Differential depot-specific effects of long-term fructose intake on lipoprotein lipase activity and adipose tissue development in lean and obese+NIDDM SHR/Ntul//-cp rats

Abstract

To determine the effects of a lower glycemic index, fructose-rich diet on parameters of weight gain and adipose tissue cellularity in principle fat depots, groups of congenic lean and obese+NIDDM SHR/tul//-cp rats were fed nutritionally complete isoenergetic diets where 54% of the calories were present as cooked cornstarch (CCS diet) or equal parts CCS and fructose (the CCSF diet) plus essential fats, proteins, minerals and dietary fibers from one until 9 months of age. Initial body weights were similar in all groups. Net weight gain and final body weights of obese >>>lean and demonstrated only a modest trend toward a greater weight gain in obese animals fed the CCSF diet. Differential effects on adipocyte size and number including marked hyperplasia and hypertrophy were observed in retroperitoneal and dorsal fat pads, while the mass and cellularity of the epididymal depots were similar in all dietary and phenotype groups. Tissue Lipoprotein Lipase activity (LPLA) was similar in EPI, RP, and Dorsal fat depots in both phenotypes, but LPLA in IBAT of lean >>> obese and demonstrated a modest diet effect (CSS > CSSF) in both phenotypes. These results indicate that the long-term consumption of the high fructose diet was neither substantially beneficial nor ameliorative in contributing to the modest excess weight gain and adiposity in WAT depots of the obese phenotype of this strain, despite the lower glycemic index and slower luminal digestibility of fructose vs cornstarch when fed in isoenergetic proportions in the diet. In contrast, IBAT mass and cellularity of obese >>> lean, while IBAT LPLA of lean >>> obese, suggestive of improved insulin sensitivity. These results suggest that the excess weight gain and adiposity often attributed to the consumption of excess dietary fructose sources may be at least in part a reflection of net caloric intake and insulinogenic responses rather than the type of carbohydrate consumed. In addition, the greater IBAT mass, cellularity, and percent lipid content of the obese are consistent with early onset hyperphagia and an impaired capacity for energy expenditure via non-shivering thermogenesis and thus represent a likely contributor to the epigenetic expression and development of obesity in the obese phenotype of this strain.