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      Antiobesity Effects of Ginsenoside Rg1 on 3T3-L1 Preadipocytes and High Fat Diet-Induced Obese Mice Mediated by AMPK

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          Abstract

          Ginsenosides Rg1 is one of the major pharmacologically active saponins in ginseng, which as an antioxidant reduces oxidative damage in the liver and can also be used to prevent cardiovascular diseases and diabetes. However, there is no research targeting the effect of lipid metabolism in high-fat diet (HFD)-induced mice. In this study, we evaluated the anti-obesity effects of Rg1 in 3T3-L1 adipocyte cells and HFD-induced obese C57BL/6J mice. Administration of Rg1 to HFD-induced obese mice significantly decreased body weight, total cholesterol, and total triglyceride levels. In addition to effects in 3T3-L1 cells, Rg1 reduced the accumulation of lipid droplets in a dose-dependent manner. Furthermore, Rg1 exhibits an anti-adipogenic effect via regulation of the expression of the transcriptional factors and lipid metabolism-related genes in vivo and in vitro. We observed that Rg1 administration significantly increased the phosphorylation level of AMP-activated protein kinase (AMPK) in both epididymal white adipose tissue and 3T3-L1 cells. These results indicated that Rg1 works both in an anti-adipogenic and anti-obesity manner through inducing AMPK activation, inhibiting lipogenesis, and decreasing intracellular lipid content, adipocyte size, and adipose weight.

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          Adipocytes as regulators of energy balance and glucose homeostasis.

          Adipocytes have been studied with increasing intensity as a result of the emergence of obesity as a serious public health problem and the realization that adipose tissue serves as an integrator of various physiological pathways. In particular, their role in calorie storage makes adipocytes well suited to the regulation of energy balance. Adipose tissue also serves as a crucial integrator of glucose homeostasis. Knowledge of adipocyte biology is therefore crucial for understanding the pathophysiological basis of obesity and metabolic diseases such as type 2 diabetes. Furthermore, the rational manipulation of adipose physiology is a promising avenue for therapy of these conditions.
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            The cell biology of fat expansion

            Adipose tissue is a complex, multicellular organ that profoundly influences the function of nearly all other organ systems through its diverse metabolite and adipokine secretome. Adipocytes are the primary cell type of adipose tissue and play a key role in maintaining energy homeostasis. The efficiency with which adipose tissue responds to whole-body energetic demands reflects the ability of adipocytes to adapt to an altered nutrient environment, and has profound systemic implications. Deciphering adipocyte cell biology is an important component of understanding how the aberrant physiology of expanding adipose tissue contributes to the metabolic dysregulation associated with obesity.
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              Adipose tissue regulates insulin sensitivity: role of adipogenesis, de novo lipogenesis and novel lipids.

              Obesity, the major cause of the current global epidemic of type 2 diabetes (T2D), induces insulin resistance in peripheral insulin target tissues. Several mechanisms have been identified related to cross-talk between adipose tissue, skeletal muscle and liver. These mechanisms involve both increased free fatty acid release and altered secretion of adipokines from adipose tissue. A major determinant of metabolic health is the ability of subcutaneous adipose tissue (SAT) to store excess fat rather than allowing it to accumulate in ectopic depots including liver (i.e. in nonalcoholic fatty liver disease), muscle and heart, or in epicardial/pericardial and visceral fat depots which promote the metabolic complications of obesity. The ability to recruit and differentiate precursor cells into adipose cells (adipogenesis) in SAT is under genetic regulation and is reduced in high-risk individuals who have first-degree relatives with T2D. Early recruitment of new adipose cells is dependent on the cross-talk between canonical WNT and BMP4 signalling; WNT enhances their undifferentiated and proliferative state whereas BMP4 induces their commitment to the adipogenic lineage. Dysregulation of these signalling pathways is associated with impaired adipogenesis and impaired ability to respond to the need to store excess lipids in SAT. This leads to hypertrophic, dysfunctional and insulin-resistant adipose cells with a reduced content of GLUT4, the major insulin-regulated glucose transporter, which in turn reduces adipose tissue glucose uptake and de novo lipogenesis. We recently identified that reduced GLUT4 and lipogenesis in adipocytes impairs the synthesis of a novel family of lipids secreted by adipose tissue (and potentially other tissues), branched fatty acid esters of hydroxy fatty acids (FAHFAs). FAHFAs have beneficial metabolic effects, including enhancing insulin-stimulated glucose transport and glucose-stimulated GLP1 and insulin secretion, as well as powerful anti-inflammatory effects. FAHFA levels are reduced in subcutaneous adipose tissue in insulin-resistant individuals, and this novel family of lipids may become of future therapeutic use.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                27 June 2018
                July 2018
                : 10
                : 7
                : 830
                Affiliations
                [1 ]College of Life Science, Jilin Agricultural University, Changchun, Jilin 130118, China; liuhuimin@ 123456jlau.edu.cn (H.L.); wangjing11151204@ 123456163.com (J.W.)
                [2 ]National Engineering Laboratory for Wheat and Corn Deep Processing, Changchun, Jilin 130118, China; liumh@ 123456jlau.edu.cn (M.L.); sanabily67@ 123456gmail.com (S.Y.); zhengmzhu@ 123456163.com (M.Z.); dan1980623@ 123456163.com (D.C.)
                [3 ]College of Food Science and Engineering, Jilin Agricultural University, Changchun, Jilin 130118, China
                [4 ]Chinese Medicine Science Academy of Jilin Province, Changchun, Jilin 130118, China; fixiov5815@ 123456126.com
                Author notes
                [* ]Correspondence: liujs1007@ 123456vip.sina.com ; Tel.: +86-431-8453-2886
                Author information
                https://orcid.org/0000-0002-2265-2961
                Article
                nutrients-10-00830
                10.3390/nu10070830
                6073290
                29954059
                bc3ee4d7-bff9-4191-9476-97dcafc4ba35
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 16 May 2018
                : 21 June 2018
                Categories
                Article

                Nutrition & Dietetics
                ginsenoside rg1,obesity,adipogenesis,lipogenesis,lipolysis,ampk
                Nutrition & Dietetics
                ginsenoside rg1, obesity, adipogenesis, lipogenesis, lipolysis, ampk

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