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Does the epigenetic expression of obesity, insulin resistance and their metabolic sequelae contribute to brain senescence?


Abstract

Cognitive senescence and brain shrinkage have been reported in Alzheimer’s disease and is often associated with obesity but the pathophysiologic factors which bring about the neural declines remain unclear. A retrospective examination of factors of Insulin resistance and obesity in lean and obese rats indicated that final body weights of obese phenotype were more than double those of their lean littermates throughout adulthood, and carcass fat content at 10.5 months of age 15-fold greater than similarly fed lean littermates. In addition, the life span of the obese phenotype wasdecreased by approximately 30% in both male and female rats compared to their lean littermates. In addition, glycemic parameters indicated that the obese rats developed significant insulin resistance, while brain lipid, protein and DNA content were significantly reduced by one third or more in the obese phenotype by ~10 months of age, when they had approached their peak body weights. These observations suggest that the onset and progression obesity and its metabolic sequelae contributes to brain shrinkage, decreased DNA and protein content, key factors in the development of cognitive senescence in aging in this strain of rat.

Keywords

obesity, brain development, hyperinsulinemia, senescence, DNA, starch, sucrose, rat

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