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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of diabetes is steadily rising, and once it occurs, it can cause multiple complications with a negative impact on the whole organism. Complications of diabetes may be macrovascular: such as stroke and ischemic heart disease as well as peripheral vascular and microvascular diseases-retinopathy, nephropathy, and neuropathy. Key factors that cause cardiovascular disease in people with diabetes include hyperglycemia, dyslipidemia, obesity, insulin resistance, inflammation, hypertension, autonomic dysfunction, and decreased vascular response capacity. Microbes can be considered a complex endocrine system capable of ensuring the proper functioning of the body but are also responsible for the development of numerous pathologies (diabetes, coronary syndromes, peripheral arterial disease, neoplasia, Alzheimer's disease, and hepatic steatosis). Changes in the intestinal microbiota may influence the host's sensitivity to insulin, body weight, and lipid and carbohydrate metabolism. Dysbiosis causes activation of proinflammatory mechanisms, metabolic toxicity, and insulin resistance. Trimethylamine N-oxide (TMAO) is a microbial organic compound generated by the large intestine, and its concentration increases in the blood after ingestion of foods rich in L-carnitine and choline, such as red meat, eggs, and fish. The interest for TMAO in cardiometabolic research has recently emerged, given the preclinical evidence that reveals a link between TMAO, diabetes, and cardiovascular complications. Intestinal microbiota can be modulated by changing one's lifestyle but also by antibiotic, probiotic, prebiotic, and fecal transplantation. The purpose of this article is to highlight issues related to the involvement of microbiota and trimethylamine N-oxide in the pathogenesis of diabetes mellitus and cardiovascular disease. Better appreciation of the interactions between food intake and intestinal floral-mediated metabolism can provide clinical insights into the definition of individuals with diabetic risk and cardiometabolic disease as well as potential therapeutic targets for reducing the risk of progression of the disease.
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PMID:Implications of the Intestinal Microbiota in Diagnosing the Progression of Diabetes and the Presence of Cardiovascular Complications. 3053 26

The metabolic syndrome (MS) is a conglomeration of inter-related common clinical disorders, including obesity, glucose intolerance, hypertension and dyslipidemia, which predispose to Type 2 diabetes (T2D) and cardiovascular diseases. Hyperinsulinemia, per se, and insulin resistance are the pathogenic factors associated with the metabolic risk factors. Since these risk factors are the most frequent causes for mortality among patients with T2D and the MS, treatments targeting normalization of both lipid and glucose homeostasis are of interest. The crucial role of L-carnitine (CA) as a regulator of lipid and glucose metabolism has raised considerable interest in its use as a potential tool for therapeutic intervention in the MS. Several clinical studies have, therefore, been undertaken to examine the efficacy and other benefits in the treatment of T2D and the MS. Studies from rodent models of MS have also shown the positive effects of CA on several components of the syndrome. CA, being an endogenous water-soluble nutrient, could be a safe adjunct and a relevant future drug for the MS. This review provides an overview on the importance of CA in T2D and the MS and the need for further evaluation of its inclusion in treatment protocols.
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PMID:L-carnitine: implications in the treatment of the metabolic syndrome and Type 2 diabetes. 3076 66

Hyperuricemia was linked to diabetes mellitus, metabolic syndrome, and oxidative stress, and could be induced by higher fructose consumption through altering energy status in liver. l-Carnitine is an antioxidant, affecting mitochondria and cellular energetics; however, little is known about its effects in hyperuricemic states. This study investigated metabolic and hepatic effects of hyperuricemia and fructose feeding, and demonstrated the role of l-Carnitine in such states. Fifty adult male Wistar rats were randomly divided into control, untreated hyperuricemic, fructose-supplemented hyperuricemic, l-Carnitine-treated hyperuricemic, and l-Carnitine-treated fructose-supplemented hyperuricemic groups. The separated plasma was used for determination of the glycemic control, lipid profile, liver function tests, uric acid level, and oxidative stress markers. Atherogenic index, HOMA-IR, and body mass index (BMI) were calculated. Left liver lobe and left kidney specimen from all groups were used for histopathological studies. Hyperuricemic rats exhibited significantly hypoalbuminemia, dyslipidemia, insulin resistance, and oxidative stress compared to the controls. Fructose-supplemented hyperuricemic group showed obesity and more deleterious effects, as well as, steatosis, and renal tubular damage compared to the hyperuricemic rats. Concomitant l-Carnitine treatment with hyperuricemia improved such effects, despite causing adiposity. While combined l-Carnitine treatment and fructose supplementation in hyperuricemia limited the aggressive hyperuricemic picture of fructose supplementation. It is concluded that hyperuricemia has detrimental metabolic and hepatic effects. Artificial fructose supplementation worsened such effects, while l-Carnitine was efficient in ameliorating these hyperuricemia and/or excess fructose-induced hyperuricemia effects, through its anti-inflammatory, antisteatotic, and antioxidant properties.
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PMID:Possible role of l-carnitine in improvement of metabolic and hepatic changes in hyperuricemic and hyperuricemic-Fructose-supplemented rats. 3178 19


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