Cinnamaldehyde Ameliorates Diet-Induced Obesity in Mice by Inducing Browning of White Adipose Tissue

Cell Physiol Biochem. 2017;42(4):1514-1525. doi: 10.1159/000479268. Epub 2017 Jul 18.

Abstract

Background/aims: Obesity has become a major health concern with few effective medications. Cinnamaldehyde (CA) has been reported to exhibit anti-diabetic and anti-inflammatory properties. However, whether CA shows anti-obesity activity remains unknown. Therefore, the present study aimed to investigate the potential anti-obesity effects of CA on mice fed a high-fat diet (HFD) and to explore the possible mechanisms involved.

Methods: Male C57BL/6J mice fed an HFD for 12 weeks were supplemented with CA (40 mg/kg/day) via gavage for an additional 8 weeks. Mice fed a standard diet were used as normal controls.

Results: The results revealed that CA treatment decreased body weight, fat mass, food intake, and serum lipid, free fatty acid and leptin levels. CA administration also improved insulin sensitivity in HFD-induced obese mice. Additionally, CA inhibited the hypertrophy of adipose tissue and induced browning of white adipose tissue. Uncoupling protein 1 (UCP1) was expressed in white adipose tissue after the oral administration of CA. Furthermore, CA enhanced the expression of the peroxisome proliferator-activated receptor γ (PPARγ), PR domain-containing 16 (PRDM16) and PPARγ coactivator 1α (PGC-1α) proteins in both brown and white adipose tissues.

Conclusions: The results suggest that CA exhibits therapeutic potency against obesity by inducing the browning of white adipose tissue in HFD-fed mice.

Keywords: Adipose tissue browning; Anti-obesity; Cinnamaldehyde; Fat mass; Mice.

MeSH terms

  • Acrolein / analogs & derivatives*
  • Acrolein / pharmacology
  • Adipose Tissue, Brown / drug effects*
  • Adipose Tissue, Brown / metabolism
  • Adipose Tissue, White / drug effects*
  • Adipose Tissue, White / metabolism
  • Administration, Oral
  • Animals
  • Anti-Obesity Agents / pharmacology*
  • Body Weight / drug effects
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Diet, High-Fat / adverse effects
  • Eating / drug effects
  • Energy Metabolism / drug effects
  • Fatty Acids, Nonesterified / blood
  • Gene Expression Regulation
  • Insulin Resistance
  • Leptin / genetics
  • Leptin / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Obesity / drug therapy*
  • Obesity / etiology
  • Obesity / genetics
  • Obesity / pathology
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / genetics
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Uncoupling Protein 1 / genetics
  • Uncoupling Protein 1 / metabolism

Substances

  • Anti-Obesity Agents
  • DNA-Binding Proteins
  • Fatty Acids, Nonesterified
  • Leptin
  • PPAR gamma
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Ppargc1a protein, mouse
  • Prdm16 protein, mouse
  • Transcription Factors
  • Ucp1 protein, mouse
  • Uncoupling Protein 1
  • Acrolein
  • cinnamaldehyde