Effect of biotin supplementation on fatty acid metabolic pathways in 3T3‐L1 adipocytes

Abstract

Several studies have shown that pharmacological concentrations of biotin decrease serum lipid concentrations and the expression of lipogenic genes. Previous studies on epididymal adipose tissue in mice revealed that 8 weeks of dietary biotin supplementation increased the protein abundance of the active form of AMPK and the inactive forms acetyl CoA carboxylase (ACC)‐1 and − 2, and decreased serum free fatty acid concentrations but did not affect lipolysis. These data suggest that pharmacological concentrations of the vitamin might affect fatty acid metabolism. In this work, we investigated the effects of pharmacological biotin concentrations on fatty acid synthesis, oxidation, and uptake in 3T3‐L1 adipocytes. Similar to observations in mice, biotin‐supplemented 3T3‐L1 adipose cells increased the protein abundance of active T172‐AMPK and inactive ACC‐1 and ‐2 forms. No changes were observed in the expression of the transcriptional factor PPARα and carnitine‐palmitoyltransferase‐1 (CPT‐1). Radiolabeled assays indicated a decrease in fatty acid synthesis; an increase in fatty acid oxidation and fatty acid incorporation rate into the lipid fraction between control cells and biotin‐supplemented cells. The data revealed an increase in the mRNA abundance of the fatty acid transport proteins Fatp1 and Acsl1 but not Cd36 or Fatp4 mRNA. Furthermore, the abundance of glycerol phosphate acyl transferase‐3 protein was increased. Triglyceride content was not affected. Lipid droplet numbers showed an increase and their areas were smaller in the biotin‐supplemented group. In conclusion, these data indicate that biotin supplementation causes a decrease in fatty acid synthesis and an increase in its oxidation and uptake. © 2018 BioFactors, 45(2):259–270, 2019

Effects of Magnesium Biotinate Supplementation on Serum Insulin, Glucose, and Lipid Parameters Along with Gene Expressions of Intermediary Metabolism in Rats

“…Low cellular energy causes activation of AMPK which inactivates both ACC isoforms, ACC-1 and ACC-2, resulting in reduced de novo lipogenesis and increased fatty acid oxidation [42]. Similarly, biotin supplementation in mice and rats has been reported to increase the active form of AMPK, which phosphorylates ACC-1 and ACC-2, resulting in decreases in the rate of lipid synthesis and increases in fatty acid oxidation rates [43,44]. Biotin supplementation in mice has also been shown to increase the gene expression of the active form of AMPK and decrease FAS and SREBP-1c expression [6,44].…”

“…Similarly, biotin supplementation in mice and rats has been reported to increase the active form of AMPK, which phosphorylates ACC-1 and ACC-2, resulting in decreases in the rate of lipid synthesis and increases in fatty acid oxidation rates [43,44]. Biotin supplementation in mice has also been shown to increase the gene expression of the active form of AMPK and decrease FAS and SREBP-1c expression [6,44]. Moreno-Méndez et al [44] found that ACC-1 and FAS reduced the acetate incorporations into total lipid fractions in response to biotin supplementation, resulting in lower fatty acid synthesis in mice adipose tissues.…”

“…Biotin supplementation in mice has also been shown to increase the gene expression of the active form of AMPK and decrease FAS and SREBP-1c expression [6,44]. Moreno-Méndez et al [44] found that ACC-1 and FAS reduced the acetate incorporations into total lipid fractions in response to biotin supplementation, resulting in lower fatty acid synthesis in mice adipose tissues.…”

Effects of magnesium biotinate supplementation on serum insulin, glucose, and lipid parameters along with liver protein levels of intermediary metabolism in rats

“…Low cellular energy causes activation of AMPK which inactivates both ACC isoforms, ACC-1, and ACC-2, resulting in reduced de novo lipogenesis and increased fatty acid oxidation [42]. Similarly, biotin supplementation in mice and rats has been reported to increase the active form of AMPK, which phosphorylates ACC-1 and ACC-2, resulting in decreases in the rate of lipid synthesis and increases in fatty acid oxidation rates [43,44]. Biotin supplementation in mice has also been shown to increase the level of the active form of AMPK and decrease FAS and SREBP-1c levels [6,44].…”

“…Similarly, biotin supplementation in mice and rats has been reported to increase the active form of AMPK, which phosphorylates ACC-1 and ACC-2, resulting in decreases in the rate of lipid synthesis and increases in fatty acid oxidation rates [43,44]. Biotin supplementation in mice has also been shown to increase the level of the active form of AMPK and decrease FAS and SREBP-1c levels [6,44]. Moreno-Méndez et al [44] found that ACC-1 and FAS reduced the acetate incorporations into total lipid fractions in response to biotin supplementation, resulting in lower fatty acid synthesis in mice adipose tissues.…”