scholarly journals Somatomedin-C and zinc status in rats as affected by Zn, protein and food intake

1986 ◽  
Vol 56 (1) ◽  
pp. 163-169 ◽  
Author(s):  
Zafrallah T. Cossack
Keyword(s):  
Food Intake ◽  
Body Weight Gain ◽  
Experimental Period ◽  
Optimal Level ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Control Group ◽  
Somatomedin C ◽  
Low Protein ◽  
Adequate Food

1. The objective of the present experiment was to study the level of plasma somatomedin-C (SM-C) and the status of zinc in rats as affected by three levels of Zn given in combinations with two levels of protein.2. Six groups of rats were fed, for 21 d, on six different diets based on combinations of two levels of dietary protein (low protein, 75 g/kg; high protein, 200 g/kg) and three levels of zinc (low Zn, 0.9 pglkg; moderate Zn, 55 pg/kg; high Zn, 110 pglkg). All groups were pair-fed with the group receiving the low-Zn-low-protein diet. An additional group of six rats served as an ad lib.-fed control group and was fed on a diet that contained 55 pg Zn/kg and 200 g protein/kg ad lib.3. Body-weight gain and food intake were recorded daily. Rats were killed at the end of the experimental period (21 d). Zn was assayed in plasma, tibia and liver by atomic absorption technique. Plasma SM-C was assayed by radioimmunoassay.4. In rats given the low-Zn-low-protein diet, the level of plasma SM-C increased in response to the increase in the amount of Zn or Zn and protein in the diet. However, no change was observed when the level of protein alone was increased.5. Among all groups tested, adlib.-fed rats showed the highest level of plasma SM-C. Thus it may be concluded that a balanced diet combined with adequate food intake is necessary to maintain an optimal level of plasma SM-C.

scholarly journals Phosphorus Supplementation Mitigated Food Intake and Growth of Rats Fed a Low-Protein Diet

2017 ◽  
Vol 1 (8) ◽  
pp. e000943 ◽  
Author(s):  
Rola U Hammoud ◽  
Mark N Jabbour ◽  
Ayman N Tawil ◽  
Hala Ghattas ◽  
Omar A Obeid
Keyword(s):  
Food Intake ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Low Protein

scholarly journals Effect of prenatal programming and postnatal rearing on glomerular filtration rate in adult rats

2015 ◽  
Vol 308 (5) ◽  
pp. F411-F419 ◽  
Author(s):  
German Lozano ◽  
Ayah Elmaghrabi ◽  
Jordan Salley ◽  
Khurrum Siddique ◽  
Jyothsna Gattineni ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Control Group ◽  
Adult Rats ◽  
Pregnant Rats ◽  
Mature Adult ◽  
Low Protein

The present study examined whether a prenatal low-protein diet programs a decrease in glomerular filtration rate (GFR) and an increase in systolic blood pressure (BP). In addition, we examined whether altering the postnatal nutritional environment of nursing neonatal rats affected GFR and BP when rats were studied as adults. Pregnant rats were fed a normal (20%) protein diet or a low-protein diet (6%) during the last half of pregnancy until birth, when rats were fed a 20% protein diet. Mature adult rats from the prenatal low-protein group had systolic hypertension and a GFR of 0.38 ± 0.03 versus 0.57 ± 0.05 ml·min−1·100 g body wt−1 in the 20% group ( P < 0.01). In cross-fostering experiments, mothers continued on the same prenatal diet until weaning. Prenatal 6% protein rats cross-fostered to a 20% mother on day 1 of life had a GFR of 0.53 ± 0.05 ml·min−1·100 g body wt−1, which was not different than the 20% group cross-fostered to a different 20% mother (0.45 ± 0.04 ml·min−1·100 g body wt−1). BP in the 6% to 20% group was comparable with the 20% to 20% group. Offspring of rats fed either 20% or 6% protein diets during pregnancy and cross-fostered to a 6% mother had elevated BP but a comparable GFR normalized to body weight as the 20% to 20% control group. Thus, a prenatal low-protein diet causes hypertension and a reduction in GFR in mature adult offspring, which can be modified by postnatal rearing.

Erratum: Factors in the reduced food intake of rats fed a low-protein diet

1968 ◽  
Vol 46 (4) ◽  
pp. 702-702
Author(s):  
J. R. Beaton ◽  
V. Feleki ◽  
J. A. F. Stevenson
Keyword(s):  
Food Intake ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Low Protein

INSULIN HYPERPHAGIA IN RATS FED A LOW-PROTEIN DIET

1965 ◽  
Vol 43 (2) ◽  
pp. 225-233 ◽  
Author(s):  
J. R. Beaton ◽  
V. Feleki ◽  
J. A. F. Stevenson
Keyword(s):  
Food Intake ◽  
Body Fat ◽  
Normal Diet ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Eating Pattern ◽  
Low Protein ◽  
Running Activity ◽  
Male Wistar Rats ◽  
Rebound Increase

This investigation was undertaken to ascertain if daily treatment with insulin, known to increase lipogenesis, fat deposition, and food intake on a normal diet, could overcome or prevent, the hypophagia of rats fed a low-protein (5% casein) diet. Male Wistar rats on 20 or 5% casein diets were injected subcutaneously daily for 25 days with 2 units/100 g body weight of protamine zinc insulin (PZI) or saline. PZI increased the food intake and weight gain on both diets but not linear growth. It increased body fat markedly and protein slightly on the low-protein diet and body fat only on the normal diet. In a second similar experiment, in which treatment was continued for 17 days, PZI caused no change in resting oxygen consumption from that of the controls on either diet but did prevent the increase in running activity that rats on a low-protein diet show. In both experiments, although the insulin-treated rats on low-protein diet ate as many calories as the saline-treated controls on the normal diet, they gained significantly less weight. This paradox remains unexplained.The rebound increase in blood sugar following injection of PZI was relatively much faster in the low-protein animals. This was associated with a more immediate and greater food intake suggesting a "meal-eating" pattern of food intake in these animals which may have also enhanced lipogenesis.

scholarly journals A low-protein diet supplemented with ketoacids plays a more protective role against oxidative stress of rat kidney tissue with 5/6 nephrectomy than a low-protein diet alone

2009 ◽  
Vol 103 (4) ◽  
pp. 608-616 ◽  
Author(s):  
Xiang Gao ◽  
Jianxiang Wu ◽  
Zheyi Dong ◽  
Can Hua ◽  
Huimin Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Tissue ◽  
Protein Restriction ◽  
Protein Malnutrition ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Glomerular Sclerosis ◽  
Control Group ◽  
Stress Injury ◽  
Low Protein

Dietary protein restriction is one major therapy in chronic kidney disease (CKD), and ketoacids have been evaluated in CKD patients during restricted-protein diets. The objective of the present study was to compare the efficacy of a low-protein diet supplemented with ketoacids (LPD+KA) and a low-protein diet alone (LPD) in halting the development of renal lesions in CKD. 5/6 Nephrectomy Sprague–Dawley rats were randomly divided into three groups, and fed with either 22 % protein (normal-protein diet; NPD), 6 % protein (LPD) or 5 % protein plus 1 % ketoacids (LPD+KA) for 24 weeks. Sham-operated rats were used as controls. Each 5/6 nephrectomy group included fifteen rats and the control group included twelve rats. Proteinuria, decreased renal function, glomerular sclerosis and tubulointerstitial fibrosis were found in the remnant kidneys of the NPD group. Protein restriction ameliorated these changes, and the effect was more obvious in the LPD+KA group after 5/6 nephrectomy. Lower body weight and serum albumin levels were found in the LPD group, indicating protein malnutrition. Lipid and protein oxidative products were significantly increased in the LPD group compared with the LPD+KA group. These findings indicate that a LPD supplemented with ketoacids is more effective than a LPD alone in protecting the function of remnant kidneys from progressive injury, which may be mediated by ketoacids ameliorating protein malnutrition and oxidative stress injury in remnant kidney tissue.

scholarly journals Low-protein diet prevents tissue lipoprotein lipase activity increase in growing rats

2000 ◽  
Vol 84 (5) ◽  
pp. 663-671 ◽  
Author(s):  
A. Boualga ◽  
M. Bouchenak ◽  
J. Belleville
Keyword(s):  
G Protein ◽  
Lipoprotein Lipase ◽  
Wheat Gluten ◽  
Lipid Storage ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Control Group ◽  
Fat Tissue ◽  
Low Protein ◽  
Epididymal Fat

The time course of changes in tissue lipolytic activities was studied in young rats during the consumption of a low-protein diet containing 50 g protein/kg (40 g wheat gluten +10 g casein/kg) for 28 d followed by balanced refeeding with 200 g protein/kg (160 g wheat gluten +40 g casein/kg) for 28 d. Lipoprotein lipase (LPL) activities were compared with the values of a control group fed a balanced diet containing 200 g protein/kg for 56 d. At the end of protein malnutrition period, the epididymal fat tissue LPL activity represented 36 %, and that of heart and gastrocnemius was 44 %, of those of the control group. These differences were accompanied by lower serum- and VLDL-triacylglycerols (TAG), respectively 47·6 % and 31 % of the control group values, probably resulting from reduced synthesis of VLDL-apolipoproteins (29 % of control group values), concomitant with liver lipid accumulation (4·8-fold) and little lipid storage in epididymal fat tissue. At day 2 of refeeding, there was no significant difference in liver and epididymal fat tissue LPL activities between experimental and control rats. At the end of the refeeding period, LPL activity of epididymal fat and liver lipolytic activity had increased and became similar to control group values. The consumption of a low-protein diet prevented the increase in extrahepatic LPL activities as observed in the control group. The alterations in LPL activity suggest that a low-protein diet limits lipid storage in adipose tissue due to reduced serum VLDL-TAG availability.

scholarly journals Intrauterine low protein diet increases fetal beta-cell sensitivity to NO and IL-1 beta: the protective role of taurine

2001 ◽  
Vol 171 (2) ◽  
pp. 299-308 ◽  
Author(s):  
S Merezak ◽  
AA Hardikar ◽  
CS Yajnik ◽  
C Remacle ◽  
B Reusens
Keyword(s):  
Beta Cell ◽  
Protective Effect ◽  
Interleukin 1 ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Control Group ◽  
Beta Alanine ◽  
Low Protein

We have demonstrated earlier that a low-protein (8% protein) diet during gestation alters fetal beta-cell development. Here, we investigated the effect of a low-protein diet as compared with a control (20% protein) diet, during gestation, on the sensitivity of fetal beta-cells against nitric oxide (NO) or interleukin-1 beta (IL-1 beta), and assessed the protective effect of taurine in vitro and in vivo. Neoformed islets from control fetuses or fetuses of dams fed a low-protein diet (LP group) were incubated with taurine, methionine or beta-alanine and then exposed to sodium nitropruside (SNP), a NO donor, or to IL-1 beta. To understand the effect of taurine in vivo, LP or control pregnant rats received 2.5% of taurine in the drinking water. Mortality and rate of apoptosis were quantified by confocal microscopy. Without treatment, rate of apoptosis was greater in LP group islets than in control islets (1.38+/-0.18% compared with 0.66+/-0.21% respectively, P<0.05). Addition of SNP 100 microM showed an augmentation in cell death, which was greater in the LP than in the control group (17.88+/-0.69% compared with 11.89+/-0.44% respectively, P<0.01). LP islets were more sensitive than control islets to IL-1 beta. Taurine was protective against SNP and IL-1 beta in both the groups, methionine provided a less protective effect than taurine, and pretreatment with beta-alanine had no protective effect. Taurine supplementation of the maternal diet reduced the rate of apoptosis induced by IL-1 beta in control islets and suppressed that induced by IL-1 beta in LP islets. Our findings indicate that a low-protein diet during gestation augments the sensitivity of fetal islet cells to NO and IL-1 beta. However, through in vitro and in vivo experiments our studies indicate that such effects can be rescued using amino acids such as taurine.

scholarly journals Prenatal programming of rat thick ascending limb chloride transport by low-protein diet and dexamethasone

2009 ◽  
Vol 297 (1) ◽  
pp. R93-R99 ◽  
Author(s):  
Amit Dagan ◽  
Sabeen Habib ◽  
Jyothsna Gattineni ◽  
Vangipuram Dwarakanath ◽  
Michel Baum
Keyword(s):  
Blood Pressure ◽  
Sodium Transport ◽  
Chloride Transport ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Control Group ◽  
Thick Ascending Limb ◽  
Prenatal Programming ◽  
Low Protein ◽  
Protein Group

Prenatal administration of dexamethasone and a low-protein diet has been shown to result in hypertension in the offspring when they are adults. The cause for the hypertension is unknown. The purpose of this study was to examine whether there was prenatal programming of thick ascending limb transport. Rats were administered either dexamethasone for 4 days (0.2 mg/kg body wt) by intraperitoneal injection daily between the 15th and 18th day of gestation, or they were fed a low-protein diet (6% protein) or an isocaloric normal protein diet (20% protein) from day 12 gestation until birth. The offspring were studied as adults. Prenatal dexamethasone and dietary protein deprivation resulted in an increase in blood pressure. Offspring of mothers fed a low-protein diet had an increase in medullary but not cortical bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) protein abundance ( P < 0.01). There was not a statistically significant increase in medullary NKCC2 by prenatal dexamethasone ( P = 0.07). Both prenatal administration of dexamethasone and a low-protein diet resulted in an increase in medullary thick ascending limb chloride transport compared with control (298 ± 33 pmoles·mm−1·min−1, 280 ± 26 pmoles·mm−1·min−1, and 191 ± 21 pmoles·mm−1·min−1, respectively P < 0.05). There was a higher lumen-positive transepithelial potential difference in the prenatal dexamethasone and low-protein group compared with control as well. Administration of furosemide for 24 h resulted in a decrease in blood pressure in the low-protein group but not the control group. This study demonstrates that insults administered to the fetus can program altered sodium transport. Increased tubular sodium transport is a likely cause for the hypertension by prenatal programming.

Factors in the reduced food intake of rats fed a low-protein diet

1968 ◽  
Vol 46 (1) ◽  
pp. 19-23 ◽  
Author(s):  
J. R. Beaton ◽  
V. Feleki ◽  
J. A. F. Stevenson
Keyword(s):  
Food Intake ◽  
Protein Diet ◽  
Male Rats ◽  
Low Protein Diet ◽  
Fasting Period ◽  
Thermostatic Control ◽  
Low Protein ◽  
Wistar Strain ◽  
Glucose Injection ◽  
Colonic Temperature

Male rats of the Wistar strain were fed either a control (20% casein) or a low-protein (5% casein) diet. Following the intraperitoneal injection of glucose solution it was observed from the blood glucose curve that low-protein fed rats had a delayed or impaired utilization of this carbohydrate. Resting oxygen consumption was not significantly different, and after glucose injection the slight increase in both groups was not significant. On refeeding after fasting, the colonic temperature of low-protein fed rats rose to a greater extent than did that of controls. Administration of protamine zinc insulin (PZI) decreased colonic temperature during fasting particularly in low-protein fed animals, and also during refeeding following a brief fasting period. From the results of these several experiments, it would appear that low-protein fed rats may have (a) an impairment in utilization of carbohydrate, and (b) a defect in immediate energy dissipation or an increased rate of energy production from ingested food. These two abnormalities may contribute to the reduced food intake of such animals. The association of a greater increase in colonic temperature on feeding and the hypophagia of rats fed a low-protein diet, as well as the hypothermic effect of PZI associated with an increase in food intake are suggestive of a thermostatic control of food intake in addition to a glucostatic control.

scholarly journals Some factors controlling food intake by zinc-deficient rats

1973 ◽  
Vol 30 (3) ◽  
pp. 555-566 ◽  
Author(s):  
J. K. Chesters ◽  
Marie Will
Keyword(s):  
Amino Acids ◽  
Food Intake ◽  
Amino Acid Content ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Effective Control ◽  
Zn Deficiency ◽  
Low Protein ◽  
Zn Concentration ◽  
Egg Albumen

1. Male hooded Lister rats given a diet containing 40 mg zinc/kg were described as Zn-adequate. Other rats were subsequently given diets containing less than 1 mg Zn/kg. After a period of approximately 5 d these animals ceased to grow and were described as Zn-deficient.2. Zn-deficient rats offered ad lib. a Zn-deficient diet containing 200 g egg albumen/kg ate only 55% of the weight eaten by Zn-adequate rats given a similar diet supplemented with Zn. The intake of the deficient rats increased when the metabolizable energy content of the diet was decreased and also when the environmental temperature was lowered.3. Zn-deficient rats offered Zn-deficient diets containing 200 g egg albumen/kg showed a high day-to-day variability of intake. When the albumen content was raised to 400 g/kg, neither the mean food intake of the rats nor the variability of food intake changed, but with diets containing only 50 g albumen/kg the quantity eaten increased and the variability of food intake decreased. Results obtained when the low-protein diet was supplemented with essential and non-essential amino acids indicated that increased variability of intake was associated with the essential amino acid content of the diet. The effect on variability of intake was greatest when the supplements contained methionine, phenylalanine, threonine and tryptophan; addition of this group of amino acids to a Zn-supplemented, low-protein diet produced the largest increase in the growth rate of Zn-adequate rats.4. When the food intake of the rats was examined for periods of 2 h throughtout the day, the Zn-deficient rats were found to eat on fewer occasions than the control rats. However, in those periods when the Zn-deficient rats did eat, the quantities eaten in 2 h showed the same distribution of weights as did those for the Zn-adequate rats.5. There were significant relationships between food intake and plasma Zn concentration; the most significant was the negative correlation between food intake in 24 h and plasma Zn concentration at the end of the 24 h period.6. Zn deficiency resulted in a failure of growth in the young rat and therefore in a reduction in its rate of energy expenditure but did not appear to cause directly a loss of appetite. It is suggested that cyclical patterns of food intake associated with Zn deficiency in young rats resulted from the slow but effective control of food intake by the energy balance of the animals.

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