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6 "Fatty acid oxidation"
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Original Article
Obesity and Metabolic Syndrome
Statins Increase Mitochondrial and Peroxisomal Fatty Acid Oxidation in the Liver and Prevent Non-Alcoholic Steatohepatitis in Mice
Han-Sol Park, Jung Eun Jang, Myoung Seok Ko, Sung Hoon Woo, Bum Joong Kim, Hyun Sik Kim, Hye Sun Park, In-Sun Park, Eun Hee Koh, Ki-Up Lee
Diabetes Metab J. 2016;40(5):376-385.   Published online April 5, 2016
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AbstractAbstract PDFPubReader   

Non-alcoholic fatty liver disease is the most common form of chronic liver disease in industrialized countries. Recent studies have highlighted the association between peroxisomal dysfunction and hepatic steatosis. Peroxisomes are intracellular organelles that contribute to several crucial metabolic processes, such as facilitation of mitochondrial fatty acid oxidation (FAO) and removal of reactive oxygen species through catalase or plasmalogen synthesis. Statins are known to prevent hepatic steatosis and non-alcoholic steatohepatitis (NASH), but underlying mechanisms of this prevention are largely unknown.


Seven-week-old C57BL/6J mice were given normal chow or a methionine- and choline-deficient diet (MCDD) with or without various statins, fluvastatin, pravastatin, simvastatin, atorvastatin, and rosuvastatin (15 mg/kg/day), for 6 weeks. Histological lesions were analyzed by grading and staging systems of NASH. We also measured mitochondrial and peroxisomal FAO in the liver.


Statin treatment prevented the development of MCDD-induced NASH. Both steatosis and inflammation or fibrosis grades were significantly improved by statins compared with MCDD-fed mice. Gene expression levels of peroxisomal proliferator-activated receptor α (PPARα) were decreased by MCDD and recovered by statin treatment. MCDD-induced suppression of mitochondrial and peroxisomal FAO was restored by statins. Each statin's effect on increasing FAO and improving NASH was independent on its effect of decreasing cholesterol levels.


Statins prevented NASH and increased mitochondrial and peroxisomal FAO via induction of PPARα. The ability to increase hepatic FAO is likely the major determinant of NASH prevention by statins. Improvement of peroxisomal function by statins may contribute to the prevention of NASH.


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GLP-1 Receptor Agonist and Non-Alcoholic Fatty Liver Disease
Jinmi Lee, Seok-Woo Hong, Eun-Jung Rhee, Won-Young Lee
Diabetes Metab J. 2012;36(4):262-267.   Published online August 20, 2012
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AbstractAbstract PDFPubReader   

Non-alcoholic fatty liver disease (NAFLD), one of the most common liver diseases, is caused by the disruption of hepatic lipid homeostasis. It is associated with insulin resistance as seen in type 2 diabetes mellitus. Glucagon-like peptide-1 (GLP-1) is an incretin that increases insulin sensitivity and aids glucose metabolism. In recent in vivo and in vitro studies, GLP-1 presents a novel therapeutic approach against NAFLD by increasing fatty acid oxidation, decreasing lipogenesis, and improving hepatic glucose metabolism. In this report, we provide an overview of the role and mechanism of GLP-1 in relieving NAFLD.


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Original Articles
Effects of Lovastatin on Free Fatty Acid Oxidation in Cultured L6 Rat Skeletal Muscle Cells.
Dong Lim Kim, Kee Ho Song, Hae Rim Kim, Suk Kyeong Kim
Korean Diabetes J. 2007;31(3):230-235.   Published online May 1, 2007
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AbstractAbstract PDF
Recent clinical studies suggest that statins improve insulin resistance and glucose metabolism in patients with metabolic syndrome and type 2 diabetes. To evaluate the possible mechanism of this action, we measured free fatty acid oxidation in cultured L6 rat skeletal muscle cell line. METHODS: Cultured L6 myotubes were treated with or without lovastatin (1, 5, 20 micrometer) for 24 hours or 48 hours and palmitate oxidation was measured. We also measured protein concentration of the cells. RESULTS: Lovastain increased palmitate oxidation in dose and time dependent manner in L6 myotubes (24 hr; 1 micrometer 119.2 +/- 11.9% of control, 5 micrometer 140.9 +/- 8.1%, 20 micrometer 150 +/- 5%, P = 0.05 vs control, respectively, 48 hr 1 micrometer 120.9 +/- 14.5%, 5 micrometer 176.6 +/- 28.2%, 20 micrometer 196.0 +/- 19.9%, P < 0.01 vs control, respectively). However, lovastatin decreased total cellular protein (24 hr: 1 micrometer 89.2 +/- 6.1% of control, 5 micrometer 79.3 +/- 7.6%, 20 micrometer 65.4 +/- 4.2%, P = 0.05 vs control, respectively, 48 hr: 1 micrometer 81.7 +/- 5.1%, 5 micrometer 58.6 +/- 11.9%, 20 micrometer 48.1 +/- 6.9%, P < 0.01 vs control, respectively). CONCLUSION: Lovastatin increased skeletal muscle free fatty acid oxidation in L6 rat skeletal muscle cells. This would be one of the mechanisms which lovastatin improves insulin resistance.


Citations to this article as recorded by  
  • Characterization and Mechanisms of Action of Avocado Extract Enriched in Mannoheptulose as a Candidate Calorie Restriction Mimetic
    Donald K. Ingram, Paul J. Pistell, Zhong Q. Wang, Yongmei Yu, Stefan Massimino, Gary M. Davenport, Michael Hayek, George S. Roth
    Journal of Agricultural and Food Chemistry.2021; 69(26): 7367.     CrossRef
Effects of PPAR-alpha and-gamma Agonists on Fatty Acid Metabolism of Muscle Cells in Hyperlipidemic and Hyperglycemic Conditions.
Yong jik Lee, Zheng Shan Zhao, Soo Kyung Kim, Hae Jin Kim, Wan Sub Shim, Chul Woo Ahn, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2006;30(5):324-335.   Published online September 1, 2006
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AbstractAbstract PDF
Studies for the regulation of fatty acid metabolism are deficient relatively in skeletal muscle and heart. The investigations in pathological conditions for malonyl-CoA decarboxylase (MCD) and for the relation of MCD and PPAR-alpha.-gamma agonists are insufficient in particular. METHODS: In the current study, fully differentiated H9c2 muscle cells were exposed to pathological conditions such as hyperlipidemic (0.1 mM Palmitate) and hyperglycemic (16.5 mM Glucose) condition with 5 uM PPAR-gamma agonist (rosiglitazone) and 10 uM PPAR-alpha agonist (WY14,643) and then experiments such as MCD activity assay, MCD real-time RT-PCR, MCD reporter gene assay, MCD Western blotting, PPAR-alpha Western blotting, and palmitate oxidation test were carried out. RESULTS: Only PPAR-alpha agonist increased MCD activity. In the result of real-time RT-PCR, both PPAR-alpha and PPAR-gamma agonists elevated MCD mRNA expression in hyperlipidemic condition. MCD protein expression was decreased in hyperlipidemic condition, however, increased in rosiglitazone, or WY14,643 treated conditions. Rosiglitazone, and WY14,643 treated groups showed incresed MCD protein expression in hyperglycemic condition. Hyperlipidemic control group and PPAR-alpha.-gamma agonists treated groups presented about 3.8 times more increased palmitate oxidation level than normolipidemic control group in hyperlipidemic condition. PPAR-alpha agonist treated group showed 49% more increased palmitate oxidation rate than hyperlipidemic control group in primary cultured rat skeletal muscle cells. The amount of palmitate oxidation from differentiated H9c2 muscle cells that had overexpressed PPAR-alpha structural genes was more increased than control group. CONCLUSION: This study suggests that PPAR-alpha agonist ameliorates the defects induced by hyperlipidemic condition through the regulation of MCD. In summary, a closely reciprocal relation among PPAR-alpha agonist, MCD, and fatty acid oxidation existed distinctly in hyperlipidemic condition, but not in hyperglycemic condition.


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    Yun Jung Lee, Hye Yoom Kim, Jung Joo Yoon, So Min Lee, You Mee Ahn, Joung Hyun Kho, Min Chul Kho, Ho Sub Lee, Kyung Min Choi, Dae Gill Kang
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    Dae-Jung Kim, Jeong-Mi Kim, Tae-Hyuk Kim, Jong-Mi Baek, Hyun-Sook Kim, Myeon Choe
    Journal of the Korean Society of Food Science and Nutrition.2010; 39(9): 1257.     CrossRef
Increase in Fatty Acid Oxidation by AICAR: the Role of p38 MAPK.
Woo Je Lee, Jin Yob Kim, Sung Jin Bae, Eun Hee Koh, Sung Min Han, Hye Sun Park, Hyun Sik Kim, Min Seon Kim, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2005;29(1):15-21.   Published online January 1, 2005
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AbstractAbstract PDF
AMPK is an enzyme that increases glucose transport and fatty acid oxidation in skeletal muscle. The activation of AMPK stimulates fatty acid oxidation by decreasing the acetyl CoA carboxylase (ACC) activity and the concentration of malonyl-CoA. However, a recent study has reported a dissociation of AMPK activity and ACC phosphorylation in skeletal muscle during periods of prolonged exercise. This suggested that there is an additional mechanism for AMPK-induced fatty acid oxidation in skeletal muscle. METHODS: Plamitate oxidation was measured via the generation of [3H]-water generation from 9,10[3H]-palmitate after treating various concentrations of AICAR on the C2C12 mouse skeletal muscle cell line. Western analysis was used to test for the possible activation of p38 MAPK by AICAR. Involvement of p38 MAPK in the AICAR-induced increase in fatty acid oxidation was tested for by using SB203580, a p38 MAPK inhibitor. RESULTS: C2C12 cell treated with AICAR exhibited a dose-dependent increase in fatty acid oxidation compared to the cells that were not treated with AICAR. Western blot analysis revealed that phosphorylation of p38 MAPK was increased 2.5 folds after AICAR treatment. The increase of fatty acid oxidation with AICAR treatment was significantly inhibited by a treatment of SB203580; this indicated the involvement of p38 MAPK on the AICAR-induced increase in fatty acid oxidation. CONCLUSION: AICAR stimulated the fatty acid oxidation by activating p38 MAPK. This is a novel pathway by which AMPK activation in skeletal muscle increases the fatty acid oxidation
AMPK Activator AICAR Inhibits Hepatic Gluconeogenesis and Fatty Acid Oxidation.
Jin Yob Kim, Eun Hee Koh, Woo Je Lee, Seong Min Han, Ji Young Youn, Hye Sun Park, Hyun Sik Kim, Min Seon Kim, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2005;29(1):6-14.   Published online January 1, 2005
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AbstractAbstract PDF
Recent studies have demonstrated that adiponectin and metformin activate AMPK in the liver, and adiponectin and metformin stimulate fatty acid oxidation while inhibiting glucose production in liver. These results are in contrast to previous studies that have demonstrated that increased fatty acid oxidation in the liver is associated with increased gluconeogenesis. The present study was undertaken to reinvestigate the effects of AMPK activation by AICAR on hepatic fatty acid oxidation and gluconeogenesis. METHODS: HePG2 cells were treated with various concentrations of AICAR, and then the fatty acid oxidation and gluconeogenesis of the cells were determined. To investigate the in vivo effect of AICAR, Sprague-Dawely rats were infused with AICAR (bolus, 40 mg/g; constant, 7.5 mg/g/min-1) for 90min. RESULTS: Incubation of the HePG2 cells with higher concentrations (=1 mM) of AICAR increased fatty acid oxidation and gluconeogenesis. On the other hand, incubation of HePG2 cells with lower concentrations (0.05 and 0.1 mM) of AICAR decreased fatty acid oxidation and gluconeogenesis. Consistent with this in vitro data, the intravenous administration of AICAR to rats lowered their plasma glucose concentration and inhibited hepatic gluconeogenesis. Fatty acid oxidation in the liver tissue was significantly decreased by the administration of AICAR. CONCLUSION: The present study has demonstrated that AICAR decreased gluconeo-genesis in the liver. In contrast to previous studies, AICAR profoundly decreased hepatic fatty acid oxidation in rats and also in cultured hepatocytes

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