Alterations in vitamin A/retinoic acid homeostasis in diet-induced obesity and insulin resistance

Proc Nutr Soc. 2017 Nov;76(4):597-602. doi: 10.1017/S0029665117001069. Epub 2017 Jun 27.

Abstract

Vitamin A is an essential micronutrient for life and the phytochemical β-carotene, also known as pro-vitamin A, is an important dietary source of this vitamin. Vitamin A (retinol) is the parent compound of all bioactive retinoids but it is retinoic acid (RA) that is the active metabolite of vitamin A. The plasma concentration of retinol is maintained in a narrow range and its normal biological activities strictly regulated since excessive intake can lead to toxicity and thus also be detrimental to life. The present review will give an overview of how vitamin A homeostasis is maintained and move on to focus on the link between circulating vitamin A and metabolic disease states. Finally, we will examine how pharmacological or genetic alterations in vitamin A homeostasis and RA-signalling can influence body fat and blood glucose levels including a novel link to the liver secreted hormone fibroblast growth factor 21, an important metabolic regulator.

Keywords: FGF fibroblast growth factor; RA retinoic acid; RBP retinol binding protein; Adiposity; Ceramide; Fibroblast growth factor 21; Glucose homeostasis; Retinoids.

Publication types

  • Review

MeSH terms

  • Diet / adverse effects*
  • Fibroblast Growth Factors / metabolism
  • Homeostasis / physiology*
  • Humans
  • Insulin Resistance / physiology*
  • Liver / metabolism
  • Obesity / blood
  • Obesity / etiology*
  • Provitamins / administration & dosage
  • Retinol-Binding Proteins, Plasma / analysis
  • Vitamin A / blood*

Substances

  • Provitamins
  • Retinol-Binding Proteins, Plasma
  • fibroblast growth factor 21
  • Vitamin A
  • Fibroblast Growth Factors