Document Detail

Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms.
MedLine Citation:
PMID:  22506074     Owner:  NLM     Status:  MEDLINE    
Short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, are metabolites formed by gut microbiota from complex dietary carbohydrates. Butyrate and acetate were reported to protect against diet-induced obesity without causing hypophagia, while propionate was shown to reduce food intake. However, the underlying mechanisms for these effects are unclear. It was suggested that SCFAs may regulate gut hormones via their endogenous receptors Free fatty acid receptors 2 (FFAR2) and 3 (FFAR3), but direct evidence is lacking. We examined the effects of SCFA administration in mice, and show that butyrate, propionate, and acetate all protected against diet-induced obesity and insulin resistance. Butyrate and propionate, but not acetate, induce gut hormones and reduce food intake. As FFAR3 is the common receptor activated by butyrate and propionate, we examined these effects in FFAR3-deficient mice. The effects of butyrate and propionate on body weight and food intake are independent of FFAR3. In addition, FFAR3 plays a minor role in butyrate stimulation of Glucagon-like peptide-1, and is not required for butyrate- and propionate-dependent induction of Glucose-dependent insulinotropic peptide. Finally, FFAR3-deficient mice show normal body weight and glucose homeostasis. Stimulation of gut hormones and food intake inhibition by butyrate and propionate may represent a novel mechanism by which gut microbiota regulates host metabolism. These effects are largely intact in FFAR3-deficient mice, indicating additional mediators are required for these beneficial effects.
Hua V Lin; Andrea Frassetto; Edward J Kowalik; Andrea R Nawrocki; Mofei M Lu; Jennifer R Kosinski; James A Hubert; Daphne Szeto; Xiaorui Yao; Gail Forrest; Donald J Marsh
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Publication Detail:
Type:  Journal Article     Date:  2012-04-10
Journal Detail:
Title:  PloS one     Volume:  7     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2012  
Date Detail:
Created Date:  2012-04-16     Completed Date:  2012-10-17     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e35240     Citation Subset:  IM    
Diabetes and In Vivo Pharmacology, Merck Research Laboratories, Rahway, New Jersey, United States of America.
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MeSH Terms
Body Weight / drug effects,  physiology
Butyrates / metabolism*,  pharmacology
Fatty Acids, Nonesterified / metabolism*
Gastric Inhibitory Polypeptide / metabolism
Gastrointestinal Hormones / metabolism*
Glucagon-Like Peptide 1 / metabolism
Homeostasis / drug effects,  physiology
Insulin Resistance / physiology
Mice, Inbred C57BL
Mice, Knockout
Obesity / metabolism*,  prevention & control
Propionates / metabolism*,  pharmacology
Receptors, G-Protein-Coupled / metabolism*
Reg. No./Substance:
0/Butyrates; 0/FFAR3 protein, human; 0/Fatty Acids, Nonesterified; 0/Gastrointestinal Hormones; 0/Propionates; 0/Receptors, G-Protein-Coupled; 59392-49-3/Gastric Inhibitory Polypeptide; 89750-14-1/Glucagon-Like Peptide 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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