Impact of an Intermittent Complex Carbohydrate Regimen on Insulin Resistance and Adiposity in Congenic, Lean and Obese LA/Ntul//-cp Rats

Abstract

Chronic nutritionally induced increases in insulin resistance contribute to the progression of cardiometabolic disorders in man and animals. To determine the impact on adiposity, complex carbohydrate in the form of Polycose® was fed ad libitum intermittently to congenic lean and obese LA/Ntul//-cp rats as a 25% (w/v) dietary carbohydrate supplement in drinking water in addition to stock Purina chow and house water from 3 until 12 months of age. Final Body weights of chow-fed obese rats were 2.2-fold greater than their lean littermates, and Polycose® supplemental feeding was associated with 17% and 19% increases in final body weight in both lean and obese phenotypes respectively. The combined mass of the primary white adipose tissue (WAT) depots was 8.6-fold greater in the obese than in their similarly fed lean littermates, and the Polycose® regimen was associated with a 2.7-fold increase in the dorsal WAT depots and a 1.5-fold increase in the retroperitoneal and inguinal WAT depots in the obese phenotype. The Polycose®-associated increases in adiposity were consistent with the result of adipocyte hypertrophy and hyperplasia in both phenotypes. Interscapular brown adipose tissue (IBAT) mass of obese >> lean, and Polycose® was associated with a 1.9-fold increase in IBAT mass in the lean phenotype but was without further increases in the obese phenotype. Baseline- and insulin stimulated in vitro glucose oxidation in diaphragm occurred normally in the lean phenotype but was impaired by over 50% in the obese phenotype, consistent with a decrease in insulin sensitivity and impaired oxidative metabolism in the obese animals. Measures of these observations confirm the marked adiposity of the obese phenotype of this strain, and suggest that long -term complex-CHO supplementations may contribute to an enhancement in the capacity for energy expenditure via non-shivering thermogenesis in IBAT in the lean phenotype, thereby partially buffering the against a propensity for overly excessive fat accretion, but that the capacity for IBAT-mediated NST and mechanisms of lipid accretion and energetic efficiency in the obese phenotype may be impaired thereby further enhancing their propensity for fat accretion and the development of obesity via a combination of depot-specific lipid accretion via hyperplasia and hypertrophy of adipocytes in both abdominal and subcutaneous depots.