The objective of this work was to evaluate how obesity would influence the changes in brown fat (BAT) thermogenic capacity during fasting-refeeding. Mice fed either chow or chow + high-fat supplement for 6 wk had body weights of 34 +/- 1 and 43 +/- 1 g, respectively. They were fasted for 48 h followed by ad libitum refeeding for up to 5 days. Loss of carcass fat was similar between food-deprived mice previously fed chow or chow + high-fat supplement. However, even after a 48-h fast, obese mice still had a carcass fat content much greater than that of chow-fed mice. Brown fat atrophy caused by food deprivation was characterized by reductions in tissue weight, fat, mitochondrial proteins and uncoupling protein (UCP), without change in tissue DNA. Obesity did not alter the rate or extent of brown fat atrophy. Upon refeeding 48-h-fasted lean and obese mice, there was recovery of BAT thermogenic capacity that was similar between the two groups. In chow-fed mice, an intact neural input was essential for recovery of BAT thermogenic capacity during refeeding. These results indicate that food deprivation triggers an immediate adaptive response in mice previously fed chow or chow + a high-fat supplement and that reduction in brown fat thermogenic capacity during fasting and its recovery during refeeding appear little affected by the size of the animal energy reserves.
Electrical stimulation of the ventromedial hypothalamic area in rats caused a significant but transient increase in interscapular brown adipose tissue temperature. This response was markedly reduced by cimetidine, a histamine H2-receptor antagonist, but not by pyrilamine, an H1-receptor antagonist. Histamine is present in substantial amounts within mast cells in brown adipose tissue as injections of compound 48/80, which cause degranulation of connective tissue mast cells, reduced the tissue histamine content by > 85%. In contrast, histamine content in brown adipose tissue was not affected by loss of sympathetic neural input (with 6-hydroxydopamine) or sensory neural input (with capsaicin). Neither cimetidine nor histamine had any effect on basal and norepinephrine-stimulated rates of O2 consumption by isolated brown adipocytes. These results indicate that histamine released from mast cells acting on H2-receptors may play an important but indirect role in the thermogenic response of brown adipose tissue to stimulation of the ventromedial hypothalamic area.
1. Nutritional deprivation was induced preweaning in Wistar rats by increasing the litter size to sixteen, while paired litters with only five pups served as controls. The nutritionally deprived pups were rehabilitated after weaning by ad lib. access to an adequate diet.2. The body-weights and body lengths were significantly lower in the nutritionally deprived group and significant differences persisted even after 9 weeks of rehabilitation.3. The body temperature of the nutritionally deprived animals was significantly lower than that of their paired controls, both before and following nutritional rehabilitation, except for a short period after weaning when the nutritionally deprived animals were initially given the diet ad lib.
4.The resting oxygen consumption of the nutritionally deprived animals was comparable to that of the controls when corrected for metabolic body size, both before and after weaning. Noradrenaline-stimulated increase in 0, consumption (non-shivering thermogenesis; NST) was reduced by 50% at weaning in the nutritionally deprived animals and returned to levels comparable to those of controls within a short period of rehabilitation.5. The decrease in NST capacity seen in the nutritionally deprived animals was associated with an inability to thermoregulate when exposed to cold (5"), resulting in death. Cold-induced thermogenesis (CIT) also reappeared soon after nutritional rehabilitation.6. Reduction in metabolic rate, NST and CIT seen in the animals nutritionally deprived preweaning was short-lived and disappeared soon after nutritional rehabilitation. Rapid reversal of these physiological changes indicates that they do not confer any long-term benefit or change in metabolic efficiency and are unlike the changes in body size and growth which do not completely recover following nutritional rehabilitation.
Aims: Inheritance of polycystic ovary syndrome (PCOS) is still a controversy. Our study aims to analyze the family history of PCOS features and related metabolic disturbances including the male members to determine the mode of their inheritance.
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