Calebin-A inhibits adipogenesis and hepatic steatosis in high-fat diet-induced obesity via activation of AMPK signaling

Ching Shu Lai, Sih Ning Liao, Mei Ling Tsai, Nagabhushanam Kalyanam, Muhammed Majeed, Anju Majeed, Chi-Tang Ho, Min Hsiung Pan

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Scope: Diet-induced obesity and associated nonalcoholic fatty liver disease have increased and become a major health problem worldwide. This study was conducted to investigate the chemopreventive effects of dietary Calebin-A, a curcuminoid, on differentiation of 3T3-L1 adipocytes and high-fat diet (HFD) induced obesity and hepatic steatosis. Potential mechanisms contributing to these effects were also elucidated. Methods and results: Calebin-A effectively and dose dependently suppressed accumulation of lipid droplets in adipocytes through the suppression of adipogenic specific factor peroxisome proliferator-activated receptor (PPAR) γ and fatty acid synthase and activated acetyl-CoA carboxylase. Dietary Calebin-A effectively decreased weight gain and relative perigonadal, retroperitoneal, and mesenteric fat weight in HFD-fed mice. Furthermore, Calebin-A markedly reduced hepatic steatosis and the serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, total cholesterol, and triacylglycerol. These effects were associated with the downregulation of PPARγ, sterol regulatory element-binding protein-1, and particularly the activation of AMP-activated protein kinase α signaling found in both adipocytes and liver tissues. Conclusion: Taken together, these results demonstrated for the first time that Calebin-A suppressed adipocyte differentiation, prevented HFD-induced obesity, and improved hepatic steatosis, suggesting a novel application for the prevention and treatment of obesity and associated nonalcoholic fatty liver disease.

Original languageEnglish (US)
Pages (from-to)1883-1895
Number of pages13
JournalMolecular Nutrition and Food Research
Volume59
Issue number10
DOIs
StatePublished - Oct 1 2015

Fingerprint

AMP-activated protein kinase
Adipogenesis
AMP-Activated Protein Kinases
fatty liver
High Fat Diet
high fat diet
adipocytes
obesity
Adipocytes
Obesity
Liver
Peroxisome Proliferator-Activated Receptors
Transaminases
Glutamic Acid
Sterol Regulatory Element Binding Protein 1
Acetyl-CoA Carboxylase
Oxaloacetic Acid
Fatty Acid Synthases
acetyl-CoA carboxylase
fatty-acid synthase

All Science Journal Classification (ASJC) codes

  • Food Science
  • Biotechnology

Keywords

  • 3T3-L1 adipocytes
  • AMP-activated protein kinase
  • Adipogenesis
  • Calebin-A
  • High-fat diet

Cite this

Lai, Ching Shu ; Liao, Sih Ning ; Tsai, Mei Ling ; Kalyanam, Nagabhushanam ; Majeed, Muhammed ; Majeed, Anju ; Ho, Chi-Tang ; Pan, Min Hsiung. / Calebin-A inhibits adipogenesis and hepatic steatosis in high-fat diet-induced obesity via activation of AMPK signaling. In: Molecular Nutrition and Food Research. 2015 ; Vol. 59, No. 10. pp. 1883-1895.
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title = "Calebin-A inhibits adipogenesis and hepatic steatosis in high-fat diet-induced obesity via activation of AMPK signaling",
abstract = "Scope: Diet-induced obesity and associated nonalcoholic fatty liver disease have increased and become a major health problem worldwide. This study was conducted to investigate the chemopreventive effects of dietary Calebin-A, a curcuminoid, on differentiation of 3T3-L1 adipocytes and high-fat diet (HFD) induced obesity and hepatic steatosis. Potential mechanisms contributing to these effects were also elucidated. Methods and results: Calebin-A effectively and dose dependently suppressed accumulation of lipid droplets in adipocytes through the suppression of adipogenic specific factor peroxisome proliferator-activated receptor (PPAR) γ and fatty acid synthase and activated acetyl-CoA carboxylase. Dietary Calebin-A effectively decreased weight gain and relative perigonadal, retroperitoneal, and mesenteric fat weight in HFD-fed mice. Furthermore, Calebin-A markedly reduced hepatic steatosis and the serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, total cholesterol, and triacylglycerol. These effects were associated with the downregulation of PPARγ, sterol regulatory element-binding protein-1, and particularly the activation of AMP-activated protein kinase α signaling found in both adipocytes and liver tissues. Conclusion: Taken together, these results demonstrated for the first time that Calebin-A suppressed adipocyte differentiation, prevented HFD-induced obesity, and improved hepatic steatosis, suggesting a novel application for the prevention and treatment of obesity and associated nonalcoholic fatty liver disease.",
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Calebin-A inhibits adipogenesis and hepatic steatosis in high-fat diet-induced obesity via activation of AMPK signaling. / Lai, Ching Shu; Liao, Sih Ning; Tsai, Mei Ling; Kalyanam, Nagabhushanam; Majeed, Muhammed; Majeed, Anju; Ho, Chi-Tang; Pan, Min Hsiung.

In: Molecular Nutrition and Food Research, Vol. 59, No. 10, 01.10.2015, p. 1883-1895.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Calebin-A inhibits adipogenesis and hepatic steatosis in high-fat diet-induced obesity via activation of AMPK signaling

AU - Lai, Ching Shu

AU - Liao, Sih Ning

AU - Tsai, Mei Ling

AU - Kalyanam, Nagabhushanam

AU - Majeed, Muhammed

AU - Majeed, Anju

AU - Ho, Chi-Tang

AU - Pan, Min Hsiung

PY - 2015/10/1

Y1 - 2015/10/1

N2 - Scope: Diet-induced obesity and associated nonalcoholic fatty liver disease have increased and become a major health problem worldwide. This study was conducted to investigate the chemopreventive effects of dietary Calebin-A, a curcuminoid, on differentiation of 3T3-L1 adipocytes and high-fat diet (HFD) induced obesity and hepatic steatosis. Potential mechanisms contributing to these effects were also elucidated. Methods and results: Calebin-A effectively and dose dependently suppressed accumulation of lipid droplets in adipocytes through the suppression of adipogenic specific factor peroxisome proliferator-activated receptor (PPAR) γ and fatty acid synthase and activated acetyl-CoA carboxylase. Dietary Calebin-A effectively decreased weight gain and relative perigonadal, retroperitoneal, and mesenteric fat weight in HFD-fed mice. Furthermore, Calebin-A markedly reduced hepatic steatosis and the serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, total cholesterol, and triacylglycerol. These effects were associated with the downregulation of PPARγ, sterol regulatory element-binding protein-1, and particularly the activation of AMP-activated protein kinase α signaling found in both adipocytes and liver tissues. Conclusion: Taken together, these results demonstrated for the first time that Calebin-A suppressed adipocyte differentiation, prevented HFD-induced obesity, and improved hepatic steatosis, suggesting a novel application for the prevention and treatment of obesity and associated nonalcoholic fatty liver disease.

AB - Scope: Diet-induced obesity and associated nonalcoholic fatty liver disease have increased and become a major health problem worldwide. This study was conducted to investigate the chemopreventive effects of dietary Calebin-A, a curcuminoid, on differentiation of 3T3-L1 adipocytes and high-fat diet (HFD) induced obesity and hepatic steatosis. Potential mechanisms contributing to these effects were also elucidated. Methods and results: Calebin-A effectively and dose dependently suppressed accumulation of lipid droplets in adipocytes through the suppression of adipogenic specific factor peroxisome proliferator-activated receptor (PPAR) γ and fatty acid synthase and activated acetyl-CoA carboxylase. Dietary Calebin-A effectively decreased weight gain and relative perigonadal, retroperitoneal, and mesenteric fat weight in HFD-fed mice. Furthermore, Calebin-A markedly reduced hepatic steatosis and the serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, total cholesterol, and triacylglycerol. These effects were associated with the downregulation of PPARγ, sterol regulatory element-binding protein-1, and particularly the activation of AMP-activated protein kinase α signaling found in both adipocytes and liver tissues. Conclusion: Taken together, these results demonstrated for the first time that Calebin-A suppressed adipocyte differentiation, prevented HFD-induced obesity, and improved hepatic steatosis, suggesting a novel application for the prevention and treatment of obesity and associated nonalcoholic fatty liver disease.

KW - 3T3-L1 adipocytes

KW - AMP-activated protein kinase

KW - Adipogenesis

KW - Calebin-A

KW - High-fat diet

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