Effects of phenobarbital, dietary protein intake, and ewe liveweight on ovulation rate and concentrations of plasma FSH and hepatic microsomal enzymes

1990 ◽  
Vol 2 (6) ◽  
pp. 623 ◽  
Author(s):  
JF Smith ◽  
E Payne ◽  
AJ Peterson ◽  
LT McGowan ◽  
B Cope ◽  
...  
Keyword(s):  
Dietary Protein ◽  
Protein Intake ◽  
Metabolic Changes ◽  
Ovulation Rate ◽  
Protein Diet ◽  
Dietary Protein Intake ◽  
Hepatic Enzyme ◽  
Microsomal Enzymes ◽  
Low Protein ◽  
Hepatic Microsomal Enzymes

Coopworth ewes were differentially fed from December 1985 to April 1986 to produce two liveweight classes: fat (55-60 kg) and thin (40-45 kg). The ewes were then fed on either high-protein (22%) or low-protein (12%) diets, with or without phenobarbital treatment for 10 days commencing on Day 7 of the oestrous cycle. Phenobarbital treatment caused an increase in ovulation rate that was most pronounced in thin ewes and those on the low-protein diet. Ewe liveweight produced an increase in ovulation rate, but increased dietary protein in the particular formulations used had no effect. Hepatic enzyme concentrations were increased by phenobarbital treatment and, to a lesser extent, by dietary protein intake and ewe liveweight. However, these metabolic changes and the increase in ovulation rate were not accompanied by interpretable changes in the plasma FSH concentrations.

scholarly journals Serum metabolites associated with dietary protein intake: results from the Modification of Diet in Renal Disease (MDRD) randomized clinical trial

2019 ◽  
Vol 109 (3) ◽  
pp. 517-525 ◽  
Author(s):  
Casey M Rebholz ◽  
Zihe Zheng ◽  
Morgan E Grams ◽  
Lawrence J Appel ◽  
Mark J Sarnak ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Amino Acid ◽  
Dietary Protein ◽  
Protein Intake ◽  
Filtration Rate ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Dietary Protein Intake ◽  
Low Protein ◽  
P 16

ABSTRACT Background Accurate assessment of dietary intake is essential, but self-report of dietary intake is prone to measurement error and bias. Discovering metabolic consequences of diets with lower compared with higher protein intake could elucidate new, objective biomarkers of protein intake. Objectives The goal of this study was to identify serum metabolites associated with dietary protein intake. Methods Metabolites were measured with the use of untargeted, reverse-phase ultra-performance liquid chromatography–tandem mass spectrometry quantification in serum specimens collected at the 12-mo follow-up visit in the Modification of Diet in Renal Disease (MDRD) Study from 482 participants in study A (glomerular filtration rate: 25–55 mL · min−1 · 1.73 m−2) and 192 participants in study B (glomerular filtration rate: 13–24 mL · min−1 · 1.73 m−2). We used multivariable linear regression to test for differences in log-transformed metabolites (outcome) according to randomly assigned dietary protein intervention groups (exposure). Statistical significance was assessed at the Bonferroni-corrected threshold: 0.05/1193 = 4.2 × 10−5. Results In study A, 130 metabolites (83 known from 28 distinct pathways, including 7 amino acid pathways; 47 unknown) were significantly different between participants randomly assigned to the low-protein diet compared with the moderate-protein diet. In study B, 32 metabolites (22 known from 8 distinct pathways, including 4 amino acid pathways; 10 unknown) were significantly different between participants randomly assigned to the very-low-protein diet compared with the low-protein diet. A total of 11 known metabolites were significantly associated with protein intake in the same direction in both studies A and B: 3-methylhistidine, N-acetyl-3-methylhistidine, xanthurenate, isovalerylcarnitine, creatine, kynurenate, 1-(1-enyl-palmitoyl)-2-arachidonoyl-GPE (P-16:0/20:4), 1-(1-enyl-stearoyl)-2-arachidonoyl-GPE (P-18:0/20:4), 1-(1-enyl-palmitoyl)-2-arachidonoyl-GPC (P-16:0/20:4), sulfate, and γ-glutamylalanine. Conclusions Among patients with chronic kidney disease, an untargeted serum metabolomics platform identified multiple pathways and metabolites associated with dietary protein intake. Further research is necessary to characterize unknown compounds and to examine these metabolites in association with dietary protein intake among individuals without kidney disease. This trial was registered at clinicaltrials.gov as NCT03202914.

Effect of dietary protein and enalapril on proximal tubular delivery and absorption of albumin in nephrotic rats

1996 ◽  
Vol 270 (6) ◽  
pp. F986-F996
Author(s):  
W. R. Fitzgibbon ◽  
S. K. Webster ◽  
A. Imamura ◽  
D. W. Ploth ◽  
F. N. Hutchison
Keyword(s):  
Proximal Tubule ◽  
Dietary Protein ◽  
Protein Intake ◽  
Left Kidney ◽  
Protein Diet ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Albumin Concentration ◽  
Dietary Protein Intake ◽  
Proximal Tubular ◽  
Albumin Permeation

In passive Heymann nephritis (PHN), angiotensin-converting enzyme inhibition (ACEI) or a low dietary protein intake decreases albuminuria (UAlbV). Although this reduction in albuminuria appears to result from an improvement in glomerular permselectivity, the effect of these treatments on albumin permeation and absorption by the nephron has not been clarified. This study used micropuncture techniques to examine the effect of these two treatments on albumin permeation (by measuring the delivery of albumin to the proximal tubule) and the tubular absorption of albumin. PHN rats (12-18 days after injection of FX1A) were switched from 23% to either 40% protein diet (HP), 40% protein diet and concomitantly treated with enalapril (40 mg.kg-1.day-1) (HPE), or to 8% (LP) protein diet for 4-6 days. Although left kidney glomerular filtration rate (GFR) did not differ among the groups, UAlbV from the left kidney in LP and HPE was only 20-40% of that observed for the HP group. In protocol 1, the fractional recovery of albumin (FRAlb) in urine was calculated following injection of artificial tubular fluid containing [14C]inulin and 125I-labeled albumin into the earliest identifiable proximal loops. There were no differences in FRAlb among the three groups. In protocol 2, timed quantitative collections of tubular fluid were obtained from proximal tubular loops. The rate of albumin delivery to the earliest accessible loops of the proximal tubule was significantly lower for the LP and HPE groups compared with the HP group. For each group, albumin concentration corrected for water absorption was not altered along the proximal tubule. The data indicate that alterations of dietary protein intake or ACEI treatment results in large changes in the delivery of albumin at the proximal tubule that could singularly account for the changes in urinary albumin excretion.

scholarly journals Dietary Protein Intake Level Modulates Mucosal Healing and Mucosa-Adherent Microbiota in Mouse Model of Colitis

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 514 ◽  
Author(s):  
Sandra Vidal-Lletjós ◽  
Mireille Andriamihaja ◽  
Anne Blais ◽  
Marta Grauso ◽  
Patricia Lepage ◽  
...  
Keyword(s):  
Dietary Protein ◽  
Protein Intake ◽  
High Protein Diet ◽  
Repair Process ◽  
Mucosal Healing ◽  
High Protein ◽  
Protein Diet ◽  
Dietary Protein Intake ◽  
Epithelial Repair ◽  
The Impact

Mucosal healing after an inflammatory flare is associated with lasting clinical remission. The aim of the present work was to evaluate the impact of the amount of dietary protein on epithelial repair after an acute inflammatory episode. C57BL/6 DSS-treated mice received isocaloric diets with different levels of dietary protein: 14% (P14), 30% (P30) and 53% (P53) for 3 (day 10), 6 (day 13) and 21 (day 28) days after the time of colitis maximal intensity. While the P53 diet worsened the DSS- induced inflammation both in intensity and duration, the P30 diet, when compared to the P14 diet, showed a beneficial effect during the epithelial repair process by accelerating inflammation resolution, reducing colonic permeability and increasing epithelial repair together with epithelial hyperproliferation. Dietary protein intake also impacted mucosa-adherent microbiota composition after inflammation since P30 fed mice showed increased colonization of butyrate-producing genera throughout the resolution phase. This study revealed that in our colitis model, the amount of protein in the diet modulated mucosal healing, with beneficial effects of a moderately high-protein diet, while very high-protein diet displayed deleterious effects on this process.

Effects of dietary protein intake on vasoactive hormones

1990 ◽  
Vol 258 (5) ◽  
pp. R1095-R1100 ◽  
Author(s):  
B. S. Daniels ◽  
T. H. Hostetter
Keyword(s):  
Amino Acid ◽  
Dietary Protein ◽  
Protein Intake ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Plasma Amino Acid ◽  
Dietary Protein Intake ◽  
Vasoactive Hormones ◽  
Amino Acid Levels

Vasoactive hormonal response to two levels of dietary protein intake was studied in seven healthy adult volunteers. The subjects were randomly placed on a 2-g.kg-1.day-1 (high) or 0.55-g.kg-1.day-1 (low) diet using a crossover design and were studied on the morning of the 5th day and again after 24 h of indomethacin treatment. Plasma renin activity (PRA), aldosterone, vasopressin, and urinary excretion of 6-ketoprostaglandin F1 alpha (PGF1 alpha) were significantly higher on the high-protein diet despite constancy of body weight, blood pressure, pulse, urinary sodium and potassium excretion, and plasma amino acid levels. After treatment with cyclooxygenase inhibitor indomethacin, 6-keto-PGF1 alpha excretion was equalized, but the elevated PRA and aldosterone levels persisted on the high-protein diet, suggesting that PRA and aldosterone elevations do not depend entirely on prostanoid release. We conclude that chronic augmentation of dietary protein intake is accompanied by alterations of vasoactive hormones, which persist for up to 10 h postprandially and are independent of elevated plasma amino acid levels. Such hormonal alterations may mediate some of the dietary protein-mediated changes in renal hemodynamics.

scholarly journals Age Modifies the Association of Dietary Protein Intake with All-Cause Mortality in Patients with Chronic Kidney Disease

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1744 ◽  
Author(s):  
Daiki Watanabe ◽  
Shinji Machida ◽  
Naoki Matsumoto ◽  
Yugo Shibagaki ◽  
Tsutomu Sakurada
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Dietary Protein ◽  
Protein Intake ◽  
Ideal Body Weight ◽  
The Elderly ◽  
Dietary Protein Intake ◽  
Low Protein ◽  
All Cause Mortality ◽  
Stage Renal Disease

Whether the effect of a low-protein diet on progression to end-stage renal disease (ESRD) and mortality risk differs between young and elderly adults with chronic kidney disease (CKD) is unclear. We conducted a retrospective CKD cohort study to investigate the association between protein intake and mortality or renal outcomes and whether age affects this association. The cohort comprised 352 patients with stage G3-5 CKD who had been followed up for a median 4.2 years, had undergone educational hospitalization, and for whom baseline protein intake was estimated from 24-h urine samples. We classified the patients into a very low protein intake (VLPI) group (<0.6 g/kg ideal body weight/day), a low protein intake (LPI) group (0.6–0.8 g), and a moderate protein intake (MPI) group (>0.8 g). Compared with the LPI group, the MPI group had a significantly lower risk of all-cause mortality (hazard ratio: 0.29; 95% confidence interval: 0.07 to 0.94) but a similar risk of ESRD, although relatively high protein intake was related to a faster decline in the estimated glomerular filtration rate. When examined per age group, these results were observed only among the elderly patients, suggesting that the association between baseline dietary protein intake and all-cause mortality in patients with CKD is age-dependent.

Food and protein intake, glucagon, and distribution of alpha-aminoisobutyrate in the rat

1980 ◽  
Vol 238 (4) ◽  
pp. E358-E363
Author(s):  
J. K. Tews ◽  
A. E. Harper
Keyword(s):  
Dietary Protein ◽  
Protein Intake ◽  
Control Diet ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Tissue Water ◽  
Low Protein ◽  
Protein Diets ◽  
Different Tissues

Distribution of alpha-aminoisobutyric acid (AIB) in the rat was modified by food, dietary protein, and glucagon. In rats last fed 24 h before AIB injection, AIB clearance from plasma and uptake into liver were greater in rats fed a high-protein diet (60% casein) than in rats fed the control diet (18% casein); AIB clearance from plasma and uptake into muscle were lowered by a low-protein diet (6% casein). Feeding rats lowered clearance of AIB from plasma in low- and high-protein groups. Distribution ratios (AIB concentration in tissue water/AIB in plasma) were low in all tissues but liver during the first 7 h after feeding high protein when compared to the control values; ratios were low in muscle, heart, and kidney after feeding low protein. Maximum ratios occurred at different times for different tissues; the time was delayed by the high-protein diet in all tissues but liver. Glucagon increased all ratios in rats fed the control or low-protein diets, with the smallest changes occurring in liver and muscle from low-protein rats.

Dietary protein intake modulates glomerular eicosanoid production in the rat

1989 ◽  
Vol 256 (4) ◽  
pp. F711-F718 ◽  
Author(s):  
B. R. Don ◽  
S. Blake ◽  
F. N. Hutchison ◽  
G. A. Kaysen ◽  
M. Schambelan
Keyword(s):  
Arachidonic Acid ◽  
Dietary Protein ◽  
Protein Intake ◽  
Enzyme Inhibitor ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Dietary Protein Intake ◽  
Eicosanoid Production ◽  
Renal Ablation

The quantity of protein in the diet modulates glomerular function. To study the effect of dietary protein intake on glomerular eicosanoid production, rats were randomized to either a high- (40%) or low- (8.5%) protein isocaloric diet. Ten to fourteen days later glomeruli were isolated and incubated in the absence (basal) and presence (stimulated conditions) of arachidonic acid, and production rates of prostaglandin (PG) E2, PGF2 alpha, and thromboxane B2 (TxB2) were determined by direct radioimmunoassay. Under basal conditions, glomerular production of all three eicosanoids was significantly greater in rats ingesting the high-protein diet. Glomerular production of PGE2 and TxB2 was also greater in animals fed the high-protein diet in the presence of arachidonic acid, suggesting that glomerular cyclooxygenase activity was augmented. In contrast, ingestion of a high-protein diet was not associated with a significant increase in eicosanoid production by renal papillae or in TxB2 release by clotting blood. To investigate the potential role of the renin-angiotensin system in the dietary protein-induced modulation of glomerular eicosanoid production, rats ingesting a high- or low-protein diet were randomized to treatment with an angiotensin-converting enzyme inhibitor or no therapy. Enalapril attenuated the dietary protein-induced augmentation in glomerular eicosanoid production. This effect occurred only when administered in vivo, since the active metabolite enalapril did not alter PGE2 production by isolated glomeruli when added in vitro. Dietary protein intake also modulated glomerular eicosanoid production in three models of experimental renal disease in the rat (streptozotocin-induced diabetes mellitus, Heymann nephritis, and partial renal ablation).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effects of dietary protein restriction on the progression of moderate renal disease in the Modification of Diet in Renal Disease Study.

1996 ◽  
Vol 7 (12) ◽  
pp. 2616-2626 ◽  
Keyword(s):  
Renal Disease ◽  
Beneficial Effect ◽  
Dietary Protein ◽  
Protein Intake ◽  
Diet Group ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Dietary Protein Restriction ◽  
Low Protein ◽  
Gfr Decline

The Modification of Diet in Renal Disease (MDRD) Study consisted of two randomized controlled trials to determine the effects of dietary protein restriction and strict blood pressure control. In 255 patients with advanced renal disease (baseline GFR, 13 to 24 mL/min per 1.73 m2; Study B), secondary analyses demonstrated a correlation between achieved protein intake and rate of decline in GFR, consistent with a beneficial effect of a low-protein diet. In 585 patients with moderate renal disease (baseline GFR, 25 to 55 mL/min per 1.73 m2; Study A), the primary analysis of the effect of the low-protein diet was inconclusive because of a nonlinear GFR decline and limited duration of follow-up. A meta-analysis of recent controlled trials, including MDRD Study A, demonstrated a beneficial effect of a low-protein diet on the incidence of renal failure. The objective of these secondary analyses is to explore further the effect of dietary protein restriction in Study A. In these analyses, a total of 585 patients were randomly assigned to follow either a low-protein diet (0.58 g/kg per day) or a usual-protein diet (1.3 g/kg day). Outcomes included the rate of GFR decline, incidence of renal failure or death, and change in urine protein excretion. Analyses included comparisons of randomized groups and correlations of outcomes with achieved protein intake. The comparisons of randomized groups revealed a faster GFR decline during the first 4 months after assignment to the low-protein diet but no difference in the variability in GFR decline between the diet groups, indicating a uniform short-term effect of the low-protein diet on GFR, probably as a result of hemodynamic adjustments. After 4 months, the mean decline in GFR in the low-protein diet group was slower, and the variability of the rate of decline was smaller, than in the usual-protein diet group (ratio of standard deviations, 0.73; 95% confidence interval, 0.55 to 0.91; P < 0.01). This suggests a greater beneficial effect of the low-protein diet in patients with a more rapid GFR decline. The net effect of the low-protein diet on GFR decline over 3 yr was no significant change in mean GFR decline, but reduced variability of the decline (ratio of standard deviations, 0.76; 95% confidence interval, 0.60 to 0.92; P < 0.01). Correlational analyses revealed trends similar to the comparisons of randomized groups. During the first 4 months, patients with a greater decline in protein intake (irrespective of diet group) had a greater decline in GFR; thereafter, patients with a lower protein intake had a slower GFR decline. Over 3 yr, there was no significant correlation between GFR decline and achieved protein intake. The correlation of protein intake with GFR decline after 4 months was less strong than observed in Study B. The relative risk of death or renal failure was 0.65 (95% confidence interval, 0.38 to 1.10; P = 0.10) in patients assigned to the low-protein diet group compared with the usual-protein diet group, which is similar to that observed in the meta-analysis. During follow-up, the increase in urine protein excretion was delayed in the low-protein diet group (P = 0.008) and in patients with lower achieved protein intake (P = 0.005). In summary, the absence of a significant difference between the diet groups in the mean change in GFR from baseline to 3 yr precludes a definitive conclusion of a beneficial effect of the diet intervention based solely on MDRD Study A. However, these secondary analyses are consistent with a beneficial effect of the low-protein diet to slow the GFR decline in patients with the most rapidly declining GFR and to reduce urine protein excretion. These results, together with the results of the recent meta-analysis (including MDRD Study A), provide some support for the hypothesis that dietary protein restriction slows the progression of moderate renal disease.

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