Gut Microbiota and Metabolic Health: The Potential Beneficial Effects of a Medium Chain Triglyceride Diet in Obese Individuals - PubMed (original) (raw)

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Gut Microbiota and Metabolic Health: The Potential Beneficial Effects of a Medium Chain Triglyceride Diet in Obese Individuals

Sabri Ahmed Rial et al. Nutrients. 2016.

Abstract

Obesity and associated metabolic complications, such as non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2D), are in constant increase around the world. While most obese patients show several metabolic and biometric abnormalities and comorbidities, a subgroup of patients representing 3% to 57% of obese adults, depending on the diagnosis criteria, remains metabolically healthy. Among many other factors, the gut microbiota is now identified as a determining factor in the pathogenesis of metabolically unhealthy obese (MUHO) individuals and in obesity-related diseases such as endotoxemia, intestinal and systemic inflammation, as well as insulin resistance. Interestingly, recent studies suggest that an optimal healthy-like gut microbiota structure may contribute to the metabolically healthy obese (MHO) phenotype. Here, we describe how dietary medium chain triglycerides (MCT), previously found to promote lipid catabolism, energy expenditure and weight loss, can ameliorate metabolic health via their capacity to improve both intestinal ecosystem and permeability. MCT-enriched diets could therefore be used to manage metabolic diseases through modification of gut microbiota.

Keywords: Bacteroidetes; Firmicutes; endotoxemia; gut microbiota; lipopolysaccharide; medium chain fatty acids; medium chain triglycerides; metabolic syndrome; metabolically healthy obese; metabolically unhealthy obese; non-alcoholic fatty liver disease; obesity.

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Figure 1

Figure 1

Crosstalk between gut, liver and peripheral metabolic tissues under 4 metabolic states. Under condition of healthy leanness (A) an optimal relative abundance of LPS-expressing vs. non-expressing bacteria contribute to gut impermeability, low intestinal and hepatic inflammation, and non-obesogenic/steatogenic nutrient supply. Under MUHO conditions (B), an elevation in the relative abundance of LPS-expressing bacteria (Gram-negative) induces LPS infiltration and leads to altered intestinal barrier integrity, local inflammation, liver injury and endotoxemia. At the same time, a high fat and carbohydrate supply contributes to adiposity, hepatic steatosis and peripheral insulin resistance. In MHO subjects (C), despite an adiposity sustained by a rich diet, a balanced gut microbiota would contribute to maintain intestinal and systemic metabolic health, prevent endotoxemia, and lower hepatic injury and peripheral insulin resistance. Our hypothetical model (D) suggests that diet MCT supplementation for MUHO subjects may facilitate a shift towards an MHO-like profile by improving lipid catabolism and lowering adiposity in part, but also by remodelling the gut microbiota into a metabolically beneficial structure. SCFA: short chain fatty acids; FA-U: Fatty acid uptake; AT: adipose tissue; DNL: de novo lipogenesis; SM: skeletal muscle; MUHO: metabolically unhealthy obese (or obesity); IR: Insulin resistance; β-ox: beta-oxidation; MHO: metabolically healthy obese (or obesity); MCT: medium chain triglycerides; MCFA: medium chain fatty acids; LPS: lipopolysaccharides; VLDL: very low density lipoproteins.

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