Abstract
Food restriction (FR) is the most commonly used intervention to prevent the overweight. However, the lost weight is usually followed by “compensatory growth” when FR ends, resulting in overweight. The present study was aimed to examining the behavior patterns and hormones mechanisms underpinning the over-weight. Energy budget and body fat content, and several endocrine markers related to leptin signals were examined in the striped hamsters under 20% FR refed by either low-fat diet (LF group) or high-fat diet (HF group). Body mass and fat content significantly regained when FR ended, and the hamsters in HF group showed 49.1% more body fat than in LF group (P < 0.01). Digestive energy intake was higher by 20.1% in HF than LF group, while metabolic thermogenesis and behavior patterns did not differed between the two groups. Gene expression of leptin receptor and anorexigenic peptides of pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript in hypothalamus were significantly up-regulated in LF group, but down-regulated in HF group. It suggests that effective leptin signals to the brain were involved in attenuation of hyperphagia in hamsters refed with LF. However, “leptin resistance” probably occurred in hamsters refed with HF, which impaired the control of hyperphagia, resulting in development of over-weight.
Highlights
Food restriction has been suggested to increase the extension of life and to lose body mass of so many mammal species[1,2,3,4]
Body mass did not differ among the four groups before food restriction started
Food restriction resulted in a significant decrease in body mass of FR groups, and it decreased, on average, by 20% on day 15 compared to that on day 0
Summary
Food restriction has been suggested to increase the extension of life and to lose body mass of so many mammal species[1,2,3,4] It is the most commonly used intervention to prevent the overweight and obesity in humans[5]. We previously found a significant decrease in body mass and fat content in food-restricted hamsters, followed by a compensatory growth without overweight when refed ad libitum[41]. On the basis of the role of leptin, striped hamsters may be becoming an animal model showing resistance to overweight or obesity This may not be the case, since we observed a considerable increase in body fat content in the hamsters subjected to a high-fat diet (HF)[42]. We hypothesized that the effective leptin signal to brain might contribute to the compensatory growth without overweight, and leptin resistance resulted in overweight
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