Gelidium elegans Regulates the AMPK-PRDM16-UCP-1 Pathway and Has a Synergistic Effect with Orlistat on Obesity-Associated Features in Mice Fed a High-Fat Diet

Nutrients. 2017 Mar 30;9(4):342. doi: 10.3390/nu9040342.

Abstract

The incidence of obesity is rising at an alarming rate throughout the world and is becoming a major public health concern with incalculable social and economic costs. Gelidium elegans (GENS), also previously known as Gelidium amansii, has been shown to exhibit anti-obesity effects. Nevertheless, the mechanism by which GENS is able to do this remains unclear. In the present study, our results showed that GENS prevents high-fat diet (HFD)-induced weight gain through modulation of the adenosine monophosphate-activated protein kinase (AMPK)-PR domain-containing16 (PRDM16)-uncoupling protein-1 (UCP-1) pathway in a mice model. We also found that GENS decreased hyperglycemia in mice that had been fed a HFD compared to corresponding controls. We also assessed the beneficial effect of the combined treatment with GENS and orlistat (a Food and Drug Administration-approved obesity drug) on obesity characteristics in HFD-fed mice. We found that in HFD-fed mice, the combination of GENS and orlistat is associated with more significant weight loss than orlistat treatment alone. Moreover, our results demonstrated a positive synergistic effect of GENS and orlistat on hyperglycemia and plasma triglyceride level in these animals. Thus, we suggest that a combination therapy of GENS and orlistat may positively influence obesity-related health outcomes in a diet-induced obese population.

Keywords: Gelidium amansii; Gelidium elegans; high-fat diet-induced obese mice; hyperglycemia; obesity.

MeSH terms

  • AMP-Activated Protein Kinases / genetics
  • AMP-Activated Protein Kinases / metabolism*
  • Adiposity / drug effects
  • Animals
  • Anti-Obesity Agents / pharmacology*
  • Blood Glucose / metabolism
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Diet, High-Fat
  • Disease Models, Animal
  • Gene Expression Regulation
  • Glucose Tolerance Test
  • Insulin / blood
  • Lactones / pharmacology*
  • Male
  • Mice
  • Mice, Inbred ICR
  • Obesity / drug therapy*
  • Organ Size / drug effects
  • Orlistat
  • Plant Extracts / pharmacology
  • Rhodophyta / chemistry*
  • Signal Transduction
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Uncoupling Protein 1 / genetics
  • Uncoupling Protein 1 / metabolism*
  • Weight Gain

Substances

  • Anti-Obesity Agents
  • Blood Glucose
  • DNA-Binding Proteins
  • Insulin
  • Lactones
  • Plant Extracts
  • Prdm16 protein, mouse
  • Transcription Factors
  • Ucp1 protein, mouse
  • Uncoupling Protein 1
  • Orlistat
  • AMP-Activated Protein Kinases