Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several epidemiological studies have shown an association between postprandial hyperglycemia and mortality from cardiovascular disease. Postprandial hyperglycemia is frequently associated with visceral obesity which plays a key role in metabolic abnormalities such as dyslipidemia and hypertension. Inhibitors of alpha-glucosidase and nateglinide have beneficial effects on the metabolic syndrome associated with visceral obesity. Voglibose in combination with diet therapy reduces visceral fat deposition and ameliorates insulin resistance. Acarbose slightly reduces blood pressure of hypertensive diabetic patients. Nateglinide, a rapidly acting insulin secretagogue, lowers postprandial glucose levels without significant body weight gain. These drugs may protect pancreatic beta-cells from postprandial glucose toxicity and prevent the progression of diabetes.
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PMID:[Pharmacological treatment of postprandial hyperglycemia in hypertensive patients with type 2 diabetes mellitus]. 1287 88

Dyslipidemia and fatty liver are important components of the metabolic syndrome and are the factors most commonly associated with the development of nonalcoholic fatty liver disease. Delayed and excessive insulin secretion in response to food intake is a key element in the onset of these risk factors. Nateglinide (NAT) is known to restore early-phase insulin secretion. We assessed the effect of NAT on postprandial hypertriglyceridemia and fatty liver in type 2 diabetic Goto-Kakizaki (GK) rats. The GK rats fed a high-fat diet containing 30% beef tallow twice a day were administered either the vehicle alone or NAT (50 mg/kg) before each meal for 12 weeks. Delayed insulin secretion and an increase of total insulin release were caused by feeding 30% beef tallow to the rats. This diet also induced postprandial hypertriglyceridemia and increased the hepatic triglyceride content. Treatment with NAT restored early-phase insulin secretion without any increase of total insulin release and also reduced postprandial hypertriglyceridemia and the hepatic triglyceride content. There was up-regulation of the hepatic expression of peroxisome proliferators-activated receptor alpha and its downstream enzymes after 12 weeks of NAT treatment, as well as normalization of the plasma total ketone body level. Furthermore, NAT also up-regulated hepatic expression of the adiponectin receptor AdipoR2, although there was no effect on the plasma adiponectin level. These findings indicate that long-term treatment with NAT prevented the development of fatty liver through the up-regulation of hepatic lipid oxidation pathways. Restoration of early-phase insulin secretion and suppression of recurrent postprandial hypertriglyceridemia might be involved in these effects of NAT. The present results may support the use of NAT to prevent the onset and progression of the metabolic syndrome and chronic liver disease.
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PMID:Nateglinide prevents fatty liver through up-regulation of lipid oxidation pathway in Goto-Kakizaki rats on a high-fat diet. 1807 71

The Nateglinide and Valsartan Impaired Glucose Tolerance Outcomes Research (NAVIGATOR) trial is exploring two pharmacological strategies (nateglinide and valsartan, both alone and in combination) in the prevention of overt diabetes mellitus (DM) and the reduction of cardiovascular disease (CVD) in subjects at high risk for these events. In this analysis, we provide baseline characteristics of the randomized NAVIGATOR study population and contrast them with those from other trials of DM prevention. Key eligibility criteria include impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), a history of CVD (in patients aged > or =50 years), and > or =1 cardiovascular risk factor (in patients aged > or =55 years). Baseline demographic characteristics, laboratory findings, cardiovascular risk factors, CVD history, and medication use are described and compared with other trials of DM prevention. The full analysis set of subjects (N = 9306) showed a clustering of risk factors consistent with the metabolic syndrome: high rates of hypertension (77.5%), dyslipidemia (44.7%), increased waist circumference (101.0 cm), and high body mass index (BMI) (47.5% with BMI > or =30 kg/m(2)). A minority of patients had a history of CVD (24.3%); of these, 11.7% had a history of myocardial infarction and most of the remainder had evidence of coronary artery disease. Subjects also had elevated blood pressure (BP) (predominantly systolic) (139.7/82.6 mm Hg), increased serum low-density lipoproteins cholesterol levels (3.27 mmol/L), and borderline elevation of triglyceride levels (1.97 mmol/L). Demographic data, BP, and lipid profiles in NAVIGATOR were similar to those of previous DM prevention trials, which were also based largely on meeting criteria for IGT. Medication use at baseline among NAVIGATOR subjects, which frequently included aspirin, beta-blockers, calcium channel blockers, diuretics, and lipid-lowering agents, reflects enhanced CVD risk. However, little prescribing of renin-angiotensin-aldosterone system blockers was observed, likely due to protocol exclusion criteria. In conclusion, the NAVIGATOR study comprises prediabetic subjects who typically have concurrent BP and metabolic disturbances and an enhanced risk of CVD, and are thus at higher risk for cardiovascular events than subjects in previous DM prevention trials.
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PMID:Baseline characteristics of the Nateglinide and Valsartan Impaired Glucose Tolerance Outcomes Research (NAVIGATOR) trial population: comparison with other diabetes prevention trials. 2018 89