Low Protein Diets and Energy Balance: Mechanisms of Action on Energy Intake and Expenditure

Pezeshki, Adel; Chelikani, Prasanth

doi:10.3389/fnut.2021.655833

Cited by 23 publications

(21 citation statements)

References 111 publications

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“…Therefore, FGF21 may mediate other effects of GCN2, and further investigation is required to understand its complete role. (ⅱ) serotonergic signaling: this signaling is associated with low protein-induced energy expenditure [ 156 ]. Administration of a non-selective 5-HT receptor antagonist, metergoline, and 5-HT3 receptor antagonist, ondansetron, can reduce energy expenditure in rats fed protein-restricted diets [ 156 ].…”

Section: Discussionmentioning

confidence: 99%

“…(ⅱ) serotonergic signaling: this signaling is associated with low protein-induced energy expenditure [ 156 ]. Administration of a non-selective 5-HT receptor antagonist, metergoline, and 5-HT3 receptor antagonist, ondansetron, can reduce energy expenditure in rats fed protein-restricted diets [ 156 ]. However, whether central or peripheral serotonergic signaling contributes to these processes remains to be studied.…”

Section: Discussionmentioning

confidence: 99%

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Impacts of essential amino acids on energy balance

Xiao

Guo

2022

Molecular Metabolism

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Background Obesity develops due to an imbalance in energy homeostasis, wherein energy intake exceeds energy expenditure. Accumulating evidence shows that manipulations of dietary protein and their component amino acids affect the energy balance, resulting in changes in fat mass and body weight. Amino acids are not only the building blocks of proteins but also serve as signals regulating multiple biological pathways. Scope of review We present the currently available evidence regarding the effects of dietary alterations of a single essential amino acid (EAA) on energy balance and relevant signaling mechanisms at both central and peripheral levels. We summarize the association between EAAs and obesity in humans and the clinical use of modifying the dietary EAA composition for therapeutic intervention in obesity. Finally, similar mechanisms underlying diets varying in protein levels and diets altered of a single EAA are described. The current review would expand our understanding of the contribution of protein and amino acids to energy balance control, thus helping discover novel therapeutic approaches for obesity and related diseases. Major Conclusions Changes in circulating EAA levels, particularly increased branched-chain amino acids (BCAAs), have been reported in obese human and animal models. Alterations in dietary EAA intake result in improvements in fat and weight loss in rodents, and each has its distinct mechanism. For example, leucine deprivation increases energy expenditure, reduces food intake and fat mass, primarily through regulation of the general control nonderepressible 2 (GCN2) and mammalian target of rapamycin (mTOR) signaling. Methionine restriction by 80% decreases fat mass and body weight while developing hyperphagia, primarily through fibroblast growth factor 21 (FGF-21) signaling. Some effects of diets with different protein levels on energy homeostasis are mediated by similar mechanisms. However, reports on the effects and underlying mechanisms of dietary EAA imbalances on human body weight are few, and more investigations are needed in future.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Impacts of essential amino acids on energy balance

Xiao

Guo

2022

Molecular Metabolism

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“…LQP and LP diets promoted a slight BW gain without altering the food intake. Accumulating evidence suggests that LP diets are associated with increased BW, hyperphagia, energy expenditure and thermogenesis [37]; however, the increase in BWs was slighter, and may have been due to an increase in fat mass. The increase in fat mass in our study was possibly attributable to the compensation for the loss of lean tissue.…”

Section: Imapct Of the Mlqp And Mlp Diets In The Damsmentioning

confidence: 93%

Chronic Effects of Maternal Low-Protein and Low-Quality Protein Diets on Body Composition, Glucose-Homeostasis and Metabolic Factors, Followed by Reversible Changes upon Rehabilitation in Adult Rat Offspring

et al. 2021

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Several studies suggest that the maternal protein content and source can affect the offspring’s health. However, the chronic impact of maternal quality and quantity protein restriction, and reversible changes upon rehabilitation, if any, in the offspring, remains elusive. This study examined the effects of maternal low-quality protein (LQP) and low-protein (LP) intake from preconception to post-weaning, followed by rehabilitation from weaning, on body composition, glucose-homeostasis, and metabolic factors in rat offspring. Wistar rats were exposed to normal protein (NP; 20% casein), LQP (20% wheat gluten) or LP (8% casein) isocaloric diets for 7 weeks before pregnancy until lactation. After weaning, the offspring were exposed to five diets: NP, LQP, LQPR (LQP rehabilitated with NP), LP, and LPR (LP rehabilitated with NP) for 16 weeks. Body composition, glucose-homeostasis, lipids, and plasma hormones were investigated. The LQP and LP offspring had lower bodyweight, fat and lean mass, insulin and HOMA-IR than the NP. The LQP offspring had higher cholesterol, T3 and T4, and lower triacylglycerides and glucose, while these were unaltered in LP compared to NP. The majority of the above outcomes were reversed upon rehabilitation. These results suggest that the chronic exposure of rats to maternal LQP and LP diets induced differential adverse effects by influencing body composition and metabolism, which were reversed upon rehabilitation.

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“…The mechanisms for this rapid recognition of IAAD involve an enzyme important in the initiation of new protein synthesis: General Control Nonderepressible 2 (GCN2) and its target, phosphorylated eIF2α can be seen in Figure 6 of [ 40 , 41 ] and has been the subject of many reviews. For example, in 2021 alone, see [ 42 , 43 , 44 , 45 ]. The mechanisms involve an accumulation of uncharged tRNA because the limiting IAA that is deficient in the plasma and brain cannot adequately charge its cognate tRNA.…”

Section: Methods: Importance Of the Prefeeding Methods In Studying The Earliest Responsementioning

confidence: 99%

Brain Signaling of Indispensable Amino Acid Deficiency

Gietzen

2021

JCM

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Our health requires continual protein synthesis for maintaining and repairing tissues. For protein synthesis to function, all the essential (indispensable) amino acids (IAAs) must be available in the diet, along with those AAs that the cells can synthesize (the dispensable amino acids). Here we review studies that have shown the location of the detector for IAA deficiency in the brain, specifically for recognition of IAA deficient diets (IAAD diets) in the anterior piriform cortex (APC), with subsequent responses in downstream brain areas. The APC is highly excitable, which makes is uniquely suited to serve as an alarm for reductions in IAAs. With a balanced diet, these neurons are kept from over-excitation by GABAergic inhibitory neurons. Because several transporters and receptors on the GABAergic neurons have rapid turnover times, they rely on intact protein synthesis to function. When an IAA is missing, its unique tRNA cannot be charged. This activates the enzyme General Control Nonderepressible 2 (GCN2) that is important in the initiation phase of protein synthesis. Without the inhibitory control supplied by GABAergic neurons, excitation in the circuitry is free to signal an urgent alarm. Studies in rodents have shown rapid recognition of IAA deficiency by quick rejection of the IAAD diet.

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Low Protein Diets and Energy Balance: Mechanisms of Action on Energy Intake and Expenditure

Cited by 23 publications

References 111 publications

Impacts of essential amino acids on energy balance

Impacts of essential amino acids on energy balance

Chronic Effects of Maternal Low-Protein and Low-Quality Protein Diets on Body Composition, Glucose-Homeostasis and Metabolic Factors, Followed by Reversible Changes upon Rehabilitation in Adult Rat Offspring

Brain Signaling of Indispensable Amino Acid Deficiency

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