title: Insulin sensitivity and abdominal obesity in African-American, Hispanic, and non-Hispanic white men and women. The Insulin Resistance and Atherosclerosis Study.
abstract: Increased abdominal obesity has been related to lower insulin sensitivity (SI), independent of overall obesity, but it has been suggested that this relationship may be weaker in non-whites. In the Insulin Resistance and Atherosclerosis Study (IRAS), SI was estimated using a minimal model analysis of the frequently sampled intravenous glucose tolerance test in 1,625 men and women aged 40-69 years. Subjects included African-Americans, Hispanics, and non-Hispanic whites from Oakland and Los Angeles, CA, San Antonio, TX, and the San Luis Valley, CO. Minimum waist circumference was significantly (P = 0.0001) associated with SI after adjusting for age, sex, height, BMI, glucose tolerance status, ethnicity, and clinic. This relationship was significantly (P = 0.0001) stronger in subjects with normal glucose tolerance (NGT) (beta = -0.030, P = 0.0001) than in those with impaired glucose tolerance (IGT) (beta = -0.010, P = 0.02; NIDDM: beta = -0.013, P = 0.0001). There were no significant ethnic differences in effect size across the spectrum of glucose tolerance. Waist circumference was also positively related to fasting insulin, an indirect measure of insulin sensitivity, in NGT (P = 0.0001), IGT (P = 0.0003), and NIDDM (P = 0.0002). The waist-fasting insulin relationship was significantly weaker in African-Americans, relative to non-Hispanic whites, in NGT and IGT (tests of statistical interaction: P = 0.04 and P = 0.02, respectively). In general, these patterns were similar in models specifying waist-to-hip ratio (WHR), rather than waist circumference, as the independent variable. While some ethnic variability exists, a negative relationship between abdominal obesity and insulin sensitivity was confirmed for all three ethnic groups across the spectrum of glucose tolerance.
authors.affiliation: Division of Research, Kaiser Permanente, Northern California Region, Oakland 94611-5714, USA. ajk@dor.kaiser.org
authors.forename: A J
authors.initials: AJ
authors.lastname: Karter
authors.forename: E J
authors.initials: EJ
authors.lastname: Mayer-Davis
authors.forename: J V
authors.initials: JV
authors.lastname: Selby
authors.forename: R B
authors.initials: RB
authors.lastname: D'Agostino
authors.forename: S M
authors.initials: SM
authors.lastname: Haffner
authors.forename: P
authors.initials: P
authors.lastname: Sholinsky
authors.forename: R
authors.initials: R
authors.lastname: Bergman
authors.forename: M F
authors.initials: MF
authors.lastname: Saad
authors.forename: R F
authors.initials: RF
authors.lastname: Hamman
mesh_terms: D000328:Adult; D001741:Black or African American; D000368:Aged; D001161:Arteriosclerosis / Q000235:genetics* / Q000503:physiopathology; D044383:Black People; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D001824:Body Constitution; D015992:Body Mass Index; D002140:California; D003120:Colorado; D003920:Diabetes Mellitus / Q000235:genetics / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000503:physiopathology*; D005260:Female; D018149:Glucose Intolerance / Q000235:genetics / Q000503:physiopathology*; D005951:Glucose Tolerance Test; D006630:Hispanic or Latino; D006801:Humans; D007328:Insulin / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000235:genetics* / Q000503:physiopathology; D012016:Reference Values; D012044:Regression Analysis; D013781:Texas; D044465:White People
chemical_list: D001786:Blood Glucose; D007328:Insulin