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)

Hyperleptinemia is considered to be one of predictors of early atherosklerosis complications. This stimulated us to investigate differences between leptinemia in persons with accelerated atherosclerosis and leptinemia in probands without atherosclerosis complications. The study also verified whether leptinemia and its relationship to other anthropometric and biochemical parameters can differ in hypolipemic-treated probands and hypolipemic-untreated individuals. We examined 89 probands with accelerated atherosclerosis. The controls were 20 persons without any signs of accelerated atherosclerosis. Probands with accelerated atherosclerosis had a slight hyperglycemia and were slightly obese, but they did not meet criteria of metabolic cardiovascular syndrome. No significant differences between both groups under study were found in terms of anthropometric and biochemical parameters (BMI, % body fat, glycemia, insulin, C-peptide, intact proinsulin, total proinsulin cholesterol, HDL, triglycerides, LDL, homeostatic model of insulin secretion and resistance). Leptin concentration was not different as well. Stratification into males and females showed that women had a significantly higher leptinemia and fat tissue mass. Other biochemical parameters were similar in both groups. We suppose that in individuals without signs of metabolic syndrome, leptinemia does not belong among predictors of accelerated atherosclerosis. The accelerated atherosclerosis persons were then divided into subgroups according to medication (28 probands--pravastatin Lipostat 20, 15 probands--phenofibrate Lipanthyl 200M, 9 probands--simvastatin Zocor 20, 47 probands--no hypolipemic medication). No significant differences between the groups were found in terms of the analysed anthropometric and biochemical parameters, except leptinemia. The pravastatin-medicated probands had a significantly lower leptinemia (significant at 99% significance level) which was evidently sex-related than other patients. The pravastatin-administered persons showed no correlation between leptinemia and body fat mass (in contrast to other groups where such a correlation was highly statistically significant). These findings can be explained by a still unclear effect of pravastatin on insulin metabolism and on other factors involved in leptin synthesis and elimination. Thus, a new therapeutic effect of pravastatin can be supposed. This may account for a highly favourable effect of pravastatin on reduced manifestations of atherosclerosis complications event at a low LDL cholesterol decrease (particularly in persons with metabolic cardiovascular syndrome).
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PMID:[Serum leptin, early atherosclerosis and hypolipidemia (a new, previously undescribed effect of pravastatin, a hypolipemic agent)]. 1042 91

Advicor (lovastatin and extended-release niacin) is the first cholesterol-lowering combination product to become available for the management of hyperlipidemia. Lovastatin significantly lowers low-density lipoprotein cholesterol, whereas niacin significantly lowers triglycerides and lipoprotein (a) and markedly increases high-density lipoprotein cholesterol. These effects are ideal for managing a variety of lipid disorders, including metabolic syndrome. Lovastatin and niacin reduce coronary heart disease mortality in primary and secondary prevention patients, respectively. The extended-release niacin component uses a unique technology to minimize adverse effects (e.g., flushing and hepatotoxicity) while retaining the same lipid-altering effects as immediate-release niacin. The combination product appears to be well tolerated, with discontinuation due to adverse effects other than flushing occurring in a similar percent of patients as for lovastatin in clinical trials. Approximately 9% of patients discontinued the combination product due to flush. No confined cases of myopathy or hepatotoxicity have been reported with this product. Once-daily dosing provides ease of administration that should improve compliance and result in a greater proportion of patients meeting their low-density lipoprotein cholesterol goals. The nomenclature surrounding niacin products used to treat dyslipidemias is confusing. While only two types of niacin formulations exist (immediate-release formulations and formulations which dissolve more slowly than immediate-release formulations), government regulations allow for slowly dissolved niacin formulations to be divided into two types of niacin products; those that are available over-the-counter (OTC) and those that are available by prescription only. Over-the-counter slowly dissolved niacin preparations are not classified as OTC per se, but are considered "nutritional supplements". For this reason, they fall under the jurisdiction of the Federal Trade Commission and do not fall under the umbrella of the FDA branch that controls dyslipidemic products (Endocrine and Metabolic Division of the Center for Drug Evaluation and Research). The slowly dissolved niacin nutritional supplements have not been reviewed by the FDA for safety nor efficacy in the treatment of dyslipidemia nor are they required to meet generic drug rules (even though various brands are available). These brands are described on their labels as "sustained-release", "timed-release", and "slow-release" for example. Only two slowly absorbed niacin products have been approved by the FDA for the treatment of dyslipidemia; they are Niaspan (Kos Pharmaceuticals, Inc., Miami, FL) and Advicor (Kos Pharmaceuticals, Inc., Miami, FL). The term "extended-release" has been given to these two products to simplify the terminology and differentiate the products from immediate-release niacin. In this review, we will use "extended-release" to refer to the FDA approved slowly dissolving niacin preparation and "sustained-release" to refer to the nutritional supplements (not FDA approved).
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PMID:Lovastatin and extended-release niacin combination product: the first drug combination for the management of hyperlipidemia. 1197 44

The objective of the study was to evaluate the efficiency of lovastatin correction of dyslipidemia and impaired intravascular platelet activity (IPA) in patients with arterial hypertension (AH) concurrent with metabolic syndrome (MS). Eighteen patients were given lovastatin for a month. The time course of changes in anthropometric parameters, blood lipid spectrum, plasma and lipid peroxidation, antioxidative protectiveness of the liquid blood part and platelets, and IPA were assessed. The results were processed by Student's test and correlation analysis. Lovastin was ascertained to correct dyslipoproteinemia and peroxidation syndrome and to optimize the intrathrombocytic mechanisms responsible for their function regulation in patients with AH + MS. Lovastatin inhibits in vivo increased platelet activity. These effects may be stabilized during its use. Body weight loss and diminished insulin resistance in patients with AH concurrent MS require long use of lovastatin along with low-calorie diet and exercises.
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PMID:[Thrombocytic hemostasis in hypertensive patients with metabolic syndrome and its correction with lovastatin]. 1558 98

Lovastatin, the progenitor of the statin family, is in fact a naturally occurring compound produced by the yeast Monascus purpureus. Red yeast rice (RYR), a traditional Chinese food made by fermenting rice with M purpureus, is an herbal medicine that has been used for 1200 y as a therapy for problems related to circulation and digestion. RYR contains a range of compounds known as monacolins, of which monacolin K-renamed lovastatin by pharmaceutical researchers-was found to be the most potent inhibitor of cholesterol synthesis. Standardized extracts of RYR, providing 10 mg of monacolins daily, have been shown to lower elevated low-density lipoprotein (LDL) cholesterol by approximately 20%. In a large secondary prevention trial in China, RYR was found to be markedly protective with respect to cardiovascular events and total mortality. Yet RYR very rarely induces the myopathy and hepatic damage commonly seen with prescription statin therapy. The Chinese herbal compound berberine, used to treat diabetes and congestive heart failure in China, has been shown to increase hepatic expression of LDL receptors and, hence, to lower LDL cholesterol, by extending the half-life of LDL receptor messenger ribonucleic acid (mRNA). This effect is complementary to the increased transcription of this mRNA promoted by statin therapy. Because berberine is well tolerated aside from transient gastrointestinal (GI) upset in some people and, in particular, has not been reported to cause myopathy or hepatic damage, the combination of RYR and berberine may have the potential to achieve reductions in LDL cholesterol comparable with those achieved with prescription statin therapy, but without the associated risks such as muscle damage and diabetes. Moreover, berberine, via its ability to activate adenosine monophosphate-activated kinase (AMPK), which it shares with the drug metformin, can lower triglycerides, improve metabolic syndrome, aid glycemic control in diabetics, and act directly on the vasculature to promote vascular health. It may also have the potential to reduce risk for various cancers, osteoporosis, osteoarthritis, nonalcoholic fatty-liver disease, and neurodegenerative disorders, although such predictions are highly speculative. Whereas statin therapy modestly increases risk for type 2 diabetes, berberine likely has the opposite effect. These considerations suggest that combined administration of RYR and berberine may provide a broader range of health protection than is afforded by prescription statin therapy, with lower risks for serious adverse effects compared with statins. Randomized, controlled trials (RCTs) assessing the effect of optimal intakes of RYR and berberine on serum lipids and other vascular risk factors are needed.
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PMID:Red Yeast Rice Plus Berberine: Practical Strategy for Promoting Vascular and Metabolic Health. 2630 59

CD62L (L-Selectin) dependent lymphocyte infiltration is known to induce inflammatory bowel disease (IBD), while its function in the liver, especially in non-alcoholic steatohepatitis (NASH), remains unclear. We here investigated the functional role of CD62L in NASH in humans as well as in two mouse models of steatohepatitis. Hepatic expression of a soluble form of CD62L (sCD62L) was measured in patients with steatosis and NASH. Furthermore, CD62L-/- mice were fed with a methionine and choline deficient (MCD) diet for 4 weeks or with a high fat diet (HFD) for 24 weeks. Patients with NASH displayed increased serum levels of sCD62L. Hepatic CD62L expression was higher in patients with steatosis and increased dramatically in NASH patients. Interestingly, compared to wild type (WT) mice, MCD and HFD-treated CD62L-/- mice were protected from diet-induced steatohepatitis. This was reflected by less fat accumulation in hepatocytes and a dampened manifestation of the metabolic syndrome with an improved insulin resistance and decreased cholesterol and triglyceride levels. Consistent with ameliorated disease, CD62L-/- animals exhibited an enhanced hepatic infiltration of Treg cells and a strong activation of an anti-oxidative stress response. Those changes finally resulted in less fibrosis in CD62L-/- mice. Additionally, this effect could be reproduced in a therapeutic setting by administrating an anti-CD62L blocking antibody. CD62L expression in humans and mice correlates with disease activity of steatohepatitis. CD62L knockout and anti-CD62L-treated mice are protected from diet-induced steatohepatitis suggesting that CD62L is a promising target for therapeutic interventions in NASH.
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PMID:L-Selectin/CD62L is a Key Driver of Non-Alcoholic Steatohepatitis in Mice and Men. 3236 32