November 2, 2015

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Diet lacking soluble fiber promotes weight gain, mouse study suggests

Eating too much high-fat, high-calorie food is considered the primary cause of obesity and obesity-related disease, including diabetes. While the excess calories consumed are a direct cause of the fat accumulation, scientists suspect that low-grade inflammation due to an altered gut microbiome may also be involved. A new study in the American Journal of PhysiologyGastrointestinal and Liver Physiology finds in mice that a diet missing soluble fiber promotes inflammation in the intestines and poor gut health, leading to weight gain. Moreover, incorporating soluble fiber back into the diet can restore gut health.

The microbiota is a community of bacteria and other microorganisms that live in the intestines. Microbiota also exists elsewhere on the body, including the skin and mouth. The gut microbiota has an important role in maintaining intestinal health and function, including helping the body digest food, producing vitamins and fighting foreign microorganisms. Changes to the gut microbiota have been linked to development of gastrointestinal diseases, including inflammatory bowel disease, and metabolic diseases, including type 2 diabetes and obesity.

A research team at Georgia State University examined the effects of diets varying in amounts of soluble and insoluble fibers, protein and fat on the structure of the intestines, and weight gain in mice. Key observations from this study are:

"If our observations were to prove applicable to humans, it would suggest that encouraging consumption of foods with high content may be a means to combat the epidemic of metabolic disease. Moreover, addition of inulin and perhaps other soluble fibers to processed foods, including calorically rich obesogenic foods, may be a means to ameliorate their detrimental effects," the researchers stated.

More information: Benoit Chassaing et al. Lack of soluble fiber drives diet-induced adiposity in mice, American Journal of Physiology - Gastrointestinal and Liver Physiology (2015). DOI: 10.1152/ajpgi.00172.2015

Journal information: American Journal of Physiology

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