TY - JOUR

T1 - Personal diet-microbiota interactions and weight loss

AU - Roager, Henrik Munch

AU - Christensen, Lars Hein

N1 - CURIS 2022 NEXS 077

PY - 2022

Y1 - 2022

N2 - 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.

AB - 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.

KW - Faculty of Science

KW - Personalised nutrition

KW - Gut microbiome

KW - Obesity

KW - Weight loss

U2 - 10.1017/S0029665122000805

DO - 10.1017/S0029665122000805

M3 - Review

C2 - 35258446

VL - 81

SP - 243

EP - 254

JO - Proceedings of the Nutrition Society

JF - Proceedings of the Nutrition Society

SN - 0029-6651

IS - 3

T2 - The Nutrition Society Winter Conference 2021

Y2 - 7 December 2021 through 8 December 2021

ER -