Determining the Effect of High Carbohydrate Diets on Brain Composition and Senescence in Aging Hyperinsulinemic Obese LA/Ntul//-cp Rats

This chapter determine the effect of obese phenotype and the carbohydrate type resulted in alterations in brain composition in the obese phenotype of the congenic LA/Ntul//-cp rat, groups (n= 8 rats/group) of male littermate lean and obese rats were fed standardized isocaloric diets containing 54% (w/w) cornstarch (ST diet) or 54% (w/w) sucrose (SUC diet) from 1 until 10.5 ± 0.5 months of age. Malnutrition is a pervasive global public health issue that contributes to several dietary-related non-communicable illnesses. In low-income nations, adult nutrition is frequently overlooked. In low- and middle-income nations, both dual malnutrition (over and undernutrition) and nutrition transition exist. The current popular emphasis on low fat diets has resulted in an upwards shift in dietary carbohydrate consumption. The strain's obese phenotype exhibits hypertrophic-hyperplastic obesity during early postweaning development and early onset chronic hyperinsulinemia without NIDDM. The total fat, protein, and DNA of typical aliquots of dissected brain tissues were analyzed. When fed the SUC food as opposed to the ST diet, body weights of obese >> lean animals were higher in both genotypes. In rats fed the SUC diet compared to the ST diet, brain mass was somewhat smaller in lean individuals compared to fat individuals. Brain total Protein and DNA content of lean rats were > obese rats and were modestly Lower in SUC than ST fed rats in both phenotypes, but the percent of lipid content was proportional to brain mass. The decreased brain mass was characterized by proportionate decreases in total lipid, brain protein and brain DNA content and were further impaired when fed the insulinogenic sucrose diet. Total body fat mass of obese was significantly greater than occurred in lean littermates and was only modestly greater in SUC than ST fed rats in both phenotypes. These results indicate that brain growth and cellular development is impaired in the aging, hyperinsulinemia-prone obese phenotype of this strain, were further impaired when fed SUC than ST diets, and the decreased brain parameters were likely associated with development of a chronic neuronal inflammatory syndrome common to excessive fat accretion and obesity, resulting in premature brain senescence.