scholarly journals Maternal protein restriction differentially alters the expression of AQP1, AQP9 and VEGFr-2 in the epididymis of rat offspring

2019 ◽  
Vol 20 (3) ◽  
pp. 469 ◽  
Author(s):  
Marilia Martins Cavariani ◽  
Talita de Mello Santos ◽  
Dhrielly Natalia Pereira ◽  
Luiz Gustavo de Almeida Chuffa ◽  
Patricia Fernanda Felipe Pinheiro ◽  
...  
Keyword(s):  
Protein Restriction ◽  
Male Rats ◽  
Standard Diet ◽  
Vascular Endothelial ◽  
Pregnant Rats ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Endothelial Growth Factor ◽  
Development Methods ◽  
Protein Diets

Background: Maternal protein restriction causes sperm alterations in the offspring, most of which are associated with epididymal functions. Because fluid reabsorption/secretion dynamics in the epididymal environment play important roles in the process of sperm maturation and concentration, we investigated the effects of maternal protein restriction on the expression of aquaporins (AQP1 and AQP9), vascular endothelial growth factor (VEGFa), and its receptor VEGFr-2 in different stages of postnatal epididymal development. Methods: Pregnant rats were divided into groups that received normoprotein (17% protein) and low-protein diets (6% protein) during gestation and lactation. After weaning, male rats only received the standard diet and were euthanized at the predetermined ages of 21, 44 and 120 days. Results: Maternal protein restriction decreased AQP1 and AQP9 expression in the initial segment and caput epididymis compared to the increased expression of these proteins observed in the corpus and cauda at all ages. Although protein restriction reduced the microvasculature density (MVD) on postnatal day (PND) 21 and 44, the MVD was unaltered on PND 120. Conclusions: Maternal protein restriction changed the structure or function of the offspring’s epididymis, specifically by affecting fluid dynamics and vasculogenesis in important stages of epididymis development.

Modest maternal protein restriction fails to program adult hypertension in female rats

2005 ◽  
Vol 289 (4) ◽  
pp. R1131-R1136 ◽  
Author(s):  
Lori L. Woods ◽  
Julie R. Ingelfinger ◽  
Ruth Rasch
Keyword(s):  
Renin Angiotensin System ◽  
Female Gender ◽  
Female Offspring ◽  
Protein Restriction ◽  
Female Rats ◽  
Male Rats ◽  
Pregnant Rats ◽  
Angiotensin System ◽  
Low Protein ◽  
Maternal Protein Restriction

Modest maternal dietary protein restriction in the rat leads to hypertension in adult male offspring. The purpose of this study was to determine whether female rats are resistant to developing the increased blood pressure seen in male rats after maternal protein restriction. Pregnant rats were fed a normal protein (19%, NP) or low-protein (8.5%, LP) diet throughout gestation. Renal renin protein and ANG II levels were reduced by 50–65% in male LP compared with NP pups, but were not suppressed in female LP compared with female NP. Mean arterial pressure in conscious, chronically instrumented adult female offspring (22 wk) was not different in LP (LP: 120 ± 3 mmHg vs. NP: 121 ± 2 mmHg), and glomerular filtration rate was also not different in LP vs. NP. The number of glomeruli per kidney was similar in adult LP and NP female offspring (LP: 26,050 ± 2,071 vs. NP: 26,248 ± 1,292, NP), and individual glomerular volume was also not different (LP: 0.92 ± 0.11 106μm3, LP vs. NP: 1.07 ± 0.11 106μm3); the total volume of all glomeruli per kidney was also not significantly different. Thus female rats are relatively resistant to the programming for adult hypertension by perinatal protein restriction that we have described in males. This resistance may be due to the fact that modest maternal protein restriction does not reduce the number of glomeruli with which females are endowed as it does in males. The intrarenal renin-angiotensin system during development may play a key role in this protective effect of female gender.

scholarly journals Maternal Protein Restriction Modulates Angiogenesis and AQP9 Expression Leading to a Delay in Postnatal Epididymal Development in Rat

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 1094 ◽  
Author(s):  
Talita de Mello Santos ◽  
Marilia Martins Cavariani ◽  
Dhrielly Natália Pereira ◽  
Bruno César Schimming ◽  
Luiz Gustavo de Almeida Chuffa ◽  
...  
Keyword(s):  
Well Being ◽  
Protein Restriction ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Pregnant Rats ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Aqp1 Expression ◽  
In The Beginning ◽  
Endothelial Growth Factor

The maternal nutritional status is essential to the health and well-being of the fetus. Maternal protein restriction during the perinatal stage causes sperm alterations in the offspring that are associated with epididymal dysfunctions. Vascular endothelial growth factor (VEGF) and its receptor, VEGFr-2, as well as aquaporins (AQPs) are important regulators of angiogenesis and the epididymal microenvironment and are associated with male fertility. We investigated the effects of maternal protein restriction on epididymal angiogenesis and AQP expression in the early stages of postnatal epididymal development. Pregnant rats were divided into two experimental groups that received either a normoprotein (17% protein) or low-protein diet (6% protein) during gestation and lactation. At postnatal day (PND)7 and PND14, male offspring were euthanized, the epididymides were subjected to morphometric and microvascular density analyses and to VEGF-A, VEGF-r2, AQP1 and AQP9 expression analyses. The maternal low-protein diet decreased AQP9 and VEGFr-2 expression, decreased epididymal microvascularity and altered the morphometric features of the epididymal epithelium; no changes in AQP1 expression were observed at the beginning of postnatal epididymal development. Maternal protein restriction alters microvascularization and affects molecules involved in the epidydimal microenvironment, resulting in morphometric alterations related to a delay in the beginning of epididymis postnatal development.

scholarly journals Diabetes in Old Male Offspring of Rat Dams Fed a Reduced Protein Diet

2001 ◽  
Vol 2 (2) ◽  
pp. 139-143 ◽  
Author(s):  
Clive J. Petry ◽  
Matthew W. Dorling ◽  
Dorota B. Pawlak ◽  
Susan E. Ozanne ◽  
C. Nicholas Hales
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Protein Restriction ◽  
Male Rats ◽  
Male Rat ◽  
Intravenous Glucose ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Increased Risk ◽  
Intravenous Glucose Tolerance Tests

Restricted fetal growth is associated with increased risk for the future development of Type 2 diabetes in humans. The study aim was to assess the glucose tolerance of old (seventeen months) male rats, which were growth restricted in early life due to maternal protein restriction during gestation and lactation. Rat mothers were fed diets containing either 20% or 8% protein and all offspring weaned onto a standard rat diet. In old-age fasting plasma glucose concentrations were significantly higher in the low protein offspring: 8.4 (1.3)mmol/l v. 5.3 (1.3)mmol/l (p = 0.005), Areas under the curves were increased by 67% for glucose (p = 0.01) and 81% for insulin (p = 0.01) in these rats in intravenous glucose tolerance tests, suggesting (a degree of) insulin resistance. These results show that early growth retardation due to maternal protein restriction leads to the development of diabetes in old male rat offspring. The diabetes is predominantly associated with insulin resistance.

scholarly journals Sodium hydrosulfide prevents hypertension and increases in vascular endothelial growth factor and soluble fms-like tyrosine kinase-1 in hypertensive pregnant rats

2016 ◽  
Vol 389 (12) ◽  
pp. 1325-1332 ◽  
Author(s):  
Jose Sergio Possomato-Vieira ◽  
Victor Hugo Gonçalves-Rizzi ◽  
Tamiris Uracs Sales Graça ◽  
Regina Aparecida Nascimento ◽  
Carlos A. Dias-Junior
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Vascular Endothelial ◽  
Pregnant Rats ◽  
Sodium Hydrosulfide ◽  
Endothelial Growth Factor

Weanling Rats Exposed to Maternal Low-Protein Diets during Discrete Periods of Gestation Exhibit Differing Severity of Hypertension

1996 ◽  
Vol 91 (5) ◽  
pp. 607-615 ◽  
Author(s):  
Simon C. Langley-Evans ◽  
Simon J. M. Welham ◽  
Rachel C. Sherman ◽  
Alan A. Jackson
Keyword(s):  
Blood Pressure ◽  
Control Diet ◽  
Plasma Renin ◽  
Late Gestation ◽  
Protein Diet ◽  
Male Rats ◽  
Low Protein Diet ◽  
Fetal Exposure ◽  
Low Protein ◽  
Protein Diets

1. In the rat, hypertension is induced by fetal exposure to maternal low-protein diets. The effect on blood pressure of undernutrition before conception and during discrete periods in early, mid or late pregnancy was assessed using an 18% casein (control) diet and a 9% casein diet to apply mild protein restriction. 2. The offspring of rats fed 9% casein developed raised blood pressure by weaning age. Feeding a low-protein diet before conception was not a prerequisite for programming of hypertension. 3. Hypertension was observed in rats exposed to low protein during the following gestational periods: days 0–7, days 8–14 and days 15–22. Blood pressure increases elicited by these discrete periods of undernutrition were lower than those induced by feeding a low-protein diet throughout pregnancy. The effect in early gestation was significant only in male animals. Post-natal growth of male rats exposed to low-protein diets was accelerated, but kidneys were small in relation to body weight. 4. Biochemical indices of glucocorticoid action in liver, hippocampus, hypothalamus and lung were elevated in rats exposed to low-protein diets in utero. The apparent hypersensitivity to glucocorticoids was primarily associated with undernutrition in mid to late gestation. 5. Plasma renin activity was elevated in rats exposed to 9% casein over days 15–22 of gestation. Animals undernourished over days 0–7 and 8–14 produced pups with lower plasma angiotensin II concentrations at weaning. 6. Fetal exposure to maternal low-protein diets for any period in gestation may programme hypertension in the rat. Alterations to renal structure, renal hormone action or the hypothalamic—pituitary-adrenal axis may all play a role in the programming phenomenon, either independently or in concert.

scholarly journals Long-Term Effects of Maternal Low-Protein Diet and Post-weaning High-Fat Feeding on Glucose Metabolism and Hypothalamic POMC Promoter Methylation in Offspring Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Jia Zheng ◽  
Ling Zhang ◽  
Jiayi Liu ◽  
Yanli Li ◽  
Junqing Zhang
Keyword(s):  
Glucose Metabolism ◽  
Critical Role ◽  
Protein Restriction ◽  
Male Offspring ◽  
Melanocortin Receptor ◽  
High Fat ◽  
Altered Expression ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Fat Feeding

Substantial evidence indicated that maternal malnutrition could increase the susceptibility to obesity, insulin resistance, and type 2 diabetes in adulthood. It is increasingly apparent that the brain, especially the hypothalamus, plays a critical role in glucose homeostasis. However, little information is known about the mechanisms linking maternal protein restriction combined with post-weaning high-fat (HF) feeding with altered expression of brain neurotransmitters, and investigations into the epigenetic modifications of hypothalamus in offspring have not been fully elucidated. Our objective was to explore the effects of maternal protein restriction combined with post-weaning HF feeding on glucose metabolism and hypothalamic POMC methylation in male offspring mice. C57/BL6 mice were fed on either low-protein (LP) or normal chow (NC) diet throughout gestation and lactation. Then, the male offspring were randomly weaned to either NC or high-fat (HF) diet until 32 weeks of age. Gene expressions and DNA methylation of hypothalamic proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R) were determined in male offspring. The results showed that birth weights and body weights at weaning were both significantly lower in male offspring mice of the dams fed with a LP diet. Maternal protein restriction combined with post-weaning high-fat feeding, predisposes higher body weight, persistent glucose intolerance (from weaning to 32 weeks of age), hyperinsulinemia, and hyperleptinemia in male offspring mice. POMC and MC4R expressions were significantly increased in offspring mice fed with maternal LP and postnatal high-fat diet (P < 0.05). Furthermore, maternal protein restriction combined with post-weaning high-fat feeding induced hypomethylation of POMC promoter in the hypothalamus (P < 0.05) and POMC-specific methylation (%) was negatively correlated with the glucose response to a glucose load in male offspring mice (r = −0.42, P = 0.039). In conclusion, maternal LP diet combined with post-weaning high-fat feeding predisposed the male offspring to impaired glucose metabolism and hypothalamic POMC hypomethylation. These findings can advance our thinking about hypothalamic POMC gene methylation between maternal LP diet combined with post-weaning high-fat feeding and metabolic health in offspring.

scholarly journals Influence of L-lactic acid on the efficacy of microbial phytase in broiler chickens

2011 ◽  
Vol 49 (No. 10) ◽  
pp. 436-443 ◽  
Author(s):  
P. Zobač ◽  
I. Kumprecht ◽  
P. Suchý ◽  
E. Straková ◽  
J. Brož ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Broiler Chickens ◽  
Standard Diet ◽  
Feed Conversion ◽  
Low Protein ◽  
Final Weight ◽  
Microbial Phytase ◽  
Dietary Treatments ◽  
Protein Diets ◽  
Growth Trial

Two growth trials and a short-term metabolism trial were conducted in broiler chickens in the period of 22 to 42 days of age in order to evaluate the effects of two dietary levels of L-lactic acid (1.03 or 2.06 g/kg) and microbial 6-phytase (750 U/kg), added either separately or in combination, on growth rate, feed conversion, dressing percentage and utilization of selected nutrients. In the first growth trial, six different dietary treatments were added to a basal grower diet containing 19.4% crude protein and a reduced level of dietary phosphorus (P) (5.9 g total and 2.9 g non-phytate P per kg). Single administration of L-lactic acid did not show any positive effect on the growth rate or feed conversion. In contrast, phytase addition to a low-P grower diet resulted in the increased final weight of birds and higher feed conversion. This beneficial effect was markedly stronger when the microbial phytase was added to the diets containing L-lactic acid. Based on two-factor analysis of variance, microbial phytase significantly increased the mean final weight by 6.5% (P < 0.01) and significantly improved feed conversion from 1.877 to 1.829 (P < 0.05). In the second growth trial, the same six dietary treatments were added to a basal diet containing a standard level of dietary P (6.7 g total and 4.0 g non-phytate P per kg), but the level of crude protein was reduced to 17.0%. L-lactic acid alone did not show any positive effects on performance. Phytase supplementation alone resulted in numerical improvement of the final weight (+1.1–2.4%), but a higher effect was observed in the diets containing L-lactic acid. In agreement with the reduced final weights of broilers fed the low-protein diets, markedly higher values of feed/gain ratio were noted. In the metabolism trial, selected dietary treatments were involved to evaluate the effects of L-lactic acid and microbial phytase, added either separately or in combination, on the digestibility of nitrogen (N) and fat as well as on the retention and excretion of N and P. Apparent digestibility of N and fat in the low-P diets was not affected by dietary treatments. Retention and utilization of N were numerically higher in all treatments fed low-P diets when compared to the treatment fed a standard diet, but the differences were not significant. Retention of P was numerically higher in all treatments fed low-P diets. When compared to the standard diet, the combination of phytase and L-lactic acid increased daily P retention by 37.6%. P excretion was significantly (P < 0.05) reduced in all treatments fed low-P diets supplemented by both test products, either separately or in combination. A numerical decrease in N excretion was noted in both treatments fed low-protein diets.    

COMPARATIVE EFFECTS OF SUCROSE AND CORNSTARCH IN LOW-PROTEIN DIETS FED TO RATS EXPOSED TO COLD

1965 ◽  
Vol 43 (2) ◽  
pp. 241-249
Author(s):  
J. R. Beaton ◽  
J. F. Sangster
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Young Male ◽  
Male Rats ◽  
Low Protein ◽  
Environmental Temperatures ◽  
Protein Diets ◽  
Starch Diet

Young male rats were fed one of three low-protein (5% casein) diets differing in the source of carbohydrate (sucrose, equal parts sucrose and cornstarch, or cornstarch) or a 20% casein (sucrose) diet at environmental temperatures of 24 °C or 5 °C. Replacement of sucrose with starch appeared to have a small but significant effect in increasing body weight gain for 15 days (but not the next 28 days) at 24 °C and also in animals exposed to cold for 28 days after a 15-day feeding period at 24 °C. In disagreement with results reported by Andik et al., cold exposure, although significantly increasing body weight gain and food intake in rats fed the 5% casein – starch diet, did not elicit a weight gain as great as that observed in 20% casein-fed animals at either 24 °C or 5 °C. The 24-hour food intake following a 24-hour fast exceeded the intake on the day before fasting on all diets for animals maintained at 5 °C but not 24 °C. The immediate ([Formula: see text] hour) and 24-hour food intakes of rats at 5 °C exceeded those of comparable dietary groups at 24 °C. At 5 °C, the 24-hour food intake, following the fast, of rats fed the 5% casein – starch diet exceeded that of the 20% casein-fed controls.

scholarly journals The maternal endocrine environment in the low-protein model of intra-uterine growth restriction

2003 ◽  
Vol 90 (4) ◽  
pp. 815-822 ◽  
Author(s):  
D. S. Fernandez-Twinn ◽  
S. E. Ozanne ◽  
S. Ekizoglou ◽  
C. Doherty ◽  
L. James ◽  
...  
Keyword(s):  
Maternal Plasma ◽  
Protein Restriction ◽  
Control Group ◽  
Adult Disease ◽  
Fetal Plasma ◽  
Low Protein ◽  
Maternal Protein Restriction ◽  
Uterine Growth ◽  
Placental Blood ◽  
Mechanistic Basis

Many adult diseases, including type 2 diabetes, hypertension and cardiovascular disease, are related to low birth weight. The mechanistic basis of this relationship is not known. To investigate the role of fetal undernutrition, we used a rat model of maternal protein restriction in which dams were fed a diet containing 80 g protein/kg (v. 200 g/kg in the control group) throughout gestation and lactation. Offspring were born smaller than controls and in adulthood developed diabetes, hyperinsulinaemia and tissue insulin resistance. To determine possible mechanisms of fetal programming, circulating levels of several hormones were measured in maternal plasma at gestational days 14, 17 and 21 and fetal plasma at gestational day 21. Several differences were noted at day 14, when glucose concentrations in maternal and feto–placental blood were raised significantly (P=0·04 and P=0·0001 respectively); insulin levels in the low-protein (LP) dams were raised (P=0·04), prolactin levels were raised (P=0·047) and progesterone levels were reduced (P=0·02). Circulating 17β-oestradiol in the LP dams was raised by 35% over those of the controls from day 17 to day 21 (P=0·008). A significant decrease in maternal leptin levels (P=0·004) was observed at gestation on day 21. Neither oestradiol nor leptin levels were altered in the fetal circulation at day 21. Maternal and fetal corticosterone levels were comparable with control levels, suggesting that they do not initiate the programming effects in this model. Our present results suggest that maternal protein restriction imposes changes in maternal levels of glucose, insulin, prolactin, progesterone, oestradiol and leptin; these changes could influence the programming of eventual adult disease in the developing fetus.

Maternal protein restriction compromises myocardial contractility in the young adult rat by changing proteins involved in calcium handling

2016 ◽  
Vol 120 (3) ◽  
pp. 344-350 ◽  
Author(s):  
Aucelia C. S. de Belchior ◽  
David D. Freire ◽  
Carlos P. da Costa ◽  
Dalton V. Vassallo ◽  
Alessandra S. Padilha ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Young Adult ◽  
Left Ventricular ◽  
Protein Restriction ◽  
Female Rats ◽  
Male Rats ◽  
Calcium Handling ◽  
Myocardial Mechanics ◽  
Maternal Protein Restriction ◽  
Calcium Handling Proteins

Maternal protein restriction (MPR) during pregnancy is associated with increased cardiovascular risk in the offspring in adulthood. In this study we evaluated the cardiac function of young male rats born from mothers subjected to MPR during pregnancy, focusing on the myocardial mechanics and calcium-handling proteins. After weaning, rats received normal diet until 3 mo old, when the following parameters were assessed: arterial and left ventricular hemodynamics and in vitro cardiac contractility in isolated papillary muscles. The body weight was lower and arterial pressure higher in the MPR group compared with young adult offspring of female rats that received standard diet (controls); and left ventricle time derivatives increased in the MPR group. The force developed by the cardiac muscle was similar; but time to peak and relaxation time were longer, and the derivatives of force were depressed in the MPR. In addition, MPR group exhibited decreased post-pause potentiation of force, suggesting reduced reuptake function of the sarcoplasmic reticulum. Corroborating, the myocardial content of SERCA-2a and phosphorylated PLB-Ser16/total PLB ratio was decreased and sodium-calcium exchanger was increased in the MPR group. The contraction dependent on transsarcolemmal influx of calcium was higher in MPR if compared with the control group. In summary, young rats born from mothers subjected to protein restriction during pregnancy exhibit changes in the myocardial mechanics with altered expression of calcium-handling proteins, reinforcing the hypothesis that maternal malnutrition is related to increased cardiovascular risk in the offspring, not only for hypertension, but also cardiac dysfunction.

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