Since the dietary guidelines were adjusted several decades ago in an effort to improve cardiovascular health by promoting diets containing fewer calories from fats, the consumption of carbohydrate calories including those from refined carbohydrate sources have increased proportionately in much of industrialized society. Refined carbohydrates including sucrose are rapidly digested by brush border glucosidases and have a higher glycemic index and stimulate greater insulinogenic responses than calories obtained from complex carbohydrate sources and tend to contribute to greater body fat accretion over time. High carbohydrate diets promote greater elevations in insulin secretion and can lead to insulin resistance and its multiple pathophysiologic sequelae including increases in body fat accretion, obesity, non-insulin dependent diabetes (NIDDM) chronic inflammation, and other comorbidities that can compromise health and longevity including neurologic demise. In the obese phenotype of the aging congenic, chronically insulin resistant non- diabetic LA/Ntul//-cp rat, measures of brain composition and cellularity as determined by brain mass and DNA content were significantly decreased and were further compromised when fed a high glycemic index, insulinogenic diet where the starch was replaced with isocaloric quantities of sucrose. These observations are consistent with the chronic insulin and amylin resistance linked to high carbohydrate diets in the obese phenotype as a contributing factor in the progression of senescence and brain atrophy and suggest that the factors of obesity and insulin resistance, compounded by the glycemic index of the diet were key factors in the neurologic demise and premature death in the obese phenotype of this strain.
Obesity, Aging, Brain composition, Hyperinsulinemia, Neuroinflammation, Neurosenescence, DNA, Cognitive Decline, Carbohydrate, Sucrose, Rat.