How does protein deficiency affect the body




















Protein plays a huge role in preserving bone density with ageing. Severe protein deficiency may even cause redness, flaky skin and depigmentation. It may also cause hair thinning, fading, hair loss and brittle nails.

Edema, which leads to puffy and swollen skin, is another classic symptom of protein deficiencies. A safe thumb rule is to consume If you weigh 60 kgs, your ideal protein intake goal is between 60 and 90 grams per day.

Consume protein from natural sources like meat, eggs, fish, dairy, legumes, soy, and if you cannot meet your goal intake, then invest in protein supplements like whey protein, vegan protein powder and BCAAs.

Tags health lifestyle protein. Brain fog Short bursts of mental energy, followed by a looming fog may be related to fluctuating blood sugar and lack of protein, Mazur offers. Eat alternative protein sources. Consider a protein powder supplement. If you need help getting more protein into your diet, try supps made from soy, egg, rice, peas, or whey. Check with your physician or dietitian. Certain supplements like digestive enzymes and Manuka honey can help.

More Videos. Account My Account Sign Out. The reduction in weight and lean mass in 5P is likely due to increased energy expenditure that is not compensated for by the hyperphagia to maintain energy balance. Interestingly, the 5P animals appear to protect their fat mass while shifting their substrate oxidation from fats towards carbohydrates.

The preferential oxidation of carbohydrates in 5P is reflective of the higher dietary carbohydrate content and is consistent with other reports 50 , and the partitioning of dietary fat towards adipose reserves is also similar to other studies with adipogenic effects of low protein-high carbohydrate diets in mice Previous studies have shown that following protein restriction, rats attempt to regain body weight and adipose reserves on refeeding with a standard protein diet 34 , 35 , 37 , 38 ; however, the time-course of changes in tissue compartments and substrate utilization was relatively unknown.

We demonstrate that during the realimentation period, 0P and 5P had decreased body weight, body fat and lean mass. Importantly, 10P had increased body weight and body fat content on realimentation to a standard protein diet despite a lack of body composition differences during restriction.

The greater feed efficiency of these animals during the realimentation resulted in increased weight gain with excess calories being partitioned towards adipose reserves. Thus, prior protein restriction exerts divergent long-term effects on body composition and substrate utilization with severe protein restriction delaying fat and lean accretion and enhancing carbohydrate use during realimentation, whereas moderate protein restriction predisposes to weight gain and obesity.

These findings have important implications for long-term consequences of protein restriction on adiposity. 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 , Therefore, despite weight loss with 0P and 5P diets, the increased hepatic lipidosis likely negated any improvements in glucose tolerance.

We next focused on key markers of amino acid metabolism in the liver and skeletal muscle. We also observed distinct changes in key regulators of amino acid metabolism. The upregulation of transcripts for the amino acid transporters SLC7A5 and SLC3A2, and the rate-limiting enzyme in branched chain amino acid catabolism in the liver and muscle BCKDH, of particularly the 0P rats, is indicative of enhanced uptake and metabolism of branched chain amino acids by these tissues.

A potential caveat with our model is that the obesity prone OP-CD rats, which were originally developed from Sprague Dawley rats, have undergone multiple generations of breeding, and we did not test the effects of low protein diets in the control obesity-resistant strain. However, it is noteworthy that the hyperphagia, augmented thermogenesis and reduction in weight gain with our 0P and 5P, and the hyperphagia with 10P, is consistent with numerous other studies reporting similar findings in normal lean Sprague Dawley rats 7 , 8 , 9 , 19 , 21 , 55 , Although, the thermogenic activity of brown adipose tissue to dietary stimuli is often weak in obese animals 57 , the augmented thermogenesis with dietary protein restriction in our OP-CD rats suggests that effects of low protein diets on energy balance might be conserved in both lean and obese phenotypes.

The potential mechanisms by which low protein diets modulate energy balance are depicted in Fig. We provide evidence that severe protein deprivation produces a state of negative energy balance that persists beyond the period of deprivation primarily due to a decrease in energy intake and an increase in energy expenditure. In contrast, moderate protein deficiency produces hyperphagia without altering energy expenditure and predisposes to weight gain, adiposity and hepatic lipidosis.

We also demonstrate that protein deficiency engages sympathetic and serotonergic signaling primarily in BAT to induce thermogenesis. Together, our findings demonstrate that dietary protein deficiency exerts divergent effects on multiple metabolic parameters in obesity-prone rats.

Given that moderately low protein diets promote hyperphagia in humans 1 , 10 , 11 , our data, with an animal model that better represents human obesity, indicate that such diets could exacerbate pre-existing susceptibility to weight gain and obesity.

Protein-free diets decrease energy intake and enhance energy expenditure resulting in loss of body weight, fat and lean mass, whereas very low protein diets promote hyperphagia and thermogenesis with resultant reduction in weight and lean mass, and moderately low protein diets are hyperphagic without altering energy expenditure and body fat and lean mass. Enhanced sympathetic, serotonergic and fibroblast growth factor FGF21 secretion and signalling likely contribute to the thermogenic effects of protein-free and very low protein diets.

It is unlikely that anorexigenic gut peptides play a role in modulating intake, however, enhanced serotonergic signalling, likely of gut origin, mediates the effects of low protein diets on food intake. Further, dietary protein deficiency promotes hepatic lipidosis. Arrows pointing upwards, downwards or horizontally indicate an increase, decrease or no change, respectively.

Pathways that need further validation are indicated by dashed lines. The colored circles represent relative proportions of protein blue , carbohydrate green and fat red in the diet, respectively.

The general maintenance and husbandry Supplementary Methods was according to our previously published procedures 5. Prior to testing, animals were acclimatized to the environment and experimental conditions for 2 weeks.

These diets represent arbitrary states of protein starvation or total deprivation 0P , very low 5P and moderately low 10P dietary protein, relative to recommended control 15P requirements Three experiments were conducted. Multiple energy balance parameters were measured in both phases.

Gross energy content kilocalories per gram of fecal samples collected towards the end of the first and second week of the study were analyzed by bomb calorimetry Plain Jacket Bomb Calorimeter, Parr Instrument Company, Moline, IL, USA and energy digestibility calculated from the differences between total energy intake and fecal energy output.

In a cross-over design, following an overnight fast, each animal received intraperitoneal injection of saline or ondansetron 0. Similarly, overnight fasted rats received subcutaneous injection of either saline or propranolol 0.

Terminal postprandial samples were used for measuring plasma amino acid concentrations Supplementary Materials and Methods. Metabolic measurements during the day protein restriction phase of experiments 1 to 3 were combined prior to analyses.

The fixed effects of dietary treatment, time and the interaction of dietary treatment and time were included in the model. In addition, energy expenditure was also analyzed by incorporating lean mass as a covariate in the above model, followed by ANCOVA at each time point. For ondansetron and propranolol effects on energy intake and energy expenditure, data were modeled to include fixed effects of dietary treatment, drug, time and interactions of dietary treatment, drug and time.

Animal nested in dietary treatment was the random variable on which repeated measures were taken and covariance structures modeled either as compound symmetry, heterogenous compound symmetry, first-order antedependence, autoregressive, heterogenous autoregressive or toeplitz.

Discrete data on plasma amino acids, AUC for drug effects on energy expenditure, digestible energy, feed efficiency, and protein and mRNA abundance of tissue markers, were analyzed by one-way ANOVA with dietary treatment as a between-subject factor. For drug effects within groups, paired t-test was used to separate means. How to cite this article : Pezeshki, A. Low protein diets produce divergent effects on energy balance. Author Contributions A.

All authors have read and approved the final manuscript. National Center for Biotechnology Information , U. Sci Rep. Published online Apr Zapata , 1 Arashdeep Singh , 1 Nicholas J. Yee , 1 and Prasanth K. Chelikani a, 1, 2. Rizaldy C. Nicholas J. Prasanth K.

Author information Article notes Copyright and License information Disclaimer. Received Jan 7; Accepted Apr This work is licensed under a Creative Commons Attribution 4. This article has been cited by other articles in PMC. Abstract Diets deficient in protein often increase food consumption, body weight and fat mass; however, the underlying mechanisms remain poorly understood.

Open in a separate window. Figure 1. Effect of low protein diets on energy balance. Figure 2. Effect of ondansetron on energy balance of rats fed low protein diets. Figure 3. Effect of propranolol on energy expenditure. Plasma amino acids, glucose and hormones The 0P, 5P and 10P had lower postprandial plasma concentrations of the essential amino acids - threonine, tryptophan, valine, phenylalanine, leucine, isoleucine and lysine compared with 15P rats see Supplementary Table S3.

Figure 4. Effect of low protein diets on plasma hormone concentrations. Figure 5. Effects of low protein diets on relative mRNA or protein abundance of key regulatory molecules of energy metabolism in liver. Figure 6. Effects of low protein diets on relative mRNA abundance of key regulatory molecules of thermogenesis in interscapular brown adipose tissue.

Figure 7. Effects of low protein diets on relative mRNA abundance of key regulatory molecules of energy metabolism in skeletal muscle. Discussion We provide evidence that isocaloric diets with graded doses of protein produce divergent effects on energy intake, energy expenditure, plasma amino acids and gut hormones, and metabolic markers in peripheral tissues in obesity-prone rats. Figure 8. Model of potential mechanisms by which low protein diets modulate energy balance.

Additional Information How to cite this article : Pezeshki, A. Supplementary Material Supplementary Information: Click here to view. Footnotes Author Contributions A. References Gosby A. Testing protein leverage in lean humans: a randomised controlled experimental study. One 6 , e Obesity: the protein leverage hypothesis.



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