Effects of dietary protein to carbohydrate balance on energy intake, fat storage, and heat production in mice

Huang, Xianming; Hancock, Dale; Gosby, Alison K.; McMahon, Aisling C.; Solon, Samantha M.C.; Couteur, David G. Le; Conigrave, Arthur D.; Raubenheimer, David; Simpson, Stephen J.

doi:10.1002/oby.20007

Cited by 66 publications

(69 citation statements)

References 31 publications

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“…In our study, the low protein diets contained 67-57% carbohydrates with 33% fat. Others reported that diets relatively high in carbohydrate and fat, similar to the ranges in our study, promoted development of fatty liver and impaired glucose tolerance in both rats [52][53][54] and mice 51 , whereas low protein-high carbohydrate diets increased adiposity and fatty liver with paradoxical improvement in glucose tolerance in mice 6,32,33 . Therefore, despite weight loss with 0P and 5P diets, the increased hepatic lipidosis likely negated any improvements in glucose tolerance.…”

Section: Discussionsupporting

confidence: 84%

“…In addition to modulating energy intake and expenditure, moderate protein restriction in rats and mice has been consistently associated with alterations in body composition including reduction in lean mass, increased body fat content and development of fatty liver 6,8,9,14,17,32,33 . Protein restricted rats attempt to catch-up on body weight and adipose reserves following refeeding on a standard protein diet [34][35][36][37][38] .…”

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confidence: 99%

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0476 Low protein diets produce divergent effects on energy balance

Zapata

Pezeshki

Singh

et al. 2016

Journal of Animal Science

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Diets deficient in protein often increase food consumption, body weight and fat mass; however, the underlying mechanisms remain poorly understood. We compared the effects of diets varying in protein concentrations on energy balance in obesity-prone rats. We demonstrate that protein-free (0% protein calories) diets decreased energy intake and increased energy expenditure, very low protein (5% protein) diets increased energy intake and expenditure, whereas moderately low protein (10% protein) diets increased energy intake without altering expenditure, relative to control diet (15% protein). These diet-induced alterations in energy expenditure are in part mediated through enhanced serotonergic and β-adrenergic signaling coupled with upregulation of key thermogenic markers in brown fat and skeletal muscle. The protein-free and very low protein diets decreased plasma concentrations of multiple essential amino acids, anorexigenic and metabolic hormones, but these diets increased the tissue expression and plasma concentrations of fibroblast growth factor-21. Protein-free and very low protein diets induced fatty liver, reduced energy digestibility, and decreased lean mass and body weight that persisted beyond the restriction period. In contrast, moderately low protein diets promoted gain in body weight and adiposity following the period of protein restriction. Together, our findings demonstrate that low protein diets produce divergent effects on energy balance.The consumption of protein triggers adaptive responses in ingestive behavior, energy expenditure and metabolism that are under homeostatic controls. The 'protein leverage' hypothesis posits that protein intake is tightly regulated in several species including rats, mice and humans, which consume to acquire their required protein rather than meet requirements for fats and carbohydrates [1][2][3] . An increase in dietary protein density would decrease intake of carbohydrates and fats with consequent reduction in energy intake. There is substantial evidence that high protein diets promote satiety, weight loss and improve glycemic control 4,5 . A corollary to this hypothesis is that a reduction in the dietary protein concentration would increase total energy intake, due to overconsumption of carbohydrates and fat, in an effort to meet protein requirements. Consistent with this, moderately protein deficient diets were found to produce hyperphagia in rodents 6-9 and in some 1,10,11 but not all human studies 12,13 , whereas, severe protein restriction below a certain threshold leads to a reduction in food intake in rodents 9,14 . However, little is known of the underlying mechanisms by which moderate protein deficiency elicits such behavioural and metabolic adaptations and promotes positive energy balance with consequent predisposition to obesity and other metabolic disorders.The hyperphagic effects of moderately low protein diets are purported to be through multiple mechanisms. These include imbalances in plasma and brain amino acid concentrations in rats [15][16][17] ,...

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Section: Discussionsupporting

confidence: 84%

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confidence: 99%

0476 Low protein diets produce divergent effects on energy balance

Zapata

Pezeshki

Singh

et al. 2016

Journal of Animal Science

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“…Interestingly, this would actually also imply that those who had low intervention points might not be obese but might also be obtaining insufficient supplies of this nutrient. A candidate for the critical nutrient is protein (30,64,66), which is suggested to leverage energy intake when it is supplied at low levels, the "protein leverage" hypothesis. Interestingly, FTO the first gene identified as linked to BMI by GWAS, has been suggested recently to be potentially involved in regulation of protein intake via sensing of essential amino acids (25).…”

Section: So Why Do We Get Fat?mentioning

confidence: 99%

If Body Fatness is Under Physiological Regulation, Then How Come We Have an Obesity Epidemic?

Speakman

2014

Physiology

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Life involves a continuous use of energy, but food intake, which supplies that energy, is episodic. Feeding is switched on and off by a complex array of predominantly gut-derived peptides (and potentially nutrients) that initiate and terminate feeding bouts. Energy is stored as glucose and glycogen to overcome the problem of the episodic nature of intake compared with the continuous demand. Intake is also adjusted to meet immediate changes in demands. Most animals also store energy as fat. In some cases, this serves the purpose of storing energy in anticipation of a known future shortfall (e.g., hibernation, migration, or reproduction). Other animals, however, store fat in the absence of such anticipated needs, and in this case the fat appears to be stored in preparation for unpredictable catastrophic shortfalls in supply. Fat storage, however, brings disadvantages as well as advantages, in particular an increased risk of predation. Hence, many animals seem to have evolved a dual intervention point system preventing them from storing too little or too much fat. The physiological basis of the lower intervention point is well established, but the upper intervention point is much less studied. Human obesity can potentially be understood in an evolutionary context as due to drift in the upper intervention point following release from predation 2 million years ago (the drifty gene hypothesis) combined with a stimulus in modern society to overconsume calories, possibly attempting to satisfy intake of a limiting microor macro-nutrient like protein (the protein leverage hypothesis).

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“…The LPHC diet increased energy intake compared to the HPLC diet because of the phenomena of protein leverage, where the protein intake is prioritized over fat and carbohydrate intake [13]. In spite of the increase in the energy intake, the LPHC diet reduced body fat mass because of increased energy expenditure (Table 2), which is consistent with increased diet-induced thermogenesis serving to consume excess energy and slow development of adiposity [14]. This study suggests that a diet replacing carbohydrate with protein may be of little advantage in body fat reduction.…”

Section: A Low Protein-high Carbohydrate Diet Decreases Body Fat In Micementioning

confidence: 75%