Effect of a High Fructose Diet on Brown Adipose Tissue Development in Adult Obese NIDDM Rats
Keywords:Obesity, Brown Fat, NIDDM, Insulin Resistance, Rat
In a recent article, the merits of brown adipose tissue as an efficient potential energy buffer that when deficient, may be a contributor to excess fat accretion and in the development of obesity. As such, it offers to be a potential target for therapies that could be developed in its treatment. To determine the effects of dietary fructose consumption on development and cellularity of brown adipose tissue in NIDDM, groups of lean and obese SHR/Ntul//-cp rats demonstrating insulin resistance (IR) were fed diets containing 54% (w/w) carbohydrate as cornstarch (CS diet) or equal parts CS plus fructose (CSF diet) plus essential proteins fats, vitamins, minerals, and dietary fiber from one to nine months of age. The SHR/Ntul//-cp rat is a congenic animal model in which the only genetic difference between the phenotypes is the epigenetic expression of the obese (-cp) trait, where it is accompanied by the development of chronic IR and non-insulin dependent diabetes (NIDDM) soon after weaning in the obese phenotype. Weight gain of obese >> lean and was greater when fed the CSF than the CS diet in both phenotypes with either diet; Interscapular brown adipose tissue (IBAT) mass of obese >> Lean and was similar in both phenotypes. IBAT Mass : Body weight of Obese >> lean, and trended greater in lean CSF vs CS but less in Obese CSF vs CS. IBAT cell size of obese >> lean, and the CS vs CSF diet was similar in lean but decreased in the obese phenotype. IBAT cell number of obese >>> lean, while IBAT cell number of lean CSF > lean CS, but IBAT cell number of obese was similar with both diets. Lipoprotein lipase activity (LPL) of lean >> obese and trended to be greater with the CSF than the CS diet in both phenotypes, and IBAT tissue lipid content of obese >> lean with a trend toward CSF > CS in both phenotypes. These results indicate that IBAT development occurs via hyperplasia and hypertrophy in the Obese phenotype of this strain, and that long term consumption of the high Fructose diet enhances IBAT cellularity in the lean phenotype while the IBAT cellularity was maximally enhanced by both diets in the obese phenotype.
These results further indicate that the impact of long-term consumption of a high fructose diet impacts the development of IBAT mass and cellularity differentially in the lean and obese+NIDDM phenotype, likely at least in part due to contributions of longstanding IR in the obese+NIDDM animals. Because IR is known to impede cellular glucose uptake in isolated brown adipocytes as an essential process in the expression of cellular thermogenic responses, any potential mechanisms to override or bypass the process or to decrease the magnitude of IR would be presumed to exert a beneficial effect. Since fructose may enter tissues independently of insulin actions, it may enhance the potential for expression of IBAT development and the expression of non-shivering thermogenesis in response to alterations in diet and environment, but overall fructose consumption was found to be neither remarkably beneficial nor ameliorative in resolving critical parameters of brown adipose tissue expression as contributors to the development of obesity in the obese phenotype present study.