Biotin augments acetyl CoA carboxylase 2 gene expression in the hypothalamus, leading to the suppression of food intake in mice

Biochem Biophys Res Commun. 2016 Jul 29;476(3):134-9. doi: 10.1016/j.bbrc.2016.04.152. Epub 2016 May 12.


It is known that biotin prevents the development of diabetes by increasing the functions of pancreatic beta-cells and improving insulin sensitivity in the periphery. However, its anti-obesity effects such as anorectic effects remain to be clarified. Acetyl CoA carboxylase (ACC), a biotin-dependent enzyme, has two isoforms (ACC1 and ACC2) and serves to catalyze the reaction of acetyl CoA to malonyl CoA. In the hypothalamus, ACC2 increases the production of malonyl CoA, which acts as a satiety signal. In this study, we investigated whether biotin increases the gene expression of ACC2 in the hypothalamus and suppresses food intake in mice administered excessive biotin. Food intake was significantly decreased by biotin, but plasma regulators of appetite, including glucose, ghrelin, and leptin, were not affected. On the other hand, biotin notably accumulated in the hypothalamus and enhanced ACC2 gene expression there, but it did not change the gene expression of ACC1, malonyl CoA decarboxylase (a malonyl CoA-degrading enzyme), and AMP-activated protein kinase α-2 (an ACC-inhibitory enzyme). These findings strongly suggest that biotin potentiates the suppression of appetite by upregulating ACC2 gene expression in the hypothalamus. This effect of biotin may contribute to the prevention of diabetes by biotin treatment.

Keywords: Acetyl CoA carboxylase 2; Biotin; Food intake; Hypothalamus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetyl-CoA Carboxylase / genetics*
  • Animals
  • Biotin / administration & dosage
  • Biotin / pharmacokinetics
  • Biotin / pharmacology*
  • Blood Glucose / analysis
  • Blood Glucose / metabolism
  • Eating / drug effects*
  • Hypoglycemic Agents / administration & dosage
  • Hypoglycemic Agents / pharmacokinetics
  • Hypoglycemic Agents / pharmacology*
  • Hypothalamus / drug effects*
  • Hypothalamus / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Obesity / blood
  • Obesity / genetics
  • Obesity / metabolism
  • Obesity / prevention & control
  • Up-Regulation / drug effects*
  • Vitamin B Complex / administration & dosage
  • Vitamin B Complex / pharmacokinetics
  • Vitamin B Complex / pharmacology*


  • Blood Glucose
  • Hypoglycemic Agents
  • Vitamin B Complex
  • Biotin
  • Acacb protein, mouse
  • Acetyl-CoA Carboxylase