Abstract

High protein diets have become popular for body weight maintenance and weight loss despite controversies regarding efficacy and safety. Although both weight gain and weight loss are determined by energy consumption and expenditure, data from rodent trials consistently demonstrate that the protein:carbohydrate ratio in high fat diets strongly influences body and fat mass gain per calorie eaten. Here, we review data from rodent trials examining how high protein diets may modulate energy metabolism and the mechanisms by which energy may be dissipated. We discuss the possible role of activating brown and so-called beige/BRITE adipocytes including non-canonical UCP1-independent thermogenesis and futile cycles, where two opposing metabolic pathways are operating simultaneously. We further review data on how the gut microbiota may affect energy expenditure. Results from human and rodent trials demonstrate that human trials are less consistent than rodent trials, where casein is used almost exclusively as the protein source. The lack of consistency in results from human trials may relate to the specific design of human trials, the possible distinct impact of different protein sources, and/or the differences in the efficiency of high protein diets to attenuate obesity development in lean subjects vs. promoting weight loss in obese subjects.

Highlights

  • It has for long been known that dietary protein content influences energy efficiency and thereby the energy cost for weight gain (Stock, 1999)

  • The ability of high protein diets using casein or whey as the protein source to prevent weight gain is well-documented in mouse studies

  • Intake of high protein diets may lead to reduced insulin signaling in adipose tissue

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Summary

INTRODUCTION

It has for long been known that dietary protein content influences energy efficiency and thereby the energy cost for weight gain (Stock, 1999). The Bäckhed group reported that cold exposure drastically altered the composition of the gut microbiota accompanied by an attenuated propensity for diet-induced obesity, and the obesity-resistant phenotype could be transferred to germ-free mice by fecal transplantation (Zietak et al, 2016) In this case the most pronounced effect in terms of inducing UCP1 expression was observed in iBAT, and in addition, increased fatty acid oxidation was observed in the liver (Zietak et al, 2016). Whether the accompanied high protein induced changes in energy expenditure and/or UCP1 expression are linked to the observed changes in gut microbiota composition requires further investigations It should be mentioned, that a high dietary protein content in diets with regular fat content led to decreased abundances of Akkermansia muciniphila, Bifidobacterium, Prevotella, Ruminococcus bromii, and Roseburia/Eubacterium rectale, and thereby a decreased number and activity of propionate- and butyrate-producing bacteria in rats (Mu et al, 2017). Recent findings would indicate that BRITE adipocytes seem to play a greater role than

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