Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Groups of 4-week old, male Osborne-Mendel rats were given high fat diet (HFD) for 12 weeks; one group was fed control diet (CON) for 28 weeks. HFD rats were transferred to control diet (HFDCON) and diets restricted to 80% (HFDR80) or 60% (HFDR60) of HFDCON intake for another 16 weeks, while one group continued on HFD. Body, liver and epididymal adipose tissue (EPI) weight, and the EPI/body weight ratio of HFDR60 group decreased significantly. EPI lipid content and total lipoprotein lipase activity also declined in response to 40% restriction. Overall, the data indicate that 40% energy restriction can stabilize body weight at a reduced level, and mobilize adipose lipid to meet the energy needs of HFD rats.
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PMID:Adaptive response of rats with diet-induced adiposity to energy restriction. 274 30

Thirteen-week-old male, Osborne-Mendel rats were exercised for 6 weeks on a motorized treadmill. Exercise depressed weight gain and cumulative light cycle food intake while cumulative dark cycle and 24-hour total food intake were unaffected. Rats in sedentary and exercise groups were killed 24 hours after the last bout of exercise to assess the effects of chronic exercise and at 48, 60, 72, and 84 hours to determine the effects of exercise termination. Compared to sedentary controls, exercise decreased plasma insulin, epididymal and retroperitoneal depot weight and cell size, and retroperitoneal lipoprotein lipase (LPL) activity. Forty-eight hours after exercise, plasma insulin concentration increased to sedentary levels. By 60 hours, dark cycle food intake was increased above and adipose LPL activity was comparable to sedentary levels. At 84 hours postexercise termination, dark cycle food intake, plasma triglyceride, and epididymal LPL activity per depot and per cell were significantly greater than sedentary values. Exercise termination resulted in a preparatory response for rapid lipid deposition probably arising from increased food intake, plasma insulin, and enhanced LPL activity within 84 hours following termination of exercise.
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PMID:Exercise termination effects on food intake, plasma insulin, and adipose lipoprotein lipase activity in the Osborne-Mendel rat. 329 38

Osborne-Mendel (OM) and S5B/Pl rats differ in their sensitivity to develop obesity when fed a high fat (HF) diet; OM rats become obese, whereas S5B/Pl rats remain thin. We have investigated the possibilities that either an impaired leptin response or resistance to leptin action underlies the sensitivity to this form of obesity in OM rats. In Experiment 1, OM and S5B/Pl rats fed a nonpurified diet were killed at d 0 or were fed either a HF (56% fat energy) or a low fat (LF, 10% fat energy) diet for 2 or 7 d. The HF diet increased serum leptin significantly by d 2 to levels that were similar in both rat strains. At 7 d, leptin levels were lower than at d 2 but remained higher than levels in the d 0 control groups. The leptin mRNA:18S RNA ratio in epididymal adipose tissue increased to higher levels in HF-fed OM rats than in S5B/Pl rats fed that diet. However, although the LF diet had no effect in S5B/Pl rats, it increased leptin mRNA levels in epididymal adipose tissue of OM rats compared with the controls fed the nonpurified diet. In Experiment 2, OM and S5B/Pl rats were fed HF or LF diets for 5 wk. At that time, their feeding response to a range of leptin doses (0, 1, 5 or 10 microgram) given intracerebroventricularly was tested after overnight food deprivation. There was a similar dose-dependent reduction in energy intake in response to leptin in both OM and S5B/Pl rats. These responses were independent of the diet. The data suggest that the susceptibility of OM rats to HF diet-induced obesity is not related to either a loss of central sensitivity to leptin or a failure to enhance leptin production acutely, although the failure to maintain chronically increased levels of serum leptin could contribute to the obesity.
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PMID:The effects of a high fat diet on leptin mRNA, serum leptin and the response to leptin are not altered in a rat strain susceptible to high fat diet-induced obesity. 977 25