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Calcitriol Reduces Hepatic Triglyceride Accumulation and Glucose Output Through Ca2+/CaMKKβ/AMPK Activation Under

S Cheng, W Y So, D Zhang

  • 1Room 609A, Lo Kwee- Seong Integrated Biomedical Sciences Building, School of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, Shatin, New Territories, Hong Kong. psleung@cuhk.edu.hk.

Current Molecular Medicine
|September 24, 2016
PubMed
Abstract

Insights

Calcitriol, vitamin D

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Type 2 diabetes is characterized by hepatic metabolic abnormalities.
  • Vitamin D deficiency is common in type 2 diabetes patients.
  • Calcitriol is the active form of vitamin D.

Purpose of the Study:

  • To investigate the effects of calcitriol on hepatic metabolic abnormalities in type 2 diabetes.
  • To elucidate the underlying mechanisms of calcitriol's action in insulin resistance.

Main Methods:

  • Type 2 diabetic db/db mice and insulin-resistant HepG2 cells were utilized.
  • Calcitriol treatment was administered for 8 weeks in vivo.
  • Cellular signaling pathways, including Ca2+/CaMKKβ/AMPK, were examined.

Main Results:

  • Calcitriol treatment improved hepatic lipid and glucose metabolism in diabetic mice.
  • In insulin-resistant cells, calcitriol activated the Ca2+/CaMKKβ/AMPK pathway.
  • This activation led to reduced hepatic triglyceride accumulation and glucose output.

Conclusions:

  • Calcitriol effectively ameliorates hepatic metabolic dysfunction in type 2 diabetes.
  • The Ca2+/CaMKKβ/AMPK pathway is a key mediator of calcitriol's beneficial effects.
  • Calcitriol shows therapeutic potential for managing type 2 diabetes complications.

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