Low protein diet changes the energetic balance and sympathetic activity in brown adipose tissue of growing rats

França, Suélem Aparecida de; Santos, Maísa Pavani dos; Garófalo, Maria Antonieta Rissato; Navegantes, Luiz Carlos Carvalho; Kettelhut, Ísis C.; Lopes, Carbene França; Kawashita, Nair Honda

doi:10.1016/j.nut.2009.03.011

Cited by 64 publications

(67 citation statements)

References 35 publications

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“…The hypophagic effect of protein-free diets, and hyperphagic effect of very low protein and moderately low protein diets, in the current study are consistent with the 'protein leverage' hypothesis 2 , as well as previous studies on protein restriction in rats, mice and humans 1,[6][7][8][9]14,17,22 . Although the low protein-induced hyperphagia is associated with a central orexigenic drive 11,[15][16][17][18] , the peripheral signals that transmit information to central neural networks are poorly defined.…”

Section: Discussionsupporting

confidence: 91%

“…Despite an initial increase in energy expenditure, this effect did not persist in the 0P likely due to the sustained anorexia and weight loss. Previous studies have shown that an increased sympathetic influx to BAT is required for the thermogenic effects of low protein diets [19][20][21][22][23] . In the present study, using propranolol, a β -AR antagonist, we demonstrate that energy expenditure was dose-dependently attenuated in animals fed low protein diets with maximal attenuation in protein deprived rats.…”

Section: Discussionmentioning

confidence: 99%

“…Low protein diets also enhance energy expenditure in rodents 17,[19][20][21][22] , however, the underlying mechanisms are poorly understood. Potential mechanisms include increased sympathetic flux via β -adrenergic receptor (β -AR) signaling to brown adipose tissue (BAT) with consequent upregulation of mitochondrial uncoupling protein-1 (UCP1) expression 19,[21][22][23] , as well as increased fibroblast growth factor-21 (FGF21) mediated thermogenesis 17 . However, the relative importance of these mechanisms, and whether gut-derived signals are associated with low protein induced hyperphagia and thermogenesis, are largely unknown.…”

mentioning

confidence: 99%

“…These include imbalances in plasma and brain amino acid concentrations in rats [15][16][17] , modulation of energy sensors in the hypothalamus and anterior piriform cortex in rats 18 , and increased activity in the reward areas such as the orbitofrontal cortex and striatum in humans 11 . Low protein diets also enhance energy expenditure in rodents 17,[19][20][21][22] , however, the underlying mechanisms are poorly understood. Potential mechanisms include increased sympathetic flux via β -adrenergic receptor (β -AR) signaling to brown adipose tissue (BAT) with consequent upregulation of mitochondrial uncoupling protein-1 (UCP1) expression 19,[21][22][23] , as well as increased fibroblast growth factor-21 (FGF21) mediated thermogenesis Scientific RepoRts | 6:25145 | DOI: 10.1038/srep25145…”

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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: 91%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

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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“…Previous data from our laboratory observed that growing rats fed a low-protein, high-carbohydrate diet (LPHC diet: 6% protein, 74% carbohydrate) for 15 days showed a decrease in the body mass gain, despite the increase in food and calorie intakes and the increased lipid content in the carcass and in white and brown adipose tissues, by comparison with rats fed a control diet (C diet: 17% protein, 63% carbohydrate); the lowest mass gain for LPHC-fed rats was attributed, at least in part, to a decrease in the mass of the skeletal muscles (Aparecida de França et al 2009). A few studies have described the changes in skeletal muscle protein metabolism induced by adaptation to an LPHC diet ; however, the contribution of specific components of the different proteolytic systems to the control of muscle mass and the biochemical mechanisms underlying the reduced rate of skeletal muscle protein synthesis and breakdown under conditions of dietary protein deficiency remain unclear.…”

Section: Introductionmentioning

confidence: 88%

Decreased rate of protein synthesis, caspase-3 activity, and ubiquitin–proteasome proteolysis in soleus muscles from growing rats fed a low-protein, high-carbohydrate diet

Batistela

Pereira

Siqueira

et al. 2014

Can. J. Physiol. Pharmacol.

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The aim of this study was to investigate the changes in the rates of both protein synthesis and breakdown, and the activation of intracellular effectors that control these processes in soleus muscles from growing rats fed a low-protein, high-carbohydrate (LPHC) diet for 15 days. The mass and the protein content, as well as the rate of protein synthesis, were decreased in the soleus from LPHC-fed rats. The availability of amino acids was diminished, since the levels of various essential amino acids were decreased in the plasma of LPHC-fed rats. Overall rate of proteolysis was also decreased, explained by reductions in the mRNA levels of atrogin-1 and MuRF-1, ubiquitin conjugates, proteasome activity, and in the activity of caspase-3. Soleus muscles from LPHC-fed rats showed increased insulin sensitivity, with increased levels of insulin receptor and phosphorylation levels of AKT, which probably explains the inhibition of both the caspase-3 activity and the ubiquitin-proteasome system. The fall of muscle proteolysis seems to represent an adaptive response that contributes to spare proteins in a condition of diminished availability of dietary amino acids. Furthermore, the decreased rate of protein synthesis may be the driving factor to the lower muscle mass gain in growing rats fed the LPHC diet.

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The futile creatine cycle and the synthesis of fatty acids in inguinal white adipose tissue from growing rats, submitted to a hypoprotein‐hyperglycidic diet for 15 days

Allebrandt Neto,

Rondon e Silva,

Santos

et al. 2024

Lipids

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The low‐protein, high‐carbohydrate (LPHC) diet administered to growing rats soon after weaning, for 15 days, promoted an increase in energy expenditure by uncoupling protein 1 (UCP1) in interscapular brown adipose tissue, and also due to the occurrence of the browning process in the perirenal white adipose tissue (periWAT). However, we believe that inguinal white adipose tissue (ingWAT) may also contribute to energy expenditure through other mechanisms. Therefore, the aim of this work is to investigate the presence of the futile creatine cycle, and the origin of lipids in ingWAT, since that tissue showed an increase in the lipids content in rats submitted to the LPHC diet for 15 days. We observed increases in creatine kinase and alkaline phosphatase activity in ingWAT, of the LPHC animals. The mitochondrial Nicotinamide adenine dinucleotide reduced/nicotinamide adenine dinucleotide oxidized ratio is lower in ingWAT of LPHC animals. In the LPHC animals treated with β‐guanidinopropionic acid, the extracellular uptake of creatine in ingWAT was lower, as was the rectal temperature. Regarding lipid metabolism, we observed that in ingWAT, lipolysis in vitro when stimulated with noradrenaline is lower, and there were no changes in baseline levels. In addition, increases in the activity of enzymes were also observed: malic, glucose‐6‐phosphate dehydrogenase, and ATP‐citrate lyase, in addition to an increase in the PPARγ content. The results show the occurrence of the futile creatine cycle in ingWAT, and that the increase in the relative mass may be due to an increase in de novo fatty acid synthesis.

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Low protein diet changes the energetic balance and sympathetic activity in brown adipose tissue of growing rats

Cited by 64 publications

References 35 publications

0476 Low protein diets produce divergent effects on energy balance

0476 Low protein diets produce divergent effects on energy balance

Decreased rate of protein synthesis, caspase-3 activity, and ubiquitin–proteasome proteolysis in soleus muscles from growing rats fed a low-protein, high-carbohydrate diet

The futile creatine cycle and the synthesis of fatty acids in inguinal white adipose tissue from growing rats, submitted to a hypoprotein‐hyperglycidic diet for 15 days

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