Lund University is celebrating 350 years.


Javascript is not activated in your browser. This website needs javascript activated to work properly.
You are here

Branched short-chain fatty acids modulate glucose and lipid metabolism in primary adipocytes

  • Emilia Heimann
  • Margareta Nyman
  • Ann-Kristin Holmén-Pålbrink
  • Karin Lindkvist-Petersson
  • Eva Degerman
Publishing year: 2016-12-21
Language: English
Pages: 359-368
Publication/Series: Adipocyte
Volume: 5
Issue: 4
Document type: Journal article
Publisher: Taylor & Francis

Abstract english

Short-chain fatty acids (SCFAs), e.g. acetic acid, propionic acid and butyric acid, generated through colonic fermentation of dietary fibers, have been shown to reach the systemic circulation at micromolar concentrations. Moreover, SCFAs have been conferred anti-obesity properties in both animal models and human subjects. Branched SCFAs (BSCFAs), e.g., isobutyric and isovaleric acid, are generated by fermentation of branched amino acids, generated from undigested protein reaching colon. However, BSCFAs have been sparsely investigated when referring to effects on energy metabolism. Here we primarily investigate the effects of isobutyric acid and isovaleric acid on glucose and lipid metabolism in primary rat and human adipocytes. BSCFAs inhibited both cAMP-mediated lipolysis and insulin-stimulated de novo lipogenesis at 10 mM, whereas isobutyric acid potentiated insulin-stimulated glucose uptake by all concentrations (1, 3 and 10 mM) in rat adipocytes. For human adipocytes, only SCFAs inhibited lipolysis at 10 mM. In both in vitro models, BSCFAs and SCFAs reduced phosphorylation of hormone sensitive lipase, a rate limiting enzyme in lipolysis. In addition, BSCFAs and SCFAs, in contrast to insulin, inhibited lipolysis in the presence of wortmannin, a phosphatidylinositide 3-kinase inhibitor and OPC3911, a phosphodiesterase 3 inhibitor in rat adipocytes. Furthermore, BSCFAs and SCFAs reduced insulin-mediated phosphorylation of protein kinase B. To conclude, BSCFAs have effects on adipocyte lipid and glucose metabolism that can contribute to improved insulin sensitivity in individuals with disturbed metabolism.


  • Physiology
  • Journal Article


  • Insulin Signal Transduction
  • Medical Structural Biology
  • ISSN: 2162-3945
Eva Degerman
E-mail: eva [dot] degerman [at] med [dot] lu [dot] se


Insulin Signal Transduction

+46 46 222 85 83

+46 70 885 83 62

BMC C1121b


Lund University Diabetes Centre, CRC, SUS Malmö, Entrance 72, House 91:12. SE-205 02 Malmö. Telephone: +46 40 39 10 00