YOUNG MALE RATS

Abdominal Adiposity, Insulin And Bone Quality In Young Male Rats Fed A High-Fat Diet Containing Soybean Or Canola Oil

Abdominal Adiposity, Insulin And Bone Quality In Young Male Rats Fed A High-Fat Diet Containing Soybean Or Canola Oil

Obesity and related metabolic disorders are prevalent health issues in modern society and are commonly attributed to lifestyle and dietary factors. Obesity and insulin resistance are both powerful predictors of cardiovascular disease risk. Insulin resistance, in uncomplicated obesity, is associated with increased left ventricular mass and precocious changes of left ventricular geometry2 and, at any given degree of obesity, accentuates the risk of cardiovascular events and type 2 diabetes. Globally, the prevalence of obesity is escalating, and insulin resistance resulting from increased adipose tissue mass has been identified as a key factor in driving parallel rises in type 2 diabetes prevalence.[1] There is increasing evidence to suggest, particularly from studies in animals, that fetus exposed to excess maternal nutrition may be prone in later life to the cardiovascular disease. The environmental factors modulating the physiological systems controlling weight regulation and metabolic disorder etiologies, which manifest in young life, may originate before birth. The 'fetal origins of young disease', 'fetal programming' or 'predictive adaptive response' paradigms are based on pre- and postnatal environmental changes9 resetting the developmental path leading to obesity, cardiovascular and metabolic disorders later in life. The pathogenesis is not based on genetic defects, but rather on altered genetic expression in adaptating to environmental changes during fetal development. With the onset of obesity, maladaptive responses to adipose excess result in pathological states of inflammation, coagulopathy, and altered insulin sensitivity.[2]

Chronic high-fat diet consumption by male rats results in hyperinsulinemia maintenance during the postweaning period, causing glucose intolerance and development of obesity for the progeny in young life. Leptin and insulin resistance lead to critical endocrine defects in the pathogenesis of programming-induced obesity and metabolic disorders, because these hormones significantly reduce the number of pancreatic polypeptide- positive cells in the pancreatic islets of high-fat diet-fed animals. Moreover, postweaning high-fat diets increase plasma concentrations of free fatty acids by accelerating the maturation of the hypothalamic-pituitary- adrenal axis (HPA), causing permanent up-regulation of this axis, as well as basal level increases in corticosterone and stress-induced adrenocorticotrophic hormone (ACTH) and corticosterone secretion. Also, postnatal overfeeding increases adipose tissue glucocorticoid sensitivity. The effect of high-fat diets during early life and/or during postweaning period on body mass, fat mass, plasma level of glucose, insulin and leptin, was investigated and also their effects on the insulin/glucose ratio and cardiovascular parameters in young rat offspring. [3]

Soybean oil, which has an optimal n-6/n-3 polyunsaturated fatty acid ratio of 7 and a polyunsaturated:saturated ratio of w4, was the only source of fat in the dams' diet. The perinatal HFC had a greater amount of soybean oil, but did not modify the quality of the lipids and the same n-6/ n-3 polyunsaturated fatty acid and polyunsaturated:saturated ratios of the SC group were maintained, to avoid differences in these parameters having an impact upon the ...