scholarly journals Restriction of dietary protein leads to conditioned protein preference and elevated palatability of protein-containing food in rats

2017 ◽  
Author(s):  
Michelle Murphy ◽  
Kate Z. Peters ◽  
Bethany S. Denton ◽  
Kathryn A. Lee ◽  
Heramb Chadchankar ◽  
...  
Keyword(s):  
Dietary Protein ◽  
Food Choice ◽  
Cluster Size ◽  
Preference Test ◽  
Protein Restriction ◽  
Restricted Diet ◽  
Adult Rats ◽  
Low Protein ◽  
Casein Protein ◽  
Over Time

AbstractThe mechanisms by which intake of dietary protein is regulated are poorly understood despite their potential involvement in determining food choice and appetite. In particular, it is unclear whether protein deficiency results in a specific appetite for protein and whether influences on diet are immediate or develop over time. To determine the effects of protein restriction on consumption, preference, and palatability for protein we assessed patterns of intake for casein (protein) and maltodextrin (carbohydrate) solutions in adult rats. To induce a state of protein restriction, rats were maintained on a low protein diet (5% casein) and compared to control rats on non-restricted diet (20% casein). Under these dietary conditions, relative to control rats, protein-restricted rats exhibited hyperphagia without weight gain. After two weeks, on alternate conditioning days, rats were given access to either isocaloric casein or maltodextrin solutions that were saccharin-sweetened and distinctly flavoured whilst consumption and licking patterns were recorded. This allowed rats to learn about the post-ingestive nutritional consequences of the two different solutions. Subsequently, during a preference test when rats had access to both solutions, we found that protein-restricted rats exhibited a preference for casein over carbohydrate whereas non-restricted rats did not. Analysis of lick microstructure revealed that this preference was associated with an increase in cluster size and number, reflective of an increase in palatability. In conclusion, protein-restriction induced a conditioned preference for protein, relative to carbohydrate, and this was associated with increased palatability.

scholarly journals Dietary protein restriction in chronic renal failure: nutritional efficacy, compliance, and progression of renal insufficiency.

1991 ◽  
Vol 2 (4) ◽  
pp. 823-831
Author(s):  
W E Mitch
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Chronic Renal Failure ◽  
Renal Insufficiency ◽  
Dietary Protein ◽  
Scientific Basis ◽  
Protein Restriction ◽  
Dietary Compliance ◽  
Dietary Protein Restriction ◽  
Low Protein

Two findings prompted investigators to examine the effects of dietary manipulation on progression of chronic renal failure: dietary protein restriction is an effective method of ameliorating uremic symptoms and the course of renal insufficiency in an individual patient is predictable. Results from studies of patients and animals with chronic renal failure suggested that a low-protein, phosphorus-restricted diet could slow the rate of loss of renal function. In evaluating these studies, three questions should be considered. First, is the diet nutritionally adequate? Second, has dietary compliance been monitored and achieved? Third, is there evidence that restricting the diet will change the rate of loss of renal function? The scientific basis for each of these questions is addressed in this review.

Effect of Dietary Protein Restriction on Renal Purines and Purine-Metabolizing Enzymes in Adriamycin Nephrosis in Rats: A Mechanism for Protection against Acute Proteinuria Involving Xanthine Oxidase Inhibition

1990 ◽  
Vol 79 (6) ◽  
pp. 647-656 ◽  
Author(s):  
Gian Marco Ghiggeri ◽  
Fabrizio Ginevri ◽  
Giovanni Cercignani ◽  
Roberta Oleggini ◽  
Alessando Garberi ◽  
...  
Keyword(s):  
Xanthine Oxidase ◽  
Dietary Protein ◽  
Purine Nucleoside Phosphorylase ◽  
Protein Restriction ◽  
Purine Nucleoside ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Dietary Protein Restriction ◽  
Low Protein ◽  
Normal Protein Diet

1. A low protein diet prevents the development of proteinuria and glomerular damage in adriamycin experimental nephrosis without affecting renal haemodynamics. In this study the hypothesis was tested as to whether protein restriction is able to modulate the purine metabolic cycle and related enzymes such as xanthine oxidase, one of the putative effectors of adriamycin nephrotoxicity. 2. Renal activities of xanthine oxidase and purine nucleoside phosphorylase were markedly depressed in adriamycin-treated rats fed a 9% casein (low protein) diet compared with the group fed a 22% casein (normal protein) diet both 1 day after adriamycin administration and at the time of appearance of heavy proteinuria (day 15), whereas the activity of renal adenosine deaminase was unchanged. 3. The concentrations of the metabolic substrates of xanthine oxidase, i.e. hypoxanthine and xanthine, were constantly lower in renal homogenates of rats fed a low protein diet compared with those on a normal protein diet. In urine, uric acid, the product of hypoxanthine-xanthine transformation, was lower 1 day after adriamycin injection in protein-restricted rats compared with the group on a normal protein diet which showed a marked increase in its excretion. At the same time, the urinary efflux of adenosine 5′-monophosphate, which is the precursor nucleotide of the above-mentioned nucleosides and bases, was very high in rats fed a low protein diet, whereas it was absent in the group on a normal protein diet. 4. The progressive increment in proteinuria of glomerular origin (i.e. increased excretion of albumin and transferrin) typical of adriamycin-treated rats fed a normal protein diet was inhibited in the protein-restricted animals, which were normoproteinuric on day 10 and were only slightly proteinuric on day 15. 5. Like protein restriction, the pharmacological suppression of renal xanthine oxidase by dietary tungstate and the scavenging by dimethylthiourea of the putative free radical deriving from the action of xanthine oxidase, were associated with a similar (quantitative and qualitative) inhibition of glomerular proteinurea. 6. These data demonstrate that dietary protein restriction is associated with a block in purine metabolism within the kidney due to a marked reduction in the activities of two main enzymes of the cycle, i.e. purine nucleoside phosphorylase and xanthine oxidase, the latter being a putative effector of adriamycin nephrotoxicity. The partial reduction of proteinuria induced by a low protein diet is quantitatively and qualitatively comparable with the reduction induced by the specific block of renal xanthine oxidase or by the scavenging of OH · deriving from hypoxanthine and xanthine transformation. The crucial factor(s) determining protection against proteinuria in adriamycin nephrosis may be decreased xanthine oxidase activity in the kidney and inhibition of the O2 · and OH · production via the xanthine oxidase system.

scholarly journals Effects of Long-Term Dietary Protein Restriction on Intestinal Morphology, Digestive Enzymes, Gut Hormones, and Colonic Microbiota in Pigs

Animals ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 180 ◽  
Author(s):  
Defu Yu ◽  
Weiyun Zhu ◽  
Suqin Hang
Keyword(s):  
Growth Performance ◽  
Dietary Protein ◽  
Hormone Secretion ◽  
Protein Restriction ◽  
Intestinal Morphology ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Low Protein ◽  
Gut Hormone

Using protein-restriction diets becomes a potential strategy to save the dietary protein resources. However, the mechanism of low-protein diets influencing pigs’ growth performance is still controversial. This study aimed to investigate the effect of protein-restriction diets on gastrointestinal physiology and gut microbiota in pigs. Eighteen weaned piglets were randomly allocated to three groups with different dietary protein levels. After a 16-week trial, the results showed that feeding a low-protein diet to pigs impaired the epithelial morphology of duodenum and jejunum (p < 0.05) and reduced the concentration of many plasma hormones (p < 0.05), such as ghrelin, somatostatin, glucose-dependent insulin-tropic polypeptide, leptin, and gastrin. The relative abundance of Streptococcus and Lactobacillus in colon and microbiota metabolites was also decreased by extreme protein-restriction diets (p < 0.05). These findings suggested that long-term ingestion of a protein-restricted diet could impair intestinal morphology, suppress gut hormone secretion, and change the microbial community and fermentation metabolites in pigs, while the moderately low-protein diet had a minimal effect on gut function and did not impair growth performance.

scholarly journals NEURONAL FGF-21 SIGNALING: A SENSOR OF DIETARY PROTEIN

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S730-S730
Author(s):  
Cristal Hill ◽  
Christopher Morrison
Keyword(s):  
Body Weight ◽  
Energy Expenditure ◽  
Glucose Homeostasis ◽  
Dietary Protein ◽  
Protein Restriction ◽  
Fibroblast Growth Factor 21 ◽  
Dietary Protein Restriction ◽  
Reduced Body ◽  
Low Protein ◽  
The Central Nervous System

Abstract Our data demonstrates that dietary protein restriction increases energy expenditure and improves glucose homeostasis, and that this effect is largely mediated by the metabolic hormone fibroblast growth factor 21(FGF21). Considering that the central nervous system (CNS) is acknowledged as a major regulator of both energy and glucose homeostasis, we have extended our studies to identify the tissue site mediating these FGF21-dependent effects via dietary protein restriction. In this study, mice with dysfunctional FGF21-signaling in either the CNS or adipose tissue were fed a control or low protein (LP)-diet to assess changes in body weight and metabolic endpoints. Our data show that LP diet increased energy expenditure and reduced body weight in control littermates, but these effects were lost in mice bearing CNS-specific deletion of Klb. These data highlight a liver to brain FGF21-signal as the first known neuroendocrine mechanism to explain the coordinated metabolic changes induced by dietary protein restriction.

Protein restriction reduces transforming growth factor-beta and interstitial fibrosis in nephrotic syndrome

1994 ◽  
Vol 266 (6) ◽  
pp. F884-F893 ◽  
Author(s):  
A. A. Eddy
Keyword(s):  
Transforming Growth Factor Beta ◽  
Dietary Protein ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Protein Restriction ◽  
Mrna Levels ◽  
Tgf Beta ◽  
Low Protein ◽  
Protein Group ◽  
Growth Factor Beta

Nephrotic syndrome induced by puromycin aminonucleoside (PAN) is characterized by tubulointerstitial (TI) inflammation, foci of TI fibrosis, and increased renal mRNA levels for matrix genes, the tissue inhibitor of metalloproteinases (TIMP), and the transforming growth factor-beta 1 (TGF-beta 1). To investigate the ability of a low-protein diet known to decrease TI inflammation to alter the degree of renal fibrosis, we studied four groups of rats: 27% protein PAN, 27% protein control, 8% protein PAN, and 8% protein control. Renal TGF-beta 1 mRNA levels correlated with the number of interstitial macrophages (r = 0.76) and were significantly reduced by dietary protein restriction. On day 10, Northern blot analysis showed that the elevated renal mRNA levels for procollagens alpha 1 (I), alpha 1(III), and alpha 2(IV) and fibronectin in the PAN-treated rats were significantly reduced by 8% dietary protein. In contrast, genes regulating matrix degradation (stromelysin and TIMP) were relatively unchanged by the low-protein diet. The number of foci of interstitial fibrosis and total renal collagen were greater in the PAN + 27% protein group than in the control groups. Both parameters of fibrosis were partially normalized in the PAN + 8% protein group. The results of this study suggest that dietary protein restriction attenuates TI fibrosis in PAN-induced nephrosis by partially reversing the increase in renal matrix synthesis. This effect was associated with decreased renal expression of the fibrogenic cytokine TGF-beta 1, which may be partially mediated by the concomitant reduction in the number of interstitial inflammatory macrophages.

Role of FGF21 and GCN2 in mediating the metabolic response to dietary protein restriction

2016 ◽  
Vol 11 (S 01) ◽  
Author(s):  
T Laeger ◽  
DC Albarado ◽  
L Trosclair ◽  
J Hedgepeth ◽  
CD Morrison
Keyword(s):  
Dietary Protein ◽  
Metabolic Response ◽  
Protein Restriction ◽  
Dietary Protein Restriction

Neuronal FGF-21 Signaling–A Sensor of Dietary Protein Restriction

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 261-LB
Author(s):  
CRISTAL M. HILL ◽  
MADELEINE V. DEHNER ◽  
DAVID MCDOUGAL ◽  
HANS-RUDOLF BERTHOUD ◽  
HEIKE MUENZBERG ◽  
...  
Keyword(s):  
Dietary Protein ◽  
Protein Restriction ◽  
Dietary Protein Restriction

238-LB: Dietary Protein Restriction Induces Myocardial Dysfunction Despite Reducing Body Weight in Aged C57BL/6J Mice

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 238-LB
Author(s):  
CHRISTOPHER L. AXELROD ◽  
WAGNER S. DANTAS ◽  
GANGARAO DAVULURI ◽  
WILLIAM T. KING ◽  
CRISTAL M. HILL ◽  
...  
Keyword(s):  
Body Weight ◽  
Dietary Protein ◽  
Myocardial Dysfunction ◽  
Protein Restriction ◽  
Dietary Protein Restriction

The impact of maternal protein restriction during perinatal life on the response to a septic insult in adult rats

2020 ◽  
pp. 1-8
Author(s):  
Reza Khazaee ◽  
Anastasiya Vinokurtseva ◽  
Lynda A. McCaig ◽  
Cory Yamashita ◽  
Daniel B. Hardy ◽  
...  
Keyword(s):  
Control Diet ◽  
Protein Restriction ◽  
Saline Control ◽  
Female Adult ◽  
Adult Rats ◽  
Male And Female ◽  
Maternal Protein Restriction ◽  
And Control ◽  
The Impact ◽  
Septic Insult

Abstract Although abundant evidence exists that adverse events during pregnancy lead to chronic conditions, there is limited information on the impact of acute insults such as sepsis. This study tested the hypothesis that impaired fetal development leads to altered organ responses to a septic insult in both male and female adult offspring. Fetal growth restricted (FGR) rats were generated using a maternal protein-restricted diet. Male and female FGR and control diet rats were housed until 150–160 d of age when they were exposed either a saline (control) or a fecal slurry intraperitoneal (Sepsis) injection. After 6 h, livers and lungs were analyzed for inflammation and, additionally, the amounts and function of pulmonary surfactant were measured. The results showed increases in the steady-state mRNA levels of inflammatory cytokines in the liver in response to the septic insult in both males and females; these responses were not different between FGR and control diet groups. In the lungs, cytokines were not detectable in any of the experimental groups. A significant decrease in the relative amount of surfactant was observed in male FGR offspring, but this was not observed in control males or in female animals. Overall, it is concluded that FGR induced by maternal protein restriction does not impact liver and lung inflammatory response to sepsis in either male or female adult rats. An altered septic response in male FGR offspring with respect to surfactant may imply a contribution to lung dysfunction.

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