Normal insulin sensitivity in lean offspring of obese parents

• Published in: Obesity (Silver Spring, Md.) Md.), 2004-04, Vol.12 (4), p.621-626
• Main Authors: Lazarin, M.A.C.T, Bennini, J.R, Pereira, C.L.C, Astiarraga, B.D, Ferrannini, E, Muscelli, E
• Format: Article
• Language: English
• Subjects: Adult; Blood Glucose - analysis; Body Composition; Body Constitution; Body Mass Index; C-Peptide - blood; C‐peptide; Female; Glucose Clamp Technique; Glucose Tolerance Test; Humans; Insulin - blood; Insulin - pharmacology; insulin clamp; Insulin Resistance - genetics; insulin secretion; insulin sensitivity; Male; Obesity - etiology; Obesity - genetics; offspring of obese; Parents
• ISSN: 1071-7323; 1930-7381; 1550-8528; 1930-739X
• DOI: 10.1038/oby.2004.71

Objective: Offspring of diabetic or hypertensive patients are insulin resistant at a prediabetic/prehypertensive stage. We tested the hypothesis that insulin action may be impaired in the offspring of obese nondiabetic parents. Research Methods and Procedures: Twenty‐one lean offspring of nonobese subjects [(OL) 22 ± 3 years of age] were matched to 23 lean offspring of obese subjects (OOb) by gender distribution, age, BMI, and waist circumference. Anthropometry, oral glucose tolerance, in vivo insulin sensitivity [by a euglycemic insulin clamp (6 pmol/min per kilogramFFM; where FFM represents fat‐free mass)], and thermogenesis (by indirect calorimetry) were measured in each subject. The study subjects were from a population of 267 nuclear families (one offspring and both his/her parents) in which there was statistically significant (χ2 = 30.2, p = 0.001) concordance of BMI between parents and offspring. Results: In comparing OOb with OL, no statistically significant difference or trend toward a difference was detected in fasting plasma glucose and insulin concentrations, glucose and insulin responses to oral glucose, insulin sensitivity [metabolism value = 45 ± 12 (OOb) vs. 47 ± 17 μmol/min per kilogramFFM (OL)], insulin‐induced inhibition of protein and lipid oxidation, stimulation of glucose oxidation and nonoxidative glucose disposal, respiratory quotient, resting energy expenditure, and glucose‐induced thermogenesis. Discussion: The metabolic similarity between lean offspring of obese parents and those of nonobese parents suggests that insulin resistance and its correlates are not co‐inherited with the predisposition to develop obesity.