scholarly journals Gomisin N from Schisandra chinensis Ameliorates Lipid Accumulation and Induces a Brown Fat-Like Phenotype through AMP-Activated Protein Kinase in 3T3-L1 Adipocytes

2020 ◽  
Vol 21 (6) ◽  
pp. 2153
Author(s):  
Kippeum Lee ◽  
Yeon-Joo Lee ◽  
Kui-Jin Kim ◽  
Sungwoo Chei ◽  
Heegu Jin ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Lipid Accumulation ◽  
Uncoupling Protein ◽  
Brown Adipocyte ◽  
Acid Oxidation ◽  
Schisandra Chinensis ◽  
White Adipocytes ◽  
Gomisin N ◽  
Amp Activated Protein Kinase

Obesity results from an imbalance between energy intake and energy expenditure, in which excess fat is stored as triglycerides (TGs) in white adipocytes. Recent studies have explored the anti-obesity effects of certain edible phytochemicals, which suppress TG accumulation and stimulate a brown adipocyte-like phenotype in white adipocytes. Gomisin N (GN) is an important bioactive component of Schisandra chinensis, a woody plant endemic to Asia. GN has antioxidant, anti-inflammatory and hepatoprotective effects in vivo and in vitro. However, the anti-obesity effects of GN in lipid metabolism and adipocyte browning have not yet been investigated. In the present study, we aimed to determine whether GN suppresses lipid accumulation and regulates energy metabolism, potentially via AMP-activated protein kinase (AMPK), in 3T3-L1 adipocytes. Our findings demonstrate that GN inhibited adipogenesis and lipogenesis in adipocyte differentiation. Also, GN not only increased the expression of thermogenic factors, including uncoupling protein 1 (UCP1), but also enhanced fatty acid oxidation (FAO) in 3T3-L1 cells. Therefore, GN may have a therapeutic benefit as a promising natural agent to combat obesity.

scholarly journals Interleukin-6 Increases Insulin-Stimulated Glucose Disposal in Humans and Glucose Uptake and Fatty Acid Oxidation In Vitro via AMP-Activated Protein Kinase

Diabetes ◽  
2006 ◽  
Vol 55 (10) ◽  
pp. 2688-2697 ◽  
Author(s):  
A. L. Carey ◽  
G. R. Steinberg ◽  
S. L. Macaulay ◽  
W. G. Thomas ◽  
A. G. Holmes ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Fatty Acid Oxidation ◽  
Interleukin 6 ◽  
Glucose Disposal ◽  
Acid Oxidation ◽  
Amp Activated Protein Kinase

scholarly journals Metformin induces oxidative stress in white adipocytes and raises uncoupling protein 2 levels

2008 ◽  
Vol 199 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Andrea Anedda ◽  
Eduardo Rial ◽  
M Mar González-Barroso
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
Protein Levels ◽  
White Adipocytes ◽  
Epididymal White Adipose Tissue ◽  
Amp Activated Protein Kinase

Metformin is a drug widely used to treat type 2 diabetes. It enhances insulin sensitivity by improving glucose utilization in tissues like liver or muscle. Metformin inhibits respiration, and the decrease in cellular energy activates the AMP-activated protein kinase that in turn switches on catabolic pathways. Moreover, metformin increases lipolysis and β-oxidation in white adipose tissue, thereby reducing the triglyceride stores. The uncoupling proteins (UCPs) are transporters that lower the efficiency of mitochondrial oxidative phosphorylation. UCP2 is thought to protect against oxidative stress although, alternatively, it could play an energy dissipation role. The aim of this work was to analyse the involvement of UCP2 on the effects of metformin in white adipocytes. We studied the effect of this drug in differentiating 3T3-L1 adipocytes and found that metformin causes oxidative stress since it increases the levels of reactive oxygen species (ROS) and lowers the aconitase activity. Variations in UCP2 protein levels parallel those of ROS. Metformin also increases lipolysis in these cells although only when the levels of ROS and UCP2 have decreased. Hence, UCP2 does not appear to be needed to facilitate fatty acid oxidation. Furthermore, treatment of C57BL/6 mice with metformin also augmented the levels of UCP2 in epididymal white adipose tissue. We conclude that metformin treatment leads to the overexpression of UCP2 in adipocytes to minimize the oxidative stress that is probably due to the inhibition of respiration caused by the drug.

scholarly journals Docosahexaenoic Acid Lessens Hepatic Lipid Accumulation and Inflammation via the AMP-Activated Protein Kinase and Endoplasmic Reticulum Stress Signaling Pathway in Grass Carp (Ctenopharyngodon Idella)

2021 ◽  
Author(s):  
Xiaocheng Huang ◽  
Jian Sun ◽  
Chenchen Bian ◽  
Shanghong Ji ◽  
Hong ji
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Kinase ◽  
Hepatic Steatosis ◽  
Grass Carp ◽  
Lipid Accumulation ◽  
Ctenopharyngodon Idella ◽  
Hepatic Inflammation ◽  
Amp Activated Protein Kinase

Abstract Background: The liver is the primary organ for frontline immune defense and lipid metabolism. Excessive lipid accumulation in the liver severely affects its metabolic homeostasis and causes metabolic diseases. Docosahexaenoic acid (DHA) is known for its beneficial effects on lipid metabolism and anti-inflammation, but its molecular mechanism remains unknown, especially in fish. In this study, we evaluated the protective effects of DHA on hepatic steatosis of grass carp (Ctenopharyngodon idella) in vivo and in vitro and mainly focused on lipogenesis and inflammation. Grass carp were fed with purified diets supplemented with 0%, 0.5% and 1% DHA for 8 weeks in vivo. Hepatocytes were treated with palmitic acid (PA) (200 μM) with or without DHA (50 or 100 μM) for 24 h in vitro. In addition, Compound C (CC, the inhibitor of AMP-activated protein kinase) was used to examine the mechanism of DHA on hepatic steatosis in vitro.Results: In this study, 1% DHA significantly decreased the liver triglyceride (TG), malondialdehyde (MDA), serum tumor necrosis factor α (TNFα) and nuclear factor kappa B (NFκB) contents. DHA (100 μM) effectively attenuated PA-induced lipid accumulation (P<0.05). Furthermore, DHA significantly inhibited endoplasmic reticulum (ER) stress and stimulated the expression of AMP-activated protein kinase (AMPK) and its downstream factors related to hepatic inflammation and lipogenesis in vivo and in vitro. However, the effects of DHA could be abrogated by CC in vitro.Conclusions: DHA exerted a protective effect on hepatic steatosis by inhibiting ER stress, improving antioxidant ability, relieving hepatic inflammation and inhibiting hepatic lipogenesis in an AMPK-dependent manner. Our findings give a theoretical foundation for further elucidation of the beneficial role of DHA in vertebrates.

Phytol stimulates the browning of white adipocytes through the activation of AMP-activated protein kinase (AMPK) α in mice fed high-fat diet

2018 ◽  
Vol 9 (4) ◽  
pp. 2043-2050 ◽  
Author(s):  
Fenglin Zhang ◽  
Wei Ai ◽  
Xiaoquan Hu ◽  
Yingying Meng ◽  
Cong Yuan ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
High Fat Diet ◽  
High Fat ◽  
White Adipocytes ◽  
Amp Activated Protein Kinase

In vivo and in vitro studies show that phytol stimulates the browning of mice iWAT and formation of brown-like adipocytes in the differentiated 3T3-L1 through the activation of the AMPKα signaling pathway.

scholarly journals Bai-Hu-Jia-Ren-Shen-Tang Decoction Reduces Fatty Liver by Activating AMP-Activated Protein Kinase In Vitro and In Vivo

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Hui-Kang Liu ◽  
Tzu-Min Hung ◽  
Hsiu-Chen Huang ◽  
I-Jung Lee ◽  
Chia-Chuan Chang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Fatty Liver ◽  
Lipid Accumulation ◽  
Serum Triglyceride ◽  
Total Lipid Content ◽  
Lipid Lowering ◽  
Acid Oxidation ◽  
Lowering Effect ◽  
Amp Activated Protein Kinase ◽  
Lipid Lowering Effect

Obesity and associated conditions, such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are currently a worldwide health problem. In Asian traditional medicine, Bai-Hu-Jia-Ren-Shen-Tang (BHJRST) is widely used in diabetes patients to reduce thirst. However, whether it has a therapeutic effect on T2DM or NAFLD is not known. The aim of this study was to examine whether BHJRST had a lipid-lowering effect using a HuS-E/2 cell model of fatty liver induced by palmitate and in a db/db mouse model of dyslipidemia. Incubation of HuS-E/2 cells with palmitate markedly increased lipid accumulation and expression of adipose triglyceride lipase (ATGL), which is involved in lipolysis. BHJRST significantly decreased lipid accumulation and increased ATGL levels and phosphorylation of AMP-activated protein kinase (AMPK) and its primary downstream target, acetyl-CoA carboxylase (ACC), which are involved in fatty acid oxidation. Furthermore, after twice daily oral administration for six weeks, BHJRST significantly reduced hepatic fat accumulation in db/db mice, as demonstrated by increased hepatic AMPK and ACC phosphorylation, reduced serum triglyceride levels, and reduced hepatic total lipid content. The results show that BHJRST has a lipid-lowering effect in the liver that is mediated by activation of the AMPK signaling pathway.

scholarly journals Dietary Silk Peptide Prevents High-Fat Diet-Induced Obesity and Promotes Adipose Browning by Activating AMP-Activated Protein Kinase in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 201 ◽  
Author(s):  
Kippeum Lee ◽  
Heegu Jin ◽  
Sungwoo Chei ◽  
Jeong-Yong Lee ◽  
Hyun-Ji Oh ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
High Fat Diet ◽  
Ex Vivo ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Silk Peptide ◽  
Amp Activated Protein Kinase

Obesity is associated with metabolic syndrome and other chronic diseases, and is caused when the energy intake is greater than the energy expenditure. We aimed to determine the mechanism whereby acid-hydrolyzed silk peptide (SP) prevents high-fat diet-induced obesity, and whether it induces browning and fatty acid oxidation (FAO) in white adipose tissue (WAT), using in vivo and ex vivo approaches. We determined the effects of dietary SP in high-fat diet-fed obese mice. The expression of adipose tissue-specific genes was quantified by western blotting, qRT-PCR, and immunofluorescence analysis. We also investigated whether SP directly induces browning in primarily subcutaneous WAT-derived adipocytes. Our findings demonstrate that SP has a browning effect in WAT by upregulating AMP-activated Protein Kinase (AMPK) phosphorylation and uncoupling protein 1 (UCP1) expression. SP also suppresses adipogenesis and promotes FAO, implying that it may have potential as an anti-obesity drug.

UCP-3 expression in skeletal muscle: effects of exercise, hypoxia, and AMP-activated protein kinase

2000 ◽  
Vol 279 (3) ◽  
pp. E622-E629 ◽  
Author(s):  
Min Zhou ◽  
Bao-Zhen Lin ◽  
Sean Coughlin ◽  
Gino Vallega ◽  
Paul F. Pilch
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Uncoupling Protein ◽  
Fold Increase ◽  
Treadmill Running ◽  
Mitochondrial Transporter ◽  
Edl Muscle ◽  
Amp Activated Protein Kinase ◽  
Carnitine Palmitoyltransferase 1

Uncoupling protein 3 (UCP-3), a member of the mitochondrial transporter superfamily, is expressed primarily in skeletal muscle where it may play a role in altering metabolic function under conditions of fuel depletion caused, for example, by fasting and exercise. Here, we show that treadmill running by rats rapidly (30 min) induces skeletal muscle UCP-3 mRNA expression (sevenfold after 200 min), as do hypoxia and swimming in a comparably rapid and substantial fashion. The expression of the mitochondrial transporters, carnitine palmitoyltransferase 1 and the tricarboxylate carrier, is unaffected under these conditions. Hypoxia and exercise-mediated induction of UCP-3 mRNA result in a corresponding four- to sixfold increase in rat UCP-3 protein. We treated extensor digitorum longus (EDL) muscle with 5′-amino-4-imidazolecarboxamide ribonucleoside (AICAR), a compound that activates AMP-activated protein kinase (AMPK), an enzyme known to be stimulated during exercise and hypoxia. Incubation of rat EDL muscle in vitro for 30 min with 2 mM AICAR causes a threefold increase in UCP-3 mRNA and a 1.5-fold increase of UCP-3 protein compared with untreated muscle. These data are consistent with the notion that activation of AMPK, presumably as a result of fuel depletion, rapidly regulates UCP-3 gene expression.

scholarly journals Resolvin D1 Enhances Necroptotic Cell Clearance Through Promoting Macrophage Fatty Acid Oxidation and Oxidative Phosphorylation

2021 ◽  
Vol 41 (3) ◽  
pp. 1062-1075
Author(s):  
Zeinab Hosseini ◽  
Michael Marinello ◽  
Christa Decker ◽  
Brian E. Sansbury ◽  
Sudeshna Sadhu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Protein Kinase ◽  
Oxidative Phosphorylation ◽  
Fatty Acid Oxidation ◽  
Therapeutic Strategy ◽  
Acid Oxidation ◽  
Resolvin D1 ◽  
Cell Clearance ◽  
Amp Activated Protein Kinase

Objective: Plaque necrosis is a key feature of defective resolution in atherosclerosis. Recent evidence suggests that necroptosis promotes plaque necrosis; therefore, we sought to determine how necroptotic cells (NCs) impact resolution programs in plaques. Approach and Results: To investigate the role(s) of necroptosis in advanced atherosclerosis, we used mice deficient of Mlkl , an effector of necroptosis. Mlkl −/− mice that were injected with a gain-of-function mutant PCSK9 (AAV8-gof-PCSK9) and fed a Western diet for 16 weeks, showed significantly less plaque necrosis, increased fibrous caps and improved efferocytosis compared with AAV8-gof-PCSK9 injected wt controls. Additionally, hypercholesterolemic Mlkl −/− mice had a significant increase in proresolving mediators including resolvin D1 (RvD1) and a decrease in prostanoids including thromboxane in plaques and in vitro. We found that exuberant thromboxane released by NCs impaired the clearance of both apoptotic cells and NCs through disruption of oxidative phosphorylation in macrophages. Moreover, we found that NCs did not readily synthesize RvD1 and that exogenous administration of RvD1 to macrophages rescued NC-induced defective efferocytosis. RvD1 also enhanced the uptake of NCs via the activation of p-AMPK (AMP-activated protein kinase), increased fatty acid oxidation, and enhanced oxidative phosphorylation in macrophages. Conclusions: These results suggest that NCs derange resolution by limiting key SPMs and impairing the efferocytic repertoire of macrophages. Moreover, these findings provide a molecular mechanism for RvD1 in directing proresolving metabolic programs in macrophages and further suggests RvD1 as a potential therapeutic strategy to limit NCs in tissues. Graphic Abstract: A graphic abstract is available for this article.

scholarly journals Expression of Uncoupling Protein 3 and GLUT4 Gene in Skeletal Muscle of Preterm Newborns: Possible Control by AMP-Activated Protein Kinase

2006 ◽  
Vol 60 (5) ◽  
pp. 569-575 ◽  
Author(s):  
Petr Brauner ◽  
Pavel Kopecky ◽  
Pavel Flachs ◽  
Ondrej Kuda ◽  
Jaroslav Vorlicek ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Uncoupling Protein ◽  
Uncoupling Protein 3 ◽  
Amp Activated Protein Kinase ◽  
Preterm Newborns
Sign in / Sign up

Export Citation Format

Share Document