Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0497406 (overweight)
 26,365 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-four overweight subjects with normal glucose tolerance (NGT) or impaired glucose tolerance (IGT) were followed for 10 years. No one from the NGT group developed diabetes, however 32% of the IGT subjects did develop diabetes. Initial data of the IGT subjects who developed diabetes were significantly different from those who did not develop diabetes. Fasting, peak and/or sigma plasma glucose (PG), IRI and CPR at 180 minutes and CPR/IRI at 0 and 180 minutes were increased, and the peak time of PG was delayed; also the prevalence of a positive family history was higher, and the body weight heavier. Seventy-nine percent of IGT subjects with the initial sigma PG of greater than or equal to 40 mM or a positive family history developed diabetes whereas only 3% of those with sigma PG of less than 40 mM and a negative family history developed diabetes. Therefore, it might be considered that among the overweight adults with IGT, those with sigma PG of greater than or equal to 40 mM or a positive family history are diabetes prone and those with sigma PG of less than 40 mM and a negative family history are diabetes resistant.
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PMID:Ten-year follow-up of Japanese overweight subjects with impaired glucose tolerance: identification of a diabetes-prone subpopulation. 145 Apr 95

In this study, 16 overweight or obese NIDDM patients with a long period of stable weight and dietary surveillance were treated with 150 mg t.i.d. of Benfluorex per os for 3 months. A significant improvement occurred in the fasting and post-meal glucose levels and in the HbA1C values, regardless of weight changes that occurred throughout the study. No significant changes were found in the fasting or meal-stimulated insulin (IRI) levels and in the glucose:IRI molar ratios. On the contrary, there were no significant variations in C-peptide levels while the glucose:CPR ratio appeared to decrease while on Benfluorex. In basal conditions, 11 patients presented insulin insensitivity (as measured by the glucose-insulin-somatostatin technique) which was unaffected by the pharmacological treatment. Benfluorex may therefore ameliorate metabolic control in overweight or obese NIDDM patients, but our data do not clarify whether its effects are mediated by an improvement in the action of insulin in peripheral tissues.
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PMID:Benfluorex action on metabolic control and insulin sensitivity in type 2 non-insulin dependent diabetics. 268 69

Liver microsomes from obese and control Sprague-Dawley rats were compared for cytochrome P-450 content and the ability to metabolize various prototype substrates. Over a 40-week period, the obesity-producing energy-dense diet increased average total body mass by 50%, liver mass by 32%, and body fat mass by 292%. Spectrally detectable cytochrome P-450 per mg protein increased by 36% in hepatic microsomes from obese rats. The livers from obese rats also contained more cytochrome P-450 (87%), while microsomal protein, NADPH-cytochrome c reductase, aryl hydrocarbon hydroxylase, and UDP-glucuronosyl transferase per organ rose slightly (12-40%) but not significantly. No change in the specific activities of these enzymes occurred. Young and adult rats were transferred from pellet diet to energy-dense diet for 3 weeks to examine the influence of diet vs. obesity. This short-term dietary change increased microsomal protein per g liver as well as cytochrome P-450 per liver, per g liver, and per mg protein. Adult animals increased in body weight by 24%, making them overweight and borderline obese. However, young animals showed no increase in body or liver weight, suggesting a direct effect of the energy-dense diet on liver P-450. Dietary obesity thus increased both the relative and total amounts of liver cytochrome P-450 in rats, but not the specific activities of other enzymes. These changes in cytochrome P-450 are consistent with the increased clearance seen for several oxidized drugs in obese humans and suggest that the obese overfed rat represents a useful animal model.
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PMID:Hepatic cytochrome P-450 and in vitro drug metabolism in an overfed rat model of obesity. 314 37