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      Beneficial Role of Bitter Melon Supplementation in Obesity and Related Complications in Metabolic Syndrome

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          Abstract

          Diabetes, obesity, and metabolic syndrome are becoming epidemic both in developed and developing countries in recent years. Complementary and alternative medicines have been used since ancient era for the treatment of diabetes and cardiovascular diseases. Bitter melon is widely used as vegetables in daily food in Bangladesh and several other countries in Asia. The fruits extract of bitter melon showed strong antioxidant and hypoglycemic activities in experimental condition both in vivo and in vitro. Recent scientific evaluation of this plant extracts also showed potential therapeutic benefit in diabetes and obesity related metabolic dysfunction in experimental animals and clinical studies. These beneficial effects are mediated probably by inducing lipid and fat metabolizing gene expression and increasing the function of AMPK and PPARs, and so forth. This review will thus focus on the recent findings on beneficial effect of Momordica charantia extracts on metabolic syndrome and discuss its potential mechanism of actions.

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          Most cited references134

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          IKK-beta links inflammation to obesity-induced insulin resistance.

          Inflammation may underlie the metabolic disorders of insulin resistance and type 2 diabetes. IkappaB kinase beta (IKK-beta, encoded by Ikbkb) is a central coordinator of inflammatory responses through activation of NF-kappaB. To understand the role of IKK-beta in insulin resistance, we used mice lacking this enzyme in hepatocytes (Ikbkb(Deltahep)) or myeloid cells (Ikbkb(Deltamye)). Ikbkb(Deltahep) mice retain liver insulin responsiveness, but develop insulin resistance in muscle and fat in response to high fat diet, obesity or aging. In contrast, Ikbkb(Deltamye) mice retain global insulin sensitivity and are protected from insulin resistance. Thus, IKK-beta acts locally in liver and systemically in myeloid cells, where NF-kappaB activation induces inflammatory mediators that cause insulin resistance. These findings demonstrate the importance of liver cell IKK-beta in hepatic insulin resistance and the central role of myeloid cells in development of systemic insulin resistance. We suggest that inhibition of IKK-beta, especially in myeloid cells, may be used to treat insulin resistance.
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            PGC-1 coactivators: inducible regulators of energy metabolism in health and disease.

            Members of the PPARgamma coactivator-1 (PGC-1) family of transcriptional coactivators serve as inducible coregulators of nuclear receptors in the control of cellular energy metabolic pathways. This Review focuses on the biologic and physiologic functions of the PGC-1 coactivators, with particular emphasis on striated muscle, liver, and other organ systems relevant to common diseases such as diabetes and heart failure.
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              Dyslipidemia in type 2 diabetes mellitus.

              Dyslipidemia is one of the major risk factors for cardiovascular disease in diabetes mellitus. The characteristic features of diabetic dyslipidemia are a high plasma triglyceride concentration, low HDL cholesterol concentration and increased concentration of small dense LDL-cholesterol particles. The lipid changes associated with diabetes mellitus are attributed to increased free fatty acid flux secondary to insulin resistance. The availability of multiple lipid-lowering drugs and supplements provides new opportunities for patients to achieve target lipid levels. However, the variety of therapeutic options poses a challenge in the prioritization of drug therapy. The prevalence of hypercholesterolemia is not increased in patients with diabetes mellitus, but mortality from coronary heart disease increases exponentially as a function of serum cholesterol levels, and lowering of cholesterol with statins reduces diabetic patients' relative cardiovascular risk. Although drug therapy for dyslipidemia must be individualized, most people with diabetes mellitus are candidates for statin therapy, and often need treatment with multiple agents to achieve therapeutic goals.

                Author and article information

                Journal
                J Lipids
                J Lipids
                JL
                Journal of Lipids
                Hindawi Publishing Corporation
                2090-3030
                2090-3049
                2015
                12 January 2015
                : 2015
                : 496169
                Affiliations
                1Department of Pharmaceutical Sciences, North South University, Dhaka 1229, Bangladesh
                2Department of Pharmacy, Stamford University Bangladesh, Dhaka 1217, Bangladesh
                3School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2678, Australia
                Author notes
                *Md Ashraful Alam: sonaliagun@ 123456yahoo.com and
                *Hasan Mahmud Reza: reza@ 123456northsouth.edu

                Academic Editor: Xian-Cheng Jiang

                Author information
                http://orcid.org/0000-0001-7596-5868
                http://orcid.org/0000-0001-8133-9732
                Article
                10.1155/2015/496169
                4306384
                25650336
                b72a1942-81a7-4390-91f2-8ec5f9ee2062
                Copyright © 2015 Md Ashraful Alam et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 30 August 2014
                : 5 December 2014
                Categories
                Review Article

                Biochemistry
                Biochemistry

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