Vitamin D and energy homeostasis: of mice and men

Area of Science:

• Endocrinology
• Metabolic Research
• Nutritional Science

Background:

• The vitamin D endocrine system impacts numerous tissues beyond bone, including adipose tissue.
• 1,25-Dihydroxyvitamin D₃, the active vitamin D form, regulates adipogenesis and gene expression in fat cells.
• Genetic disruption of vitamin D action in mice leads to fat loss and increased energy expenditure.

Purpose of the Study:

• To investigate the role of vitamin D receptor (Vdr) signaling in adipose tissue and its impact on energy homeostasis.
• To explore the discrepancy between mouse models and human data regarding vitamin D status and obesity.

Main Methods:

• Analysis of mice with genetic disruptions in vitamin D action (Vdr or Cyp27b1 gene deletion).
• Assessment of fat mass, energy expenditure, and gene expression (including uncoupling proteins) in mouse models.
• Review of human epidemiological data and intervention studies on vitamin D status and body weight.

Main Results:

• Mice lacking Vdr signaling lose fat mass due to increased energy expenditure.
• Enhanced Vdr signaling in adipose tissue promotes obesity in mice.
• Disrupted Vdr signaling in mice increases uncoupling protein expression and bile acid pools, contributing to energy expenditure.
• Human obesity is linked to poor vitamin D status, but supplementation trials show limited effects on body weight.

Conclusions:

• Vitamin D action significantly influences energy homeostasis and fat mass, particularly in mouse models.
• A notable discrepancy exists between mouse and human data concerning vitamin D's effect on obesity.
• Further research is needed to clarify the role of vitamin D in human obesity and metabolic syndrome.