Dietary Fiber: Potential Mechanism of Appetite Suppression Discovered

Professor Gary Frost PhD RD Head of the Nutrition and Dietetic Research Group NIHR Senior Investigator Division of Diabetes, Endocrinology and Metabolism Faculty of Medicine Imperial College Hammersmith Campus London W12 ONNMedicalResearch.com Interview with:
Professor Gary Frost PhD RD
Head of the Nutrition and Dietetic Research Group
NIHR Senior Investigator
Division of Diabetes, Endocrinology and Metabolism
Faculty of Medicine Imperial College Hammersmith Campus
London W12 ONN

MedicalResearch.com: What are the main findings of the study? 

Prof. Frost: That acetate that is derived from the fermentation of dietary fiber in the colon by the microbiota is taken up by the hypothalamus in the brain.  In the hypothalamus the way the cells metabolize acetate creates a signal that suppresses appetite

MedicalResearch.com: Were any of the findings unexpected? 

Prof. Frost: No, most people thought that acetate from the colon did not reach the brain it was all metabolised by the liver.  Also other scientist have shown that the fermentation of dietary fiber leads to an increase release of hormones from the colon that make you feal full (PYY and GLP-1).  What we are beginning to see is that dietary fiber has many ways of working.

MedicalResearch.com: What should clinicians and patients take away from your report? 

Prof. Frost: It is to early, we need to translate these observation to humans.  We need to understand how much fiber you would need to eat to have these effects.  What we do know is if you eat large amounts of fiber it makes you feel full but you need to eat about double the recommendation (30g)

MedicalResearch.com: What recommendations do you have for future research as a result of this study? 

Prof. Frost: At the moment we are working with humans to see if the results are the same.  If they are then we can start to develop targeted dietary methods to suppress appetite

Citation:

The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism
Gary Frost et al

Nature Communications5, Article number: 3611 doi:10.1038/ncomms4611Received 16 July 2013 Accepted 11 March 2014 Published 29 April 2014

 

 

Last Updated on May 4, 2014 by Marie Benz MD FAAD