Diabetes, Metabolic Syndrome Linked to Dietary Fiber in Study

Diabetes, Metabolic Syndrome Linked to Dietary Fiber in Study

In a new study, researchers have found that an excess of gut bacteria, together with the production and liver accumulation of short-chain fatty acids, increases the risk of developing metabolic syndrome. The research paper entitled “Microbiota-Dependent Hepatic Lipogenesis Mediated by Stearoyl CoA Desaturase 1 (SCD1) Promotes Metabolic Syndrome in TLR5-Deficient Mice” was recently published in the journal Cell Metabolism.

Metabolic syndrome is the medical term to describe a group of conditions, such as high blood pressure, high levels of triglycerides, high blood sugar, and a large waist circumference, which can lead to a higher risk of developing serious conditions such as obesity and type 2 diabetes. According to the International Diabetes Federation, a quarter of the world’s adult population has metabolic syndrome.

Researchers investigated the effect of over-proliferating gut bacteria in the development of fat deposits in the liver and consequent onset of metabolic syndrome. When dietary fiber (indigestible fiber derived from plants) is consumed, gut bacteria ferments it to short-chain fatty acids (SCFAs) that reach the liver and are converted to lipids that form fat deposits. The deregulation of this process might hinder liver function.

To understand this process, scientists studied the metabolic profiles of mice lacking the toll-like receptor 5 (TLR5), a bacterial flagellin receptor that keeps the gut bacteria homeostasis and prevents bacteria overgrowth. TLR5 is mutated in 10% of the world population. Although several studies point to a beneficial effect of SCFA for overall health, uncontrolled production in individuals with these receptor defects might lead to liver damage and metabolic disorders.

Indeed, the scientists observed that TLR5-deficient mice are prone to develop metabolic syndrome with increased liver lipid deposits. Moreover, consumption of dietary fiber aggravated the metabolic syndrome in these mice. When the scientists deleted the hepatic Stearoyl CoA Desaturase 1 (SCD1), an important fatty acid metabolism enzyme that has been associated with development of obesity in humans, there was an improvement in the metabolic syndrome. This observation led researchers to believe that SCD1 plays a key role in the development of metabolic syndrome in these mice.

Dr. Vishal Singh, the study’s first author and postdoctoral fellow in nutritional sciences at Penn State, commented on the objectives following these findings in a news release, saying, “Our next goal is to analyze the long-term effects of short-chain fatty acids, specifically in experimental models of type 2 diabetes and/or metabolic syndrome. We envision that our studies would drive the field towards ‘personalized’ cautioned dietary intake of plant-derived fiber in immunocompromised individuals.”

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