Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Otsuka Long-Evans Tokushima fatty (OLETF) rat is a model of hyperphagic obesity in which the animals retain the desire to run voluntarily. Running wheels were provided for 4-wk-old OLETF rats for 16 wk before they were killed 5 h (WL5), 53 h (WL53), or 173 h (WL173) after the wheels were locked. Sedentary (SED) OLETF rats that were not given access to running wheels served as age-matched cohorts. Epididymal fat pad mass, adipocyte volume, and adipocyte number were 58%, 39%, and 47% less, respectively, in WL5 than SED rats. Contrary to cessation of daily running in Fischer 344 x Brown Norway rats, epididymal fat did not increase during the first 173 h of running cessation in the OLETF runners. Serum insulin and glucose levels were 77% and 29% less, respectively, in WL5 than SED rats. Oil red O staining for intramyocellular lipid accumulation was not statistically different among groups. However, lipid peroxidation levels, as determined by total trans-4-hydroxy-2-nonenal (4-HNE) and 4-HNE normalized to oil red O, was higher in epitrochlearis muscles of SED than WL5, WL53, and WL173 rats. mRNA levels of glutathione S-transferase-alpha type 4, an enzyme involved in cellular defense against electrophilic compounds such as 4-HNE, were higher in epitrochlearis muscle of WL53 than WL173 and SED rats. In contrast, 4-HNE levels in omental fat were unaltered. Epitrochlearis muscle palmitate oxidation and relative transcript levels for peroxisome proliferator-activated receptor-delta and peroxisome proliferator-activated receptor-gamma coactivator type 1 were surprisingly not different between runners and SED rats. In summary, voluntary running was associated with lower levels of lipid peroxidation in skeletal muscle without significant changes in intramyocellular lipids or mitochondrial markers in OLETF rats at 20 wk of age. Therefore, even in a genetic animal model of extreme overeating, daily physical activity promotes improved health of skeletal muscle.
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PMID:Exercise-induced attenuation of obesity, hyperinsulinemia, and skeletal muscle lipid peroxidation in the OLETF rat. 1807 66

Many studies, both national and international, have shown that tea has protective effects on many chronic diseases and their risk factors. In cancer prevention, our studies indicated that tea drinking could inhibit the carcinogenicity of various chemical carcinogens, including oral tumors induced by 7,12-dimethylbenz[a]anthracene (DMBA) in Golden hamsters, esophageal tumors in rats by blocking in vivo synthesis of N-Nitroso-methylbenzylamine (NMBzA), esophageal cancer induced by NMBzA in rats, precancerous liver lesions (r-GT and GST-P) induced by diethylnitrosamine (DENA) in rats, intestinal preneoplastic lesion (ACF) and intestinal tumors induced by 1,2-dimethyl-hydrazine (DMH) in rats, lung carcinoma induced by nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK) in A/J mice. Our studies have also shown that the protective effects of tea against cancer is a combined effects of various tea ingredients, among which the major ones are polyphenols and tea pigments. Based on animal studies, antioxidant properties, protection against DNA damage and modulation of immune functions were found to be the main mechanisms of anticancer effects of tea. In human trials, tea drinking showed protective effects against oxidative damage and DNA damage caused by cigarette smoking. Mixed tea drinking significantly blocked lesion progress in patients with oral mucosa leukoplakia, therefore, demonstrated its protective effects on oral cancer. Our studies have also shown effects of tea on prevention of cardiovascular diseases (CVD). For example, tea pigments was found to significantly inhibit LDL oxidation induced by Cu2+, Fe2+ in in vitro studies. In vivo studies showed that tea could prevent blood coagulation, facilitate fibrinogen dissolution, inhibit platelet aggregation, lower endothelin levels, enhance GSH-Px activities, protect against oxidated LDL-induced damage in endothelium cells, and prevent atherosclerosis of coronary arteries. The mechanisms of these protective effects of tea are possibly related to its antioxidant properties or its inhibition of lipid oxidation. Green tea and pigments was also found to inhibit cardiac hypertrophy induced by renal hypertension in rat models, whose mechanisms might, at least partly, involve its modulation on nitric oxide, angiotensin II and endothelin-1. Clinical intervention trials have indicated that tea and tea extracts decreased blood lipid, improved blood flow of coronary artery, and played an important role in atherosis inhibition and prevention. Our studies also showed that tea drinking has protective effects on diabetes. White tea drinking could significantly relieve symptoms including polyuria, polydipsia, polyphagia and weight loss in diabetic mice, decrease fasting plasma glucose level and improve glucose tolerance. In human trial, continuous white tea drinking could significantly improve symptoms of diabetic patients, such as relieve polydipsia, decrease plasma glucose levels, both fasting and 2 hours after meal, and increase insulin secretion. The effective rate for glucose lowering is 48% in clinical study.
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PMID:[Studies on tea and health]. 2227 81