Ethanolic extract of seabuckthorn (Hippophae rhamnoides L) prevents high-fat diet-induced obesity in mice through down-regulation of adipogenic and lipogenic gene expression

Nutr Res. 2012 Nov;32(11):856-64. doi: 10.1016/j.nutres.2012.09.015.

Abstract

Phenolic compounds and flavonoids ameliorate bodyweight, blood glucose, and serum lipid profile. Since seabuckthorn (Hippophae rhamnoides L.) is known as a rich source of isoflavones and flavonoids, we hypothesized that ethanolic extract of seabuckthorn leaves (SL) may have anti-obesity and hypoglycemic effects. To investigate the effect of ethanolic extract of SL, 32 C57BL/6J mice were randomly divided into 4 dietary groups, containing 8 mice in each group: normal diet group; high-fat diet (HD) control group; high-fat diet with SL extract, 500 mg/kg body weight (BW) (SL1) group; and high-fat diet with SL extract, 1000 mg/kg BW (SL2) group. After 13 weeks, it was observed that oral administration of SL extract significantly reduced the energy intake; BW gain; epididymal fat pad weight; hepatic triglyceride, hepatic, and serum total cholesterol levels; and serum leptin levels in the SL groups compared to the HD group. However, differences in serum triglyceride and insulin levels in the SL groups were not significant in comparison to the HD group. The hepatic mRNA expression of peroxisome proliferator-activated receptor (PPAR) α and carnitine palmitoyltransferase 1 along with PPAR-γ were significantly increased in SL groups, whereas the level of acetyl-CoA carboxylase was significantly reduced in SL groups compared to HD group. Our results indicated that SL is effective in preventing BW gain and fat accumulation in the liver; it also reduced adipose tissue mass, hepatic lipid profile, and serum leptin level in the mouse. Together, these observations suggest that SL is a potential agent to study in the management of obesity and related disorders.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetyl-CoA Carboxylase / metabolism
  • Adipogenesis / drug effects*
  • Adipogenesis / genetics
  • Adipose Tissue / drug effects*
  • Adipose Tissue / metabolism
  • Administration, Oral
  • Animals
  • Anti-Obesity Agents / pharmacology
  • Anti-Obesity Agents / therapeutic use
  • Carnitine O-Palmitoyltransferase / genetics
  • Carnitine O-Palmitoyltransferase / metabolism
  • Cholesterol / metabolism
  • Diet, High-Fat / adverse effects
  • Down-Regulation
  • Energy Intake / drug effects
  • Flavonoids / pharmacology
  • Flavonoids / therapeutic use
  • Hippophae / chemistry*
  • Insulin / blood
  • Leptin / blood
  • Lipogenesis / drug effects*
  • Lipogenesis / genetics
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Obesity / etiology
  • Obesity / prevention & control*
  • PPAR alpha / genetics
  • PPAR alpha / metabolism
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Phytotherapy*
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use
  • RNA, Messenger / metabolism
  • Random Allocation
  • Triglycerides / metabolism
  • Weight Gain / drug effects

Substances

  • Anti-Obesity Agents
  • Flavonoids
  • Insulin
  • Leptin
  • PPAR alpha
  • PPAR gamma
  • Plant Extracts
  • RNA, Messenger
  • Triglycerides
  • Cholesterol
  • Carnitine O-Palmitoyltransferase
  • Acetyl-CoA Carboxylase