Melatonin Alleviates Glucose and Lipid Metabolism Disorders in Guinea Pigs Caused by Different Artificial Light

Wei Liu1, Yunchao Zhang1, Qi Chen1

  • 1Department of Endocrinology and Metabolism, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China.

Insights

Melatonin may help reduce obesity and insulin resistance caused by artificial light exposure. This study shows melatonin activates the AMPKα/PPARα pathway, improving metabolic health.

Area of Science:

  • Metabolic research
  • Endocrinology
  • Chronobiology

Background:

  • Modern lifestyles, including high-calorie diets and artificial light, disrupt glucose and lipid metabolism.
  • Melatonin shows potential for managing obesity and diabetes, but its mechanisms are unclear.

Purpose of the Study:

  • To investigate melatonin's effects on fat deposition, lipid metabolism, and insulin resistance induced by constant artificial light.
  • To explore the molecular pathways, specifically the AMPKα/PPARα signaling pathway, involved in melatonin's metabolic effects.

Main Methods:

  • Guinea pigs were exposed to different light conditions (12h light, 24h light) and/or high-fat diets, with some receiving melatonin treatment.
  • Metabolic parameters including insulin resistance and obesity were assessed after 10 weeks.
  • Gene and protein expression of the AMPKα/PPARα pathway and CPT1A were analyzed using qPCR and Western blotting.

Main Results:

  • Constant artificial light (24HL) worsened insulin resistance and obesity compared to intermittent light (12HL).
  • Melatonin treatment significantly reduced insulin resistance and obesity markers compared to the 24HL group.
  • Melatonin upregulated key pathway proteins: AMPKα, p-AMPKα, PPARα, and CPT1A.

Conclusions:

  • Melatonin may mitigate insulin resistance and obesity associated with prolonged artificial light exposure in guinea pigs.
  • The beneficial effects of melatonin appear to be mediated through the activation of the AMPKα/PPARα signaling pathway.

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