1.5 mU/kg FFM/min) euglycemic clamp. To maintain identical plasma glucose levels, Asian Indians required a substantially lower glucose infusion rate than European American controls (42.3 ± 4.0 vs. 68.3 ± 4.2 µmol/Kg FFM/min,p<0.001). Percutaneous needle biopsy samples were collected for gene array analysis. Total RNA was extracted from snap frozen muscle biopsy samples, amplified, labeled with fluorescent probe, fragmented and hybridized to the U133 Pins 2.0 Affymetrix genechip and GCRMA software was used to analyze microarray data. Out of about 47,000 transcripts surveyed, 58 genes transcript levels were altered (52 increased and 6 decreased) in Asian Indians compared to European Americans. Examples are as follows: Lipid metabolism: Fatty acid binding protein 7 (↑3.7); Glucose metabolism: GAPDH (↑1.03), Lactate dehydrogenase A (↑1.3); Chaperone: heat shock proteins 70 (↓0.65); and Energy metabolism: NADH1 (↑1.07), ATP synthase (↑1.1), Cytochrome C oxidase Va (↑1.20), Cytochrome C oxidase VLLc (↑1.1). In conclusion, nondiabetic Asian Indians are significantly more insulin resistant and have altered skeletal muscle gene transcript levels involving multiple metabolic pathways including mitochondrial bioenergetics. The results indicate potential mechanisms for higher susceptibility of Asian Indians to become diabetic. [ABSTRACT FROM AUTHOR]

Provides information on several studies about insulin action to be presented at the 65th Scientific Sessions of the American Diabetes Association at the San Diego Convention Center in California from June 10 to 14, 2005. Correlation of low birth weight with adult insulin resistance in Asian Indian children; Effect of high-fat feed to induced insulin resistance on male and female rats; Background on the mechanism of pancreatic islet cell insulin resistance in high-fat-diet obese rats.

Asian Indians (AI) are insulin resistant and have a higher risk of diabetes compared to Caucasians (C). However, potential abnormalities in insulin secretion and their relationship to the severity of insulin resistance in AI have not been carefully studied. To address this question we examined l) first (0-10 min) and second (l0-120 min) phase insulin secretion during a 2-hr hyperglycemic clamp at +90 mg/dl, 2) insulin secretion in response to a non-glucose secretagogue (arginine, 5 gm IV) at euglycemia and at the end of the hyperglycemic clamp, and 3) insulin sensitivity (M) during a 1 mU/kg⋅min hyperinsulinemic euglycemic clamp. Four healthy AI and 6 C of similar age (29±2 vs 38±6 yrs) and BMI (25.3±2.3 vs 24.7±1.3 kg/msup2;) were studied. AI and C had similar FPG (94±2 vs 90±2. mg/dl), but AI had higher fasting insulin levels (9.1±2.2 vs 3.4±0.6 µU/ml, p<0.05) and were very insulin resistant during the euglycemic clamp (M = 4.0±0.5 vs 9.7±0.6 mg/kg/min, p<0.001). During the hyperglycemic clamp, first phase (321±106 vs 102±22 µU/ml⋅0 min, p<0.05) and second phase (4920±959 vs 1340±174 pU/ml. 110 min, p<0.01) insulin secretion were significantly increased in AI vs C. The insulin responses to arginine at euglycemia (314±43 vs 145±9 µU/ml. l0 min, p<0.01) and hyperglycemia (2399±415 vs 1203±235 #U/ml. 10 min, p<0.05) also were significantly higher in AI. All measures of insulin secretion were inversely correlated with M (r = -0.69 to -0.82, p<0.05 to 0.005). The glucose disposition index (M x first phase insulin secretion) was increased moderately (by 29%), but not significantly, in AI vs C. Conclusion: Non-diabetic AI are characterized by l) marked insulin resistance, 2) enhanced first- and second-phase insulin responses to hyperglycemia, 3) increased insulin response to arginine at euglycemia and hyperglycemia, and 4) a moderate increase in the glucose disposition index. These data suggest that beta cell function remains intact in non-diabetic AI despite the presence of significant insulin resistance. [ABSTRACT FROM AUTHOR]