5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Helminthostachys zeylanica alleviates hepatic steatosis and insulin resistance in diet-induced obese mice

      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 and its associated health conditions, type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are worldwide health problems. It has been shown that insulin resistance is associated with increased hepatic lipid and causes hepatic steatosis through a myriad of mechanisms, including inflammatory signaling.

          Methods

          Helminthostachys zeylanica (HZ) is used widely as a common herbal medicine to relieve fever symptoms and inflammatory diseases in Asia. In the present study, we evaluated whether HZ has therapeutic effects on obesity, NAFLD and insulin resistance. The protective effects of HZ extract were examined using free fatty acid-induced steatosis in human HuS-E/2 cells and a high-fat diet-induced NAFLD in mice.

          Results

          The major components of the HZ extract are ugonins J and K, confirmed by HPLC. Incubation of human hepatocytes, HuS-E/2 cells, with palmitate markedly increased lipid accumulation and treatment with the HZ extract significantly decreased lipid deposition and facilitated AMPK and ACC activation. After 12 weeks of a high-fat diet with HZ extract treatment, the HFD mice were protected from hyperlipidemia and hyperglycemia. HZ extract prevented body weight gain, adipose tissue expansion and adipocyte hypertrophy in the HFD mice. In addition, fat accumulation was reduced in mice livers. Moreover, the insulin sensitivity-associated index, which evaluates insulin function, was also significantly restored.

          Conclusions

          These results suggest that HZ has a promising pharmacological effect on high-fat diet-induced obesity, hepatic steatosis and insulin resistance, which may have the potential for clinical application.

          Related collections

          Most cited references37

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

          AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy.

          D Hardie (2007)
          The SNF1/AMP-activated protein kinase (AMPK) family maintains the balance between ATP production and consumption in all eukaryotic cells. The kinases are heterotrimers that comprise a catalytic subunit and regulatory subunits that sense cellular energy levels. When energy status is compromised, the system activates catabolic pathways and switches off protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. Surprisingly, recent results indicate that the AMPK system is also important in functions that go beyond the regulation of energy homeostasis, such as the maintenance of cell polarity in epithelial cells.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Mouse models in non-alcoholic fatty liver disease and steatohepatitis research.

            Non-alcoholic fatty liver disease (NAFLD) represents a histological spectrum of liver disease associated with obesity, diabetes and insulin resistance that extends from isolated steatosis to steatohepatitis and cirrhosis. As well as being a potential cause of progressive liver disease in its own right, steatosis has been shown to be an important cofactor in the pathogenesis of many other liver diseases. Animal models of NAFLD may be divided into two broad categories: those caused by genetic mutation and those with an acquired phenotype produced by dietary or pharmacological manipulation. The literature contains numerous different mouse models that exhibit histological evidence of hepatic steatosis or, more variably, steatohepatitis; however, few replicate the entire human phenotype. The genetic leptin-deficient (ob/ob) or leptin-resistant (db/db) mouse and the dietary methionine/choline-deficient model are used in the majority of published research. More recently, targeted gene disruption and the use of supra-nutritional diets to induce NAFLD have gained greater prominence as researchers have attempted to bridge the phenotype gap between the available models and the human disease. Using the physiological processes that underlie the pathogenesis and progression of NAFLD as a framework, we review the literature describing currently available mouse models of NAFLD, highlight the strengths and weaknesses of established models and describe the key findings that have furthered the understanding of disease pathogenesis.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              Nonalcoholic Fatty Liver Disease and Insulin Resistance: New Insights and Potential New Treatments

              Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver disorders worldwide. It is associated with clinical states such as obesity, insulin resistance, and type 2 diabetes, and covers a wide range of liver changes, ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), liver cirrhosis, and hepatocellular carcinoma. Metabolic disorders, such as lipid accumulation, insulin resistance, and inflammation, have been implicated in the pathogenesis of NAFLD, but the underlying mechanisms, including those that drive disease progression, are not fully understood. Both innate and recruited immune cells mediate the development of insulin resistance and NASH. Therefore, modifying the polarization of resident and recruited macrophage/Kupffer cells is expected to lead to new therapeutic strategies in NAFLD. Oxidative stress is also pivotal for the progression of NASH, which has generated interest in carotenoids as potent micronutrient antioxidants in the treatment of NAFLD. In addition to their antioxidative function, carotenoids regulate macrophage/Kupffer cell polarization and thereby prevent NASH progression. In this review, we summarize the molecular mechanisms involved in the pathogenesis of NAFLD, including macrophage/Kupffer cell polarization, and disturbed hepatic function in NAFLD. We also discuss dietary antioxidants, such as β-cryptoxanthin and astaxanthin, that may be effective in the prevention or treatment of NAFLD.
                Bookmark

                Author and article information

                Contributors
                drtingchen@gmail.com
                kobe31815@gmail.com
                lyh21@ulive.pccu.edu.tw
                ylhuang@nricm.edu.tw
                jane@mail.nd.nthu.edu.tw
                ycliang@tmu.edu.tw
                hk.liu@nricm.edu.tw
                chengh@ym.edu.tw
                Journal
                BMC Complement Altern Med
                BMC Complement Altern Med
                BMC Complementary and Alternative Medicine
                BioMed Central (London )
                1472-6882
                13 December 2019
                13 December 2019
                2019
                : 19
                : 368
                Affiliations
                [1 ]ISNI 0000 0000 9337 0481, GRID grid.412896.0, Ph.D. Program in Medical Biotechnology, College of Medical Science and Technology, , Taipei Medical University, ; Taipei, 11001 Taiwan
                [2 ]ISNI 0000 0001 0425 5914, GRID grid.260770.4, Department of Biotechnology and Laboratory Science in Medicine, , National Yang-Ming University, ; No. 155, Sec. 2, Linong St., Beitou District, Taipei, 11221 Taiwan
                [3 ]ISNI 0000 0001 2225 1407, GRID grid.411531.3, Department of Chemistry, , Chinese Culture University, ; Taipei, 11114 Taiwan
                [4 ]ISNI 0000 0001 0357 4948, GRID grid.419746.9, National Research Institute of Chinese Medicine, Ministry of Health and Welfare, ; Taipei, 11221 Taiwan
                [5 ]GRID grid.418428.3, Department of Cosmetic Science, , Chang Gung University of Science and Technology, ; Taoyuan, Taiwan
                [6 ]ISNI 0000 0004 0532 0580, GRID grid.38348.34, Department of Applied Science, , National Tsing Hua University, ; Hsinchu, 30014 Taiwan
                [7 ]ISNI 0000 0000 9337 0481, GRID grid.412896.0, School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, , Taipei Medical University, ; Taipei, 11001 Taiwan
                [8 ]ISNI 0000 0000 9337 0481, GRID grid.412896.0, Ph.D. Program in Clinical Drug Development of Chinese Herbal Medicine, , Taipei Medical University, ; Taipei, 11001 Taiwan
                [9 ]Department of Earth and Life Sciences, University of Taipei, Taipei, 11153 Taiwan
                Author information
                http://orcid.org/0000-0001-8220-1815
                Article
                2782
                10.1186/s12906-019-2782-3
                6911300
                31836013
                e36efffd-e93e-42aa-af88-6b03f9aec7bd
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 11 September 2019
                : 29 November 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100004663, Ministry of Science and Technology, Taiwan;
                Award ID: MOST 104-2320-B-077-003-
                Award ID: MOST 106-2320-B-010-038-
                Award Recipient :
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2019

                Complementary & Alternative medicine
                helminthostachys zeylanica,hepatic steatosis,insulin resistance,obesity

                Comments

                Comment on this article