27
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      ReishiMax, mushroom based dietary supplement, inhibits adipocyte differentiation, stimulates glucose uptake and activates AMPK

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Obesity is a health hazard which is closely associated with various complications including insulin resistance, hypertension, dyslipidemia, atherosclerosis, type 2 diabetes and cancer. In spite of numerous preclinical and clinical interventions, the prevalence of obesity and its related disorders are on the rise demanding an urgent need for exploring novel therapeutic agents that can regulate adipogenesis. In the present study, we evaluated whether a dietary supplement ReishiMax (RM), containing triterpenes and polysaccharides extracted from medicinal mushroom Ganoderma lucidum, affects adipocyte differentiation and glucose uptake in 3T3-L1 cells.

          Methods

          3T3-L1 pre-adipocytes were differentiated into adipocytes and treated with RM (0-300 μg/ml). Adipocyte differentiation/lipid uptake was evaluated by oil red O staining and triglyceride and glycerol concentrations were determined. Gene expression was evaluated by semi-quantitative RT-PCR and Western blot analysis. Glucose uptake was determined with [ 3H]-glucose.

          Results

          RM inhibited adipocyte differentiation through the suppresion of expression of adipogenic transcription factors peroxisome proliferator-activated receptor-γ (PPAR-γ), sterol regulatory element binding element protein-1c (SREBP-1c) and CCAAT/enhancer binding protein-α (C/EBP-α). RM also suppressed expression of enzymes and proteins responsible for lipid synthesis, transport and storage: fatty acid synthase (FAS), acyl-CoA synthetase-1 (ACS1), fatty acid binding protein-4 (FABP4), fatty acid transport protein-1 (FATP1) and perilipin. RM induced AMP-activated protein kinase (AMPK) and increased glucose uptake by adipocytes.

          Conclusion

          Our study suggests that RM can control adipocyte differentiation and glucose uptake. The health benefits of ReishiMax warrant further clinical studies.

          Related collections

          Most cited references55

          • Record: found
          • Abstract: found
          • Article: not found

          Adipose tissue, adipokines, and inflammation.

          White adipose tissue is no longer considered an inert tissue mainly devoted to energy storage but is emerging as an active participant in regulating physiologic and pathologic processes, including immunity and inflammation. Macrophages are components of adipose tissue and actively participate in its activities. Furthermore, cross-talk between lymphocytes and adipocytes can lead to immune regulation. Adipose tissue produces and releases a variety of proinflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as TNF-alpha, IL-6, monocyte chemoattractant protein 1, and others. Proinflammatory molecules produced by adipose tissue have been implicated as active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. In contrast, reduced leptin levels might predispose to increased susceptibility to infection caused by reduced T-cell responses in malnourished individuals. Altered adipokine levels have been observed in a variety of inflammatory conditions, although their pathogenic role has not been completely clarified.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The medical risks of obesity.

            Obesity is at epidemic proportions in the United States and in other developed and developing countries. The prevalence of obesity is increasing not only in adults, but especially among children and adolescents. In the United States in 2003 to 2004, 17.1% of children and adolescents were overweight, and 32.2% of adults were obese. Obesity is a significant risk factor for and contributor to increased morbidity and mortality, most importantly from cardiovascular disease (CVD) and diabetes, but also from cancer and chronic diseases, including osteoarthritis, liver and kidney disease, sleep apnea, and depression. The prevalence of obesity has increased steadily over the past 5 decades, and obesity may have a significant impact on quality-adjusted life years. Obesity is also strongly associated with an increased risk of all-cause mortality as well as cardiovascular and cancer mortality. Despite the substantial effects of obesity, weight loss can result in a significant reduction in risk for the majority of these comorbid conditions. Those comorbidities most closely linked to obesity must be identified to increase awareness of potential adverse outcomes. This will allow health care professionals to identify and implement appropriate interventions to reduce patient risk and mortality. A systematic search strategy was used to identify published literature between 1995 and 2008 that reported data from prospective longitudinal studies of obesity and comorbid medical conditions. This article will review evidence for significant associations of obesity with comorbidities to provide information useful for optimal patient management.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              PPAR gamma is required for the differentiation of adipose tissue in vivo and in vitro.

              The process of adipogenesis is known to involve the interplay of several transcription factors. Activation of one of these factors, the nuclear hormone receptor PPAR gamma, is known to promote fat cell differentiation in vitro. Whether PPAR gamma is required for this process in vivo has remained an open question because a viable loss-of-function model for PPAR gamma has been lacking. We demonstrate here that mice chimeric for wild-type and PPAR gamma null cells show little or no contribution of null cells to adipose tissue, whereas most other organs examined do not require PPAR gamma for proper development. In vitro, the differentiation of ES cells into fat is shown to be dependent on PPAR gamma gene dosage. These data provide direct evidence that PPAR gamma is essential for the formation of fat.
                Bookmark

                Author and article information

                Journal
                BMC Complement Altern Med
                BMC Complementary and Alternative Medicine
                BioMed Central
                1472-6882
                2011
                19 September 2011
                : 11
                : 74
                Affiliations
                [1 ]Cancer Research Laboratory, Methodist Research Institute, Indiana University Health, 1800 N Capitol Ave, E504, Indianapolis, IN 46202, USA
                [2 ]Department of Medicine, School of Medicine, Indiana University, Indianapolis, IN, USA
                [3 ]Indiana University Simon Cancer Center, Indianapolis, IN, 46202, USA
                Article
                1472-6882-11-74
                10.1186/1472-6882-11-74
                3224355
                21929808
                e88a2665-776a-46ad-8bc9-a81f7c4c7b1a
                Copyright ©2011 Thyagarajan-Sahu et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 5 August 2011
                : 19 September 2011
                Categories
                Research Article

                Complementary & Alternative medicine
                Complementary & Alternative medicine

                Comments

                Comment on this article