ABSTRACT
BACKGROUND:The animal model of high fat diet-induced obesity is the first choice for the study of human obesity. Leptin and its receptor expression play an important role in the high fat diet-induced obesity and obesity resistant, but the exact mechanism and the role of swimming are not clear. OBJECTIVE:To explore the effect of 7-week swimming on serum leptin and leptin receptor expression in hypothalamus in rats with high fat diets. METHODS:A total of 60 Sprague-Dawley rats were fed with high fat diets for 8 weeks. Thediet-induced obeseand obese resistant rats were selected based on the body weight. 14 obese rats were equaly divided into two groups: obese group and obese-exercise group; and 14 obese resistant rats were equaly divided into two groups: obese resistantgroup and obese resistant-exercise group. Al the rats were continualy given high fat diets. Exercise groups accepted free swimming training for 7 weeks at the same time. RESULTS AND CONCLUSION:Compared with the obese group, obese-exercise group had obviously decreased in body weight, fat pad weight, fat pad weight/body weight and serum leptin concentration. And obese-exercise group had obviously increased receptor mRNA expression in hypothalamus. There was no significant change in above indexes betweenthe obese resistant group and obese resistant-exercise group. Theresults showed that swimming exercise can increase energy consumption and improve metabolism, which decreased the concentration of leptin and effectively improved leptin receptor expressionin the hypothalamus to ease leptin resistance and improve the body’s metabolism.
ABSTRACT
BACKGROUND:Overweight and obesity can lead to a disorder of sex hormone in men. The increase in female hormone levels may inhibit the synthesis and secretion of male hormone, increase fat accumulation and form a vicious circle. Exercise can effectively reduce body fat. OBJECTIVE: To investigate the effects of different exercise loads on sex hormone and the quality of sperm in obese male mice. METHODS: Weanling male C57BL/6J mice were divided into normal control group and obesity group. Mice in the obesity group were given high fat diet for 10 weeks to establish mouse model of obesity. The amount of food and water was recorded daily. Body weight was weighed once every week. After model induction, models were assigned to obesity moderate load exercise group and obesity high load exercise group. These models did exercises for 8 weeks. Body length was measured. Body weight, abdominal fat, testis, epididymis and seminal vesicle were weighed. Sperm activity and motility were observed by the sperm counting method in the epididymis tail. Enzyme linked immunosorbent assay was used to measure serum progesterone, folicle stimulating hormone, testosterone and estradiol. RESULTS AND CONCLUSION:Compared with the normal control group, body weight, abdominal fat weight, and lee’s index were increased (P < 0.01); the coefficient of testis and seminal vesicle were significantly decreased (P < 0.01); serum levels of luteinizing hormone, folicle stimulating hormone and testosterone were significantly decreased and estradiol level was significantly increased (P< 0.05); sperm count and activity were significantly decreased in the obesity group (P < 0.01). Compared with the obesity group, body weight, abdominal fat weight and lee’s index were significantly decreased (P < 0.05 orP < 0.01); the coefficient of testis and seminal vesicle were significantly increased in the obesity moderate load exercise group and obesity high load exercise group (P < 0.05 orP < 0.01). Serum luteinizing hormone, folicle stimulating hormone and testosterone levels were significantly increased (P < 0.05 orP < 0.01); estradiol levels were significantly decreased (P < 0.05); sperm count and activity were significantly increased (P < 0.01,P < 0.05) in the obesity moderate load exercise group. Compared with the obesity moderate load exercise group, abdominal fat weight and lee’s index were significantly reduced (P < 0.05); serum luteinizing hormone, folicle stimulating hormone, testosterone, sperm count and activity were decreased in the obesity high load exercise group (P < 0.01). These results indicate that long-term high fat diet leads to early obesity in males, inhibits the development of the reproductive gland and reproductive organs, and causes the decrease of the level of male hormone and sperm quality. Long-term moderate load exercise effectively reduces body fat, improves the inhibitory effect on male reproductive organs and glands, and relieves the negative effect of obesity on reproductive function. The effect of long-term large load exercise on reducing body fat is better than medium load exercise, but it has little effect on improving the level of male hormone in obese mice or on relieving the negative effect of obesity on reproductive function, even has a tendency to aggravate.
ABSTRACT
The nature of renal tubular cell injury in ischemic acute renal failure includes not only cell death (necrosis or apoptosis) but also sublethal injury causing cell dysfunction. The role of intracellu- lar calcium, calcium - dependent enzymes calpain, nitric oxide, phospholipase A2, loss of tubule cell polarity and tubular obstruction in the pathophysiology of the renal tubular cell injury during hypoxia/ischemia is described. The effects of vascular factors, infiltrating activited leukocytes, apoptosis and growth factors on renal tubular cell injury are discussed. Potential mechanisms that tubular injury leads to a profound fall in glomerular filtration rate are proposed.