Exenatide improves hepatic steatosis by enhancing lipid use in adipose tissue in nondiabetic rats

Kosuke Tanaka, Yuko Masaki, Masatake Tanaka, Masayuki Miyazaki, Munechika Enjoji, Makoto Nakamuta, Masaki Kato, Masatoshi Nomura, Toyoshi Inoguchi, Kazuhiro Kotoh, Ryoichi Takayanagi

研究成果: ジャーナルへの寄稿記事

13 引用 (Scopus)

抄録

AIM: To investigate the metabolic changes in skeletal muscle and/or adipose tissue in glucagon-like peptide- 1-induced improvement of nonalcoholic fatty liver disease (NAFLD). METHODS: Male Wistar rats were fed either a control diet (control group) or a high-fat diet (HFD). After 4 wk, the HFD-fed rats were subdivided into two groups; one group was injected with exenatide [HFD-Ex(+) group] and the other with saline [HFD-Ex(-) group] every day for 12 wk. The control group received saline and were fed a control diet. Changes in weight gain, energy intake, and oxygen consumption were analyzed. Glucose tolerance tests were performed after 8 wk of treatment. Histological assessments were performed in liver and adipose tissue. RNA expression levels of lipid metabolism related genes were evaluated in liver, skeletal muscle, and adipose tissue. RESULTS: Exenatide attenuated weight gain [HFDEx(-) vs HFD-Ex(+)] and reduced energy intake, which was accompanied by an increase in oxygen consumption and a decrease in the respiratory exchange ratio [HFD-Ex(-) vs HFD-Ex(+)]. However, exenatide did not affect glucose tolerance. Exenatide reduced lipid content in the liver and adipose tissue. Exenatide did not affect the expression of lipid metabolism-related genes in the liver or skeletal muscle. In adipose tissue, exenatide significantly upregulated lipolytic genes, including hormone-sensitive lipase, carnitine palmitoyltransferase- 1, long-chain acyl-CoA dehydrogenase, and acyl-CoA oxidase 1 [HFD-Ex(-) vs HFD-Ex(+)]. Exenatide also upregulated catalase and superoxide dismutase 2 [HFD-Ex(-) vs HFD-Ex(+)]. CONCLUSION: In addition to reducing appetite, enhanced lipid use by exenatide in adipose tissue may reduce hepatic lipid content in NAFLD, most likely by decreasing lipid influx into the liver.

元の言語英語
ページ(範囲)2653-2663
ページ数11
ジャーナルWorld Journal of Gastroenterology
20
発行部数10
DOI
出版物ステータス出版済み - 3 14 2014

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High Fat Diet
Adipose Tissue
Lipids
Liver
Skeletal Muscle
Energy Intake
Lipid Metabolism
Oxygen Consumption
Weight Gain
exenatide
Long-Chain Acyl-CoA Dehydrogenase
Acyl-CoA Oxidase
Genes
Diet
Sterol Esterase
Carnitine O-Palmitoyltransferase
Muscles
Control Groups
Glucagon-Like Peptide 1
Appetite

All Science Journal Classification (ASJC) codes

  • Gastroenterology

これを引用

Exenatide improves hepatic steatosis by enhancing lipid use in adipose tissue in nondiabetic rats. / Tanaka, Kosuke; Masaki, Yuko; Tanaka, Masatake; Miyazaki, Masayuki; Enjoji, Munechika; Nakamuta, Makoto; Kato, Masaki; Nomura, Masatoshi; Inoguchi, Toyoshi; Kotoh, Kazuhiro; Takayanagi, Ryoichi.

:: World Journal of Gastroenterology, 巻 20, 番号 10, 14.03.2014, p. 2653-2663.

研究成果: ジャーナルへの寄稿記事

Tanaka, K, Masaki, Y, Tanaka, M, Miyazaki, M, Enjoji, M, Nakamuta, M, Kato, M, Nomura, M, Inoguchi, T, Kotoh, K & Takayanagi, R 2014, 'Exenatide improves hepatic steatosis by enhancing lipid use in adipose tissue in nondiabetic rats', World Journal of Gastroenterology, 巻. 20, 番号 10, pp. 2653-2663. https://doi.org/10.3748/wjg.v20.i10.2653
Tanaka, Kosuke ; Masaki, Yuko ; Tanaka, Masatake ; Miyazaki, Masayuki ; Enjoji, Munechika ; Nakamuta, Makoto ; Kato, Masaki ; Nomura, Masatoshi ; Inoguchi, Toyoshi ; Kotoh, Kazuhiro ; Takayanagi, Ryoichi. / Exenatide improves hepatic steatosis by enhancing lipid use in adipose tissue in nondiabetic rats. :: World Journal of Gastroenterology. 2014 ; 巻 20, 番号 10. pp. 2653-2663.
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abstract = "AIM: To investigate the metabolic changes in skeletal muscle and/or adipose tissue in glucagon-like peptide- 1-induced improvement of nonalcoholic fatty liver disease (NAFLD). METHODS: Male Wistar rats were fed either a control diet (control group) or a high-fat diet (HFD). After 4 wk, the HFD-fed rats were subdivided into two groups; one group was injected with exenatide [HFD-Ex(+) group] and the other with saline [HFD-Ex(-) group] every day for 12 wk. The control group received saline and were fed a control diet. Changes in weight gain, energy intake, and oxygen consumption were analyzed. Glucose tolerance tests were performed after 8 wk of treatment. Histological assessments were performed in liver and adipose tissue. RNA expression levels of lipid metabolism related genes were evaluated in liver, skeletal muscle, and adipose tissue. RESULTS: Exenatide attenuated weight gain [HFDEx(-) vs HFD-Ex(+)] and reduced energy intake, which was accompanied by an increase in oxygen consumption and a decrease in the respiratory exchange ratio [HFD-Ex(-) vs HFD-Ex(+)]. However, exenatide did not affect glucose tolerance. Exenatide reduced lipid content in the liver and adipose tissue. Exenatide did not affect the expression of lipid metabolism-related genes in the liver or skeletal muscle. In adipose tissue, exenatide significantly upregulated lipolytic genes, including hormone-sensitive lipase, carnitine palmitoyltransferase- 1, long-chain acyl-CoA dehydrogenase, and acyl-CoA oxidase 1 [HFD-Ex(-) vs HFD-Ex(+)]. Exenatide also upregulated catalase and superoxide dismutase 2 [HFD-Ex(-) vs HFD-Ex(+)]. CONCLUSION: In addition to reducing appetite, enhanced lipid use by exenatide in adipose tissue may reduce hepatic lipid content in NAFLD, most likely by decreasing lipid influx into the liver.",
author = "Kosuke Tanaka and Yuko Masaki and Masatake Tanaka and Masayuki Miyazaki and Munechika Enjoji and Makoto Nakamuta and Masaki Kato and Masatoshi Nomura and Toyoshi Inoguchi and Kazuhiro Kotoh and Ryoichi Takayanagi",
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T1 - Exenatide improves hepatic steatosis by enhancing lipid use in adipose tissue in nondiabetic rats

AU - Tanaka, Kosuke

AU - Masaki, Yuko

AU - Tanaka, Masatake

AU - Miyazaki, Masayuki

AU - Enjoji, Munechika

AU - Nakamuta, Makoto

AU - Kato, Masaki

AU - Nomura, Masatoshi

AU - Inoguchi, Toyoshi

AU - Kotoh, Kazuhiro

AU - Takayanagi, Ryoichi

PY - 2014/3/14

Y1 - 2014/3/14

N2 - AIM: To investigate the metabolic changes in skeletal muscle and/or adipose tissue in glucagon-like peptide- 1-induced improvement of nonalcoholic fatty liver disease (NAFLD). METHODS: Male Wistar rats were fed either a control diet (control group) or a high-fat diet (HFD). After 4 wk, the HFD-fed rats were subdivided into two groups; one group was injected with exenatide [HFD-Ex(+) group] and the other with saline [HFD-Ex(-) group] every day for 12 wk. The control group received saline and were fed a control diet. Changes in weight gain, energy intake, and oxygen consumption were analyzed. Glucose tolerance tests were performed after 8 wk of treatment. Histological assessments were performed in liver and adipose tissue. RNA expression levels of lipid metabolism related genes were evaluated in liver, skeletal muscle, and adipose tissue. RESULTS: Exenatide attenuated weight gain [HFDEx(-) vs HFD-Ex(+)] and reduced energy intake, which was accompanied by an increase in oxygen consumption and a decrease in the respiratory exchange ratio [HFD-Ex(-) vs HFD-Ex(+)]. However, exenatide did not affect glucose tolerance. Exenatide reduced lipid content in the liver and adipose tissue. Exenatide did not affect the expression of lipid metabolism-related genes in the liver or skeletal muscle. In adipose tissue, exenatide significantly upregulated lipolytic genes, including hormone-sensitive lipase, carnitine palmitoyltransferase- 1, long-chain acyl-CoA dehydrogenase, and acyl-CoA oxidase 1 [HFD-Ex(-) vs HFD-Ex(+)]. Exenatide also upregulated catalase and superoxide dismutase 2 [HFD-Ex(-) vs HFD-Ex(+)]. CONCLUSION: In addition to reducing appetite, enhanced lipid use by exenatide in adipose tissue may reduce hepatic lipid content in NAFLD, most likely by decreasing lipid influx into the liver.

AB - AIM: To investigate the metabolic changes in skeletal muscle and/or adipose tissue in glucagon-like peptide- 1-induced improvement of nonalcoholic fatty liver disease (NAFLD). METHODS: Male Wistar rats were fed either a control diet (control group) or a high-fat diet (HFD). After 4 wk, the HFD-fed rats were subdivided into two groups; one group was injected with exenatide [HFD-Ex(+) group] and the other with saline [HFD-Ex(-) group] every day for 12 wk. The control group received saline and were fed a control diet. Changes in weight gain, energy intake, and oxygen consumption were analyzed. Glucose tolerance tests were performed after 8 wk of treatment. Histological assessments were performed in liver and adipose tissue. RNA expression levels of lipid metabolism related genes were evaluated in liver, skeletal muscle, and adipose tissue. RESULTS: Exenatide attenuated weight gain [HFDEx(-) vs HFD-Ex(+)] and reduced energy intake, which was accompanied by an increase in oxygen consumption and a decrease in the respiratory exchange ratio [HFD-Ex(-) vs HFD-Ex(+)]. However, exenatide did not affect glucose tolerance. Exenatide reduced lipid content in the liver and adipose tissue. Exenatide did not affect the expression of lipid metabolism-related genes in the liver or skeletal muscle. In adipose tissue, exenatide significantly upregulated lipolytic genes, including hormone-sensitive lipase, carnitine palmitoyltransferase- 1, long-chain acyl-CoA dehydrogenase, and acyl-CoA oxidase 1 [HFD-Ex(-) vs HFD-Ex(+)]. Exenatide also upregulated catalase and superoxide dismutase 2 [HFD-Ex(-) vs HFD-Ex(+)]. CONCLUSION: In addition to reducing appetite, enhanced lipid use by exenatide in adipose tissue may reduce hepatic lipid content in NAFLD, most likely by decreasing lipid influx into the liver.

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