Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although diagnostic criteria for metabolic syndrome (MtS) vary among various health professionals and organizations, blood glucose dysregulation and insulin resistance are common to all definitions. Red ginseng is beneficial for glucose regulation and insulin sensitivity but the mechanism is not yet elucidated. Ginsenosides Rh1 and Rg3 act as ligands of the estrogen receptor, and Rh2 and compound K act as ligands of the glucocorticoid receptors, which may influence the diabetes markers. The objective of this study was to test the hypothesis that there are significant causal relationships among diabetes-related markers and several hormones, and assess whether or not the consumption of fermented red ginseng (FRG) influences these causal relationships by multiple group path analysis and conventional statistical analyses. The 93 postmenopausal women were randomly divided into two groups for a double-blind trial. FRG powder and placebo were provided for 2 weeks. The data were analyzed by multiple group path analysis and the mean between groups were compared. The model's goodness of fit was excellent, with a root mean square error of approximation of 0.00, and comparative fit index of 1.00. The FRG group exhibited significantly increased levels of dehydroepiandrosterone sulfate (DHEAS), growth hormone (GH), and estradiol (E2), and they exhibited decreased levels of glycosylated hemoglobin (HbA1c), insulin, and homeostatic model assessment of insulin resistance. With regard to the hypothesis, the blood glucose lowering effects of FRG were due to the negative effects of aldosterone and increased GH, which was associated with DHEAS and E2. Even though the differences of variables between both groups were small, the total effects of these variables may indicate beneficial changes for the prevention of diabetes in healthy postmenopausal women.
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PMID:Diabetes-ameliorating effects of fermented red ginseng and causal effects on hormonal interactions: testing the hypothesis by multiple group path analysis. 2367 90

Metabolic syndrome including obesity, dyslipidemia and hypertension is a cluster of risk factors of cardiovascular disease. Fermentation of medicinal herbs improves their pharmacological efficacy. Red ginseng (RG), a widely used traditional herbal medicine, was reported with anti-inflammatory and anti-oxidant activity. Aim in the present study was to investigate that the effects of fermented red ginseng (FRG) on a high-fructose (HF) diet induced metabolic disorders, and those effects were compared to RG and losartan. Animals were divided into four groups: a control group fed a regular diet and tap water, and fructose groups that were fed a 60% high-fructose (HF) diet with/without RG 250 mg/kg/day or FRG 250 mg/kg/day for eight weeks, respectively. Treatment with FRG significantly suppressed the increments of body weight, liver weight, epididymal fat weight and adipocyte size. Moreover, FRG significantly prevented the development of metabolic disturbances such as hyperlipidemia and hypertension. Staining with Oil-red-o demonstrated a marked increase of hepatic accumulation of triglycerides, and this increase was prevented by FRG. FRG ameliorated endothelial dysfunction by downregulation of endothelin-1 (ET-1) and adhesion molecules in the aorta. In addition, FRG induced markedly upregulation of Insulin receptor substrate 1 (IRS-1) and glucose transporter type 4 (Glut4) in the muscle. These results indicate that FRG ameliorates obesity, dyslipidemia, hypertension and fatty liver in HF diet rats. More favorable pharmacological effects on HF diet induced metabolic disorders were observed with FRG, compared to an equal dose of RG. These results showed that the pharmacological activity of RG was enhanced by fermentation. Taken together, fermentated red ginseng might be a beneficial therapeutic approach for metabolic syndrome.
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PMID:Fermented Red Ginseng Potentiates Improvement of Metabolic Dysfunction in Metabolic Syndrome Rat Models. 2732 12