Spermatogenesis recovery in protein-restricted rats subjected to a normal protein diet after weaning

2014 ◽  
Vol 26 (6) ◽  
pp. 787 ◽  
Author(s):  
Michelle C. Melo ◽  
Fernanda R. C. L. Almeida ◽  
André L. Caldeira-Brant ◽  
Gleydes G. Parreira ◽  
Hélio Chiarini-Garcia
Keyword(s):  
Sertoli Cell ◽  
Cell Number ◽  
Protein Restriction ◽  
Protein Diet ◽  
Negative Effects ◽  
Adult Rat ◽  
Old Rats ◽  
Normal Protein Diet ◽  
Tubular Diameter ◽  
Protein Restricted Diet

This study investigated the pre- and postnatal effects of protein restriction (8% vs 20% crude protein) on different parameters of spermatogenesis in adult rat offspring. Body and testis weights as well as the seminiferous tubular diameter were reduced in those animals that received the protein-restricted diet after weaning, although these parameters recovered when a 20% protein diet was offered subsequently. The numbers of spermatogonia, spermatocytes, spermatids and Leydig cells were reduced in undernourished animals, whilst the Sertoli cell number did not change. Prenatal programming effect was observed only in the spermatogonial or proliferative phase of spermatogenesis. However, the intake of the normal protein diet after weaning brought many of the testicular parameters evaluated back to normal in 70-day-old rats. A significant reduction of the meiotic index, Sertoli cell supporting capacity and spermatogenic efficiency was observed in animals subjected to protein undernutrition throughout their lives. The data presented show that protein restriction impairs the normal development of the testis in different ways, depending on the period during which the restriction was imposed, and the negative effects on spermatogenesis are more severe when undernutrition occurs from conception to adulthood; however, the return to a normal protein diet after weaning recovers the spermatogenic process.

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 Impact of gestational low-protein intake on embryonic kidney microRNA expression and in the nephron progenitor cells of the male offspring fetus

2020 ◽  
Author(s):  
Leticia B Sene ◽  
Wellerson R Scarano ◽  
Adriana Zapparoli ◽  
Jose AR Gontijo ◽  
Patricia A Boer
Keyword(s):  
Target Genes ◽  
Expression Patterns ◽  
Cell Number ◽  
Protein Restriction ◽  
Protein Diet ◽  
Ki 67 ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Cell Proliferation And Differentiation ◽  
Protein Supply

Abstract Background: Authors demonstrated that gestational low-protein (LP) intake offspring presents a lower birthweight, reduced nephrons numbers and renal salt excretion, arterial hypertension and renal failure development when compared to normal protein (NP) intake rats in adulthood. The current study evaluated the miRNAs and predicted gene expression patterns in the 17-days LP (17-DG) fetal kidney to elucidate the molecular pathways and renal cell proliferation and differentiation profile. Methods: Pregnant Wistar rats were allocated into two groups, according to protein supply during pregnancy: NP (normal protein diet- 17%) or LP (low protein diet-6%). miRNA transcriptome sequencing (miRNA-Seq) was performed on the MiSeq platform and, RT-qPCR of predicted target genes, immunohistochemistry and morphological quantification from 17-DG offspring kidneys using previously described methods. Results: Forty-four expressed miRNAs, which 19 miRNA were up- and 25 downregulated, were identified in 17-DG LP fetuses compared to age-matched NP offspring. The study selected 7 miRNAs related to proliferation, differentiation, and cellular apoptosis processes. The study showed a reduced cell number, Six-2 and c-Myc immunoreactivity in metanephros cap (CM) and ureter bud (UB) in 17-DG LP fetuses. Also, Ki-67 immunoreactivity in CM was 48% lesser in LP compared to NP age-matched fetus. Conversely, in LP CM and UB β-catenin was 154% and 85% markedly enhanced, respectively and, mTOR immunoreactivity was also higher in LP CM (139%) and UB (104%) compared to the NP offspring. UB TGFβ-1 staining cells increased (about 30%) in the LP offspring. Otherwise, Zeb1 metanephros-stained, enhanced 30% in LP offspring without Zeb2 staining in both groups. Conclusions: The present study demonstrates that maternal protein restriction change miRNAs, mRNAs, and critical proteins expression involved in the processes of proliferation, differentiation, and apoptosis that occurs during renal development. The renal ontogenic dysfunction caused by maternal protein restriction promotes a reduced reciprocal interaction between CM and UB, and consequently, a programmed and expressive decrease in the nephron number fetuses.

scholarly journals Morphometric Studies of Compensatory Testicular Hypertrophy in the Rat after Hemicastration

1982 ◽  
Vol 35 (3) ◽  
pp. 287 ◽  
Author(s):  
DKH Putra ◽  
AW Blackshaw
Keyword(s):  
Sertoli Cell ◽  
Germ Cells ◽  
Cell Number ◽  
Compensatory Hypertrophy ◽  
Male Rats ◽  
Testis Weight ◽  
Cross Sectional ◽  
Old Rats ◽  
Testicular Hypertrophy ◽  
Quantitative Nature

The quantitative nature of the compensatory testicular hypertrophy following unilateral castration was examined in groups of immature Wistar-derived male rats hemicastrated at 10, 20, 30, 40 and 50 days of age and completely castrated 20 days later. Hemicastration resulted in compensatory hypertrophy of the remaining testis and it decreased as the animals aged. In 30-day-old rats compensatory testicular hypertrophy was 33 % while at 70 days of age hypertrophy was reduced to 2 %. The increase in testis weight of hemicastrated rats was correlated with an increase in total seminiferous tubule length and a larger cross-sectional area which was due in part to the greater number of germ cells per testis. Sertoli cell number did not increase significantly in the hemicastrated testis but more germ cells were associated with each Sertoli cell.

scholarly journals The Colonic Microbiome and Epithelial Transcriptome Are Altered in Rats Fed a High-Protein Diet Compared with a Normal-Protein Diet

2016 ◽  
Vol 146 (3) ◽  
pp. 474-483 ◽  
Author(s):  
Chunlong Mu ◽  
Yuxiang Yang ◽  
Zhen Luo ◽  
Leluo Guan ◽  
Weiyun Zhu
Keyword(s):  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Normal Protein Diet

Arachidonic acid mediates dual effect of TNF-α on Ca2+ transients and contraction of adult rat cardiomyocytes

2002 ◽  
Vol 282 (6) ◽  
pp. C1339-C1347 ◽  
Author(s):  
Aïssata Amadou ◽  
Artur Nawrocki ◽  
Martin Best-Belpomme ◽  
Catherine Pavoine ◽  
Françoise Pecker
Keyword(s):  
Arachidonic Acid ◽  
Cyclooxygenase Inhibitors ◽  
High Dose ◽  
Negative Effects ◽  
Dual Effect ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Tnf Α ◽  
Biphasic Effect

Tumor necrosis factor (TNF)-α has a biphasic effect on heart contractility and stimulates phospholipase A2 (PLA2) in cardiomyocytes. Because arachidonic acid (AA) exerts a dual effect on intracellular Ca2+ concentration ([Ca2+]i) transients, we investigated the possible role of AA as a mediator of TNF-α on [Ca2+]i transients and contraction with electrically stimulated adult rat cardiac myocytes. At a low concentration (10 ng/ml) TNF-α produced a 40% increase in the amplitude of both [Ca2+]i transients and contraction within 40 min. At a high concentration (50 ng/ml) TNF-α evoked a biphasic effect comprising an initial positive effect peaking at 5 min, followed by a sustained negative effect leading to 50–40% decreases in [Ca2+]i transients and contraction after 30 min. Both the positive and negative effects of TNF-α were reproduced by AA and blocked by arachidonyltrifluoromethyl ketone (AACOCF3), an inhibitor of cytosolic PLA2. Lipoxygenase and cyclooxygenase inhibitors reproduced the high-dose effects of TNF-α and AA. The negative effects of TNF-α and AA were also reproduced by sphingosine and were abrogated by the ceramidase inhibitor n-oleoylethanolamine. These results point out the key role of the cytosolic PLA2/AA pathway in mediating the contractile effects of TNF-α.

Increase in Cell Number as a Factor in the Growth of the Organs and Tissues of the Young Male Rat

Development ◽  
1962 ◽  
Vol 10 (4) ◽  
pp. 530-562
Author(s):  
M. Enesco ◽  
C. P. Leblond
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Room Temperature ◽  
Young Male ◽  
Cell Number ◽  
The Body ◽  
Male Rat ◽  
The Past ◽  
Old Rats ◽  
Young Rat

While the organs and tissues of the young rat are known to increase in size with age (Donaldson, 1924), little is known of the role played by the component cells in this increase. There is evidence that cells enlarge (Levi, 1906; Plenk, 1911) and new cells are added (Strasburger, 1893), but we do not know to what extent the enlargement and proliferation of the cells cause the growth of organs and tissues. The present work is an attempt to clarify this problem. In the past, the growth of organs and tissues has often been measured by weight gain (Donaldson, 1924). However, this approach might be misleading, since the body-weight may increase in the absence of growth, for instance as a result of fat-storage in old rats, of pregnancy in females, and even of changes in room temperature.

Antecedent protein restriction exacerbates development of impaired insulin action after high-fat feeding

1999 ◽  
Vol 276 (1) ◽  
pp. E85-E93 ◽  
Author(s):  
Mark J. Holness ◽  
Mary C. Sugden
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Action ◽  
Protein Restriction ◽  
Protein Diet ◽  
Glucose Disposal ◽  
High Fat ◽  
Impaired Insulin ◽  
Impaired Insulin Action ◽  
Fat Feeding

The study investigated whether a persistent impairment of insulin secretion resulting from mild protein restriction predisposes to loss of glucoregulatory control and impaired insulin action after the subsequent imposition of the diabetogenic challenge of high-fat feeding. Offspring of dams provided with either control (20% protein) diet (C) or an isocaloric restricted (8%) protein diet (PR) were weaned onto the maintenance diet with which their mothers had been provided. At 20 wk of age, protein restriction enhanced glucose tolerance despite impaired insulin secretion and an augmented and sensitized lipolytic response to norepinephrine in adipocytes. C and PR rats were then transferred to a high-fat diet (HF, 19% protein, 22% lipid, 34% carbohydrate) and sampled after 8 wk. These groups are termed C-HF and PR-HF. Glucose tolerance was impaired in PR-HF, but not C-HF, rats. Insulin-stimulated glucose disposal rates were significantly lower (by 30%; P < 0.01) in the PR-HF group than in the C-HF group, and a specific impairment of antilipolytic response of insulin was unmasked in adipocytes from PR-HF, but not C-HF, rats. The study demonstrates that antecedent protein restriction accelerates and augments the development of impaired glucoregulation and insulin resistance after high-fat feeding.

scholarly journals Survival on dialysis among chronic renal failure patients treated with a supplemented low-protein diet before dialysis.

1995 ◽  
Vol 6 (5) ◽  
pp. 1379-1385
Author(s):  
J Coresh ◽  
M Walser ◽  
S Hill
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Mortality Rate ◽  
Serum Creatinine ◽  
Dietary Treatment ◽  
Mortality Rates ◽  
Protein Restriction ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Low Protein

Concerns have been raised about the possibility of protein restriction resulting in malnutrition and poor subsequent survival on dialysis. However, no studies have examined patients treated with protein restriction to determine their subsequent survival on dialysis. This study prospectively monitored 67 patients with established chronic renal failure (mean initial serum creatinine of 4.3 mg/dL) who were treated with a very low-protein diet (0.3 g/kg per day) supplemented with either essential amino acids or a ketoacid-amino acid mixture and observed closely for clinical complications. Forty-four patients required dialysis. Once dialysis was started, dietary treatment was no longer prescribed. The cumulative mortality rate during the first 2 yr after starting dialysis was 7% (95% confidence interval, 0 to 16%). During this period, only two deaths occurred compared with 11.5 deaths expected on the basis of national mortality rates adjusted for age, sex, race, and cause of renal disease (P = 0.002). However, the protective effect was limited to the first 2 yr on dialysis. Thereafter, mortality rates increased, resulting in a total of 10 deaths during 96.4 person-years of follow-up, which was not significantly lower than the 14.9 deaths expected (P = 0.25). Extrapolation of sequential serum creatinine measurements made before dietary treatment suggests that the improved survival cannot be due to the early initiation of dialysis. Although the lack of an internal control group and data on dialysis lends uncertainty, the large difference in mortality rate between these patients and the nationwide experience indicates that protein restriction and close clinical monitoring predialysis does not worsen and may substantially improve survival during the first 2 yr on dialysis. These findings point out the importance of studying predialysis treatments as a means for lowering mortality on dialysis.

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