
Eva Degerman
Research team manager

Propionic acid and butyric acid inhibit lipolysis and de novo lipogenesis and increase insulin-stimulated glucose uptake in primary rat adipocytes.
Author
Summary, in English
Fermentation of dietary fibers by colonic microbiota generates short-chain fatty acids (SCFAs), e.g., propionic acid and butyric acid, which have been described to have "anti-obesity properties" by ameliorating fasting glycaemia, body weight and insulin tolerance in animal models. In the present study, we therefore investigate if propionic acid and butyric acid have effects on lipolysis, de novo lipogenesis and glucose uptake in primary rat adipocytes. We show that both propionic acid and butyric acid inhibit isoproterenol- and adenosine deaminase-stimulated lipolysis as well as isoproterenol-stimulated lipolysis in the presence of a phosphodiesterase (PDE3) inhibitor. In addition, we show that propionic acid and butyric acid inhibit basal and insulin-stimulated de novo lipogenesis, which is associated with increased phosphorylation and thus inhibition of acetyl CoA carboxylase, a rate-limiting enzyme in fatty acid synthesis. Furthermore, we show that propionic acid and butyric acid increase insulin-stimulated glucose uptake. To conclude, our study shows that SCFAs have effects on fat storage and mobilization as well as glucose uptake in rat primary adipocytes. Thus, the SCFAs might contribute to healthier adipocytes and subsequently also to improved energy metabolism with for example less circulating free fatty acids, which is beneficial in the context of obesity and type 2 diabetes.
Department/s
- EXODIAB: Excellence of Diabetes Research in Sweden
- Insulin Signal Transduction
- Department of Food Technology, Engineering and Nutrition
Publishing year
2015
Language
English
Pages
81-88
Publication/Series
Adipocyte
Volume
4
Issue
2
Full text
- Available as PDF - 600 kB
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Links
Document type
Journal article
Publisher
Taylor & Francis
Topic
- Endocrinology and Diabetes
Status
Published
Project
- ANTIDIABETIC FOOD CENTRE
Research group
- Insulin Signal Transduction
ISBN/ISSN/Other
- ISSN: 2162-3945