The multifactorial interplay of diet, the microbiome and appetite control: current knowledge and future challenges

Abstract

The recent availability of high-throughput nucleic acid sequencing technologies has rapidly advanced approaches to analysing the role of the gut microbiome in governance of human health, including gut health, and also metabolic, cardiovascular and mental health, inter alia. Recent scientific studies suggest that energy intake (EI) perturbations at the population level cannot account for the current obesity epidemic, and significant work is investigating the potential role of the microbiome, and in particular its metabolic products, notably SCFA, predominantly acetate, propionate and butyrate, the last of which is an energy source for the epithelium of the large intestine. The energy yield from dietary residues may be a significant factor influencing energy balance. This review posits that the contribution towards EI is governed by EI diet composition (not just fibre), the composition of the microbiome and by the levels of physical activity. Furthermore, we hypothesise that these factors do not exist in a steady state, but rather are dynamic, with both short-and medium-term effects on appetite regulation. We suggest that the existing modelling strategies for bacterial dynamics, specifically for growth in chemostat culture, are of utility in understanding the dynamic interplay of diet, activity and microbiomic organisation. Such approaches may be informative in optimising the application of dietary and microbial therapy to promote health. OverviewThe availability of high-throughput nucleic acid sequencing technologies has facilitated a range of new approaches to analysing the role of the gut microbiome in governance of human health (1) . Modern techniques suggest a role for the microbiome maintenance of, not only gut health but also systemic conditions, including cardiovascular health (2) , mental health (3) and obesity (3) . Despite wide media focus on excess energy intake (EI), recent scientific studies suggest EI perturbations at the population level cannot account for the current obesity epidemic (4) . The microbiome is responsible for the production of a highly complex and highly dynamic metaexometabolome. Well-known components of this include the SCFA acetate, propionate and butyrate, the last of which is an energy source for the epithelium of the large intestine (5) , as well as an inhibitor of histone deacetylation (and thereby cell fate determination) (6) . The energy yield from dietary residues entering the large intestine may account for as much as 10 % of EI (7) and is therefore a significant factor influencing energy balance. The guiding theme of this review is that this contribution towards EI is governed by EI, diet composition, the composition of the microbiome and levels of physical activity. Furthermore, we hypothesise that these factors do not exist in a steady state, but rather are dynamic, with both short-and medium-term effects

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Weight‐loss interventions and gut microbiota changes in overweight and obese patients: a systematic review

“…More recently, the gut microbiota, which is made up of the collection of microorganisms that inhabits human intestines, has been implicated in the aetiology of obesity . These bacteria play an important role in physiological processes such as digestion and metabolism, and they are suggested to participate in obesity and metabolic disorder development because they are able to increase energy production from the diet, induce low‐grade inflammation, regulate the fatty acid tissue composition and participate in appetite regulation through the gut–brain axis .…”

From Epidemiology to Epigenetics: Evidence for the Importance of Nutrition to Optimal Health Development Across the Life Course

“…Moreover, recent research suggests that not only are the metabolic products that result from carbohydrate digestion important in the etiology of obesity (e.g., short-chain fatty acids such as acetate, propionate, and butyrate) but that these factors may also have effects on appetite regulation through signaling of the hypothalamic region of the brain (Corfe et al 2015).…”