Personal diet–microbiota interactions and weight loss

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Abstract

The aim of this review is to provide an overview of how person-specific interactions between diet and the gut microbiota could play a role in affecting diet-induced weight loss responses. The highly person-specific gut microbiota, which is shaped by our diet, secretes digestive enzymes and molecules that affect digestion in the colon. Therefore, weight loss responses could in part depend on personal colonic fermentation responses, which affect energy extraction of food and production of microbial metabolites, such as short-chain fatty acids (SCFAs), which exert various effects on host metabolism. Colonic fermentation is the net result of the complex interplay between availability of dietary substrates, the functional capacity of the gut microbiome and environmental (abiotic) factors in the gut such as pH and transit time. While animal studies have demonstrated that the gut microbiota can causally affect obesity, causal and mechanistic evidence from human studies is still largely lacking. However, recent human studies have proposed that the baseline gut microbiota composition may predict diet-induced weight loss-responses. In particular, individuals characterised by high relative abundance of Prevotella have been found to lose more weight on diets rich in dietary fibre compared to individuals with low Prevotella abundance. Although harnessing of personal diet–microbiota interactions holds promise for more personalised nutrition and obesity management strategies to improve human health, there is currently insufficient evidence to unequivocally link the gut microbiota and weight loss in human subjects. To move the field forward, a greater understanding of the mechanistic underpinnings of personal diet–microbiota interactions is needed.

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Diet rapidly and reproducibly alters the human gut microbiome

Lawrence A David, Corinne F. Maurice, Rachel Carmody … (2013)

Long-term diet influences the structure and activity of the trillions of microorganisms residing in the human gut 1–5 , but it remains unclear how rapidly and reproducibly the human gut microbiome responds to short-term macronutrient change. Here, we show that the short-term consumption of diets composed entirely of animal or plant products alters microbial community structure and overwhelms inter-individual differences in microbial gene expression. The animal-based diet increased the abundance of bile-tolerant microorganisms (Alistipes, Bilophila, and Bacteroides) and decreased the levels of Firmicutes that metabolize dietary plant polysaccharides (Roseburia, Eubacterium rectale, and Ruminococcus bromii). Microbial activity mirrored differences between herbivorous and carnivorous mammals 2 , reflecting trade-offs between carbohydrate and protein fermentation. Foodborne microbes from both diets transiently colonized the gut, including bacteria, fungi, and even viruses. Finally, increases in the abundance and activity of Bilophila wadsworthia on the animal-based diet support a link between dietary fat, bile acids, and the outgrowth of microorganisms capable of triggering inflammatory bowel disease 6 . In concert, these results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles.

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An obesity-associated gut microbiome with increased capacity for energy harvest.

Peter J Turnbaugh, Ruth E Ley, Michael A Mahowald … (2006)

The worldwide obesity epidemic is stimulating efforts to identify host and environmental factors that affect energy balance. Comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant bacterial divisions, the Bacteroidetes and the Firmicutes. Here we demonstrate through metagenomic and biochemical analyses that these changes affect the metabolic potential of the mouse gut microbiota. Our results indicate that the obese microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a significantly greater increase in total body fat than colonization with a 'lean microbiota'. These results identify the gut microbiota as an additional contributing factor to the pathophysiology of obesity.

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From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites.

Ara Koh, Filipe De Vadder, Petia Kovatcheva-Datchary … (2016)

A compelling set of links between the composition of the gut microbiota, the host diet, and host physiology has emerged. Do these links reflect cause-and-effect relationships, and what might be their mechanistic basis? A growing body of work implicates microbially produced metabolites as crucial executors of diet-based microbial influence on the host. Here, we will review data supporting the diverse functional roles carried out by a major class of bacterial metabolites, the short-chain fatty acids (SCFAs). SCFAs can directly activate G-coupled-receptors, inhibit histone deacetylases, and serve as energy substrates. They thus affect various physiological processes and may contribute to health and disease.