Studies on the role of liver cytochrome P-450 and oestradiol metabolism in the effects of nutrition and phenobarbital on ovulation rate in the ewe

1991 ◽  
Vol 3 (6) ◽  
pp. 725 ◽  
Author(s):  
E Payne ◽  
JF Smith ◽  
BC Cope ◽  
LT McGowan
Keyword(s):  
G Protein ◽  
Dry Matter ◽  
Liver Weight ◽  
Microsomal Protein ◽  
Ovulation Rate ◽  
Protein Diet ◽  
Treatment Protocols ◽  
Low Protein ◽  
Cytochrome P 450

Coopworth ewes were differentially fed to produce 60 heavy (62 kg) and 80 light (45 kg) ewes. They were then fed a low protein (100 g protein kg-1 dry matter) pelleted ration. On Day 7 of the oestrous cycle after synchronization the following treatments were commenced in groups of 10 ewes: 4 low liveweight groups received low protein (LP), high protein (HP; 230 g protein kg-1 dry matter), LP + phenobarbital (PB; 1 g per os per day in gelatin capsules for 10 days) and LP + triacetyloleandomycin (TAO, 0.5 g day-1 in capsule for 10 days); while 3 high liveweight groups received LP, HP and HP + carbon tetrachloride (CCl4, 0.1 mL kg-1 bodyweight as a single dose). The experiment was repeated using another 7 groups of 10 ewes at an interval of 3 weeks. PB, TAO, high liveweight, and protein diet increased the ovulation rate whereas treatment with CCl4 reduced the ovulation rate. Because of the small number of ewes in some treatment protocols, only changes due to liveweight and protein diet were statistically significant. Liver weight and microsomal protein were increased by all treatments except CCl4 which caused a decrease. PB and TAO increased cytochrome P-450 and associated enzyme activities, in particular those related to cytochrome P-450p or P-450NF (including oestradiol 2-hydroxylation) in the human liver. In vitro, TAO binding indicated that the specific cytochrome was induced by PB and TAO but there were no direct effects of protein diet and liveweight. Most of the data support the theory that nutritionally induced increases in ovulation rate in ewes could result from changes in oestradiol metabolism, but the lack of induction of the specific cytochrome by protein diet and high liveweight suggests that increased ovulation caused by these factors may be the physiological response to several metabolic changes.

scholarly journals Protein and energy relations in the broiler chicken

1989 ◽  
Vol 61 (2) ◽  
pp. 223-233 ◽  
Author(s):  
R. W. Rosebrough ◽  
J. P. McMurtry ◽  
N. C. Steele
Keyword(s):  
G Protein ◽  
Broiler Chickens ◽  
Control Diet ◽  
Glucose Production ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Intermittent Feeding ◽  
Low Protein ◽  
Feeding Regimen

1. Broiler chickens growing from 7 to 28 d of age were given: (1) a 210 g protein/kg control diet for the entire experimental period, (2) an intermittent feeding regimen (210 g protein/kg diet for either 1 or 2 d followed by a 1 d fast), or (3) a daily change in the dietary protein level from 120 to 300 g/kg diet. Treatment variables examined were lipogenesis and glucose production in vitro, and circulating concentrations of insulin, triiodothyronine (T3) and thyroxine (T4) to determine the effects of chronic or acute dietary treatments.2. Giving the 300 g protein/kg diet or withholding feed for 1 d decreased (P < 0.05) lipogenesis in vitro compared with controls.3. Giving the 120 g protein/kg diet or refeeding with a 210 g protein/kg diet for 1 or 2 d increased (P < 0.05) lipogenesis in vitro compared with controls. Glucose production was affected in the same manner.4. Fasting decreased (P < 0.05) plasma insulin and T3 and increased T4. Both refeeding and a low-protein diet increased T3. Refeeding increased and a low-protein diet decreased insulin.5. Chronic use (7-28 d of age) of either an alternating protein or intermittent feeding regimen caused greater responses compared with acute bouts (single cycle) of either of the regimens.

scholarly journals Biochemical effects of the porphyrinogenic drug allylisopropylacetamide. A comparative study with phenobarbital

1973 ◽  
Vol 134 (4) ◽  
pp. 859-868 ◽  
Author(s):  
Manchanahalli R. Satyanarayana Rao ◽  
Govindarajan Padmanaban
Keyword(s):  
Reductase Activity ◽  
Time Lag ◽  
Liver Weight ◽  
Microsomal Protein ◽  
Female Rats ◽  
Biochemical Effects ◽  
Increase Liver Weight ◽  
Cytochrome P 450

Successive administrations of allylisopropylacetamide, a potent porphyrinogenic drug, increase liver weight, microsomal protein and phospholipid contents. There is an increase in the rate of microsomal protein synthesis in vivo and in vitro. The drug decreases microsomal ribonuclease activity and increases NADPH–cytochrome c reductase activity. Phenobarbital, which has been reported to exhibit all these changes mentioned, is a weaker inducer of δ-aminolaevulinate synthetase and increases the rate of haem synthesis only after a considerable time-lag in fed female rats, when compared with the effects observed with allylisopropylacetamide. Again, phenobarbital does not share the property of allylisopropylacetamide in causing an initial decrease in cytochrome P-450 content. Haematin does not counteract most of the biochemical effects caused by allylisopropylacetamide, although it is quite effective in the case of phenobarbital. Haematin does not inhibit the uptake of [2-14C]allylisopropylacetamide by any of the liver subcellular fractions.

scholarly journals Effect of short-term protein deprivation on hemopoietic functions of healthy volunteers

Blood ◽  
1980 ◽  
Vol 55 (4) ◽  
pp. 625-628 ◽  
Author(s):  
R Catchatourian ◽  
G Eckerling ◽  
W Fried
Keyword(s):  
Body Weight ◽  
G Protein ◽  
Protein Deprivation ◽  
Low Protein ◽  
Leukocyte Function ◽  
Leukocyte Chemotaxis ◽  
Complete Blood Counts ◽  
Excretion Rates

Abstract To ascertain the effects of protein deprivation on hemopoietic parameters in otherwise healthy subjects, three volunteers were placed on diets containing 0.15 g protein/kg body weight for 8 days followed in 2 mo by another 8-day study period during which they ingested their usual diets containing more than 0.9 g protein/kg body weight. Complete blood counts, serum protein determinations, and tests of in vitro and in vivo leukocyte chemotaxis were performed prior to and at the conclusion of each study period. Subjects were phlebotomized of 500 ml on day 7 of each study period. Twenty-four-hour urinary erythropoietin excretion rates were assayed just prior to and again postphlebotomy. Reticulocyte counts were performed at intervals up to 1 wk postphlebotomy. Some of these determinations were replicated during a subsequent study. The hemoglobin and hematocrits decrased slightly but significantly after 8 days on low protein diets. Erythropoietin excretion rates and reticulocyte responses to phlebotomy were also less marked while subjects were on protein depleted diets. Leukocyte chemotaxis, measured both in vitro and in vivo, was also markedly reduced while subjects were on protein-depleted diets. We conclude that 8 days of moderately severe protein deprivation significantly impairs erythropoiesis and leukocyte function in otherwise healthy individuals.

scholarly journals Post-ruminal effects of rumen-protected methionine supplementation with low protein diet using long-term simulation and in vitro digestibility technique

AMB Express ◽  
2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Imtiaz Hussain Raja Abbasi ◽  
Farzana Abbasi ◽  
Mohamed E. Abd El-Hack ◽  
Ayman A. Swelum ◽  
Junhu Yao ◽  
...  
Keyword(s):  
Protein Diet ◽  
Low Protein Diet ◽  
In Vitro Digestibility ◽  
Low Protein ◽  
Methionine Supplementation

scholarly journals Isocaloric maternal low-protein diet alters IGF-I, IGFBPs, and hepatocyte proliferation in the fetal rat

2003 ◽  
Vol 285 (5) ◽  
pp. E991-E1000 ◽  
Author(s):  
Ilham El Khattabi ◽  
Francine Grégoire ◽  
Claude Remacle ◽  
Brigitte Reusens
Keyword(s):  
Cell Proliferation ◽  
Fetal Liver ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Hepatocyte Proliferation ◽  
Liver Growth ◽  
Fetal Plasma ◽  
Low Protein ◽  
Igf I

We investigated the effect of an isocaloric maternal low-protein diet during pregnancy in rats on the proliferative capacity of cultured fetal hepatocytes. The potential roles of these changes on the IGF-IGF-binding protein (IGFBP) axis, and the role of insulin and glucocorticoids in liver growth retardation, were also evaluated. Pregnant Wistar rats were fed a control (C) diet (20% protein) or a low-protein (LP) diet (8%) throughout gestation. In primary culture, the DNA synthesis of hepatocytes derived from LP fetuses was decreased by ∼30% compared with control hepatocytes ( P < 0.05). In parallel, in vivo moderate protein restriction in the dam reduced the fetal liver weight and IGF-I level in fetal plasma ( P < 0.01) and augmented the abundance of 29- to 32-kDa IGFBPs in fetal plasma ( P < 0.01) and fetal liver ( P < 0.01). By contrast, the abundance of IGF-II mRNA in liver of LP fetuses was unaffected by the LP diet. In vitro, the LP-derived hepatocytes produced less IGF-I ( P < 0.01) and more 29- to 32-kDa IGFBPs ( P < 0.01) than hepatocytes derived from control fetuses. These alterations still appeared after 3–4 days of culture, indicating some persistence in programming. Dexamethasone treatment of control-derived hepatocytes decreased cell proliferation (54 ± 2.3%, P < 0.01) and stimulated 29- to 32-kDa IGFBPs, whereas insulin promoted fetal hepatocyte growth (127 ± 5.5%, P < 0.01) and inhibited 29- to 32-kDa IGFBPs. These results show that liver growth and cell proliferation in association with IGF-I and IGFBP levels are affected in utero by fetal undernutrition. It also suggests that glucocorticoids and insulin may modulate these effects.

scholarly journals Effect of feeding pattern on the energy metabolism of rats given low-protein diets

1975 ◽  
Vol 33 (2) ◽  
pp. 277-289 ◽  
Author(s):  
K. J. McCracken
Keyword(s):  
G Protein ◽  
Energy Intake ◽  
Dietary Protein ◽  
Protein Level ◽  
Dry Matter ◽  
Dietary Protein Level ◽  
Low Protein ◽  
Gastric Intubation ◽  
Energy Retention ◽  
Protein Diets

1. The deposition of fat and protein and the utilization of energy by growing rats offered diets ad lib. or in controlled amounts by gastric intubation has been investigated. Diets contained 50, 75, 100 or 200 g protein/kg, mainly as caseinGain of body-weight and protein increased with increasing dietary protein concentration when animals received the same energy intake, although the reverse was true for fat deposition. However, the differences in live-weight gain were almost entirely due to changes in body water. The dry-matter content of the gain in animals given low-protein diets was 770 g/kg compared to 360 g/kg in those given the control diet2. Energy retention was unaffected by dietary protein level in groups given the same energy intake by gastric intubation. In Expt 1 daily heat production increased significantly (P < 0·05) with increasing protein level (50, 75 and 200 g protein/kg diet) when energy intake was constant, but in Expt 2 there was no significant effect of protein level (50, 100 and 200 g protein/kg diet). Problems arose in the selection of a suitable basis for comparison of heat production between groups because of the differences in body-weight and body composition3. The energy requirement for zero energy balance was approximately 10% lower for the low-protein groups than for those given the diet containing 200 g protein/kg when food intake was just above the maintenance level. When the requirement was expressed per unit metabolic body size (W0·75 kg) dietary protein level had no significant effect. The mean values for Expts 1 and 2 were 452 and 436 kJ respectively4. The energy cost of weight gain increased as dietary protein level decreased in pairs of groups gaining at the same rate. The extra energy ingested by the animals given the lower protein level was converted to body tissue with an efficiency of at least 0·705. Striking differences were observed in body composition and energy retention of the two pairs of groups used for the comparison of tube-feeding and ad lib. feeding. With the diet containing 50 g protein/kg, tube-fed rats gained significantly more weight (P < 0·01) and more fat, dry matter and energy (P < 0·001) than their ad lib. counterparts given an iso-energetic intake6. The results demonstrate that dietary protein level has little or no effect on the utilization of energy by growing rats when the pattern of intake is controlled by gastric intubation.

scholarly journals A Low Protein Diet Alters Bone Material Level Properties and the Response toIn VitroRepeated Mechanical Loading

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Victor Dubois-Ferrière ◽  
René Rizzoli ◽  
Patrick Ammann
Keyword(s):  
Cyclic Loading ◽  
Mechanical Loading ◽  
Protein Diet ◽  
Female Rats ◽  
Low Protein Diet ◽  
Nanoindentation Test ◽  
Displacement Curve ◽  
Bone Material ◽  
Low Protein

Low protein intake is associated with an alteration of bone microstructure and material level properties. However, it remains unknown whether these alterations of bone tissue could influence the response to repeated mechanical loading. The authors investigated thein vitroeffect of repeated loading on bone strength in humeri collected from 20 6-month-old female rats pair-fed with a control (15% casein) or an isocaloric low protein (2.5% casein) diet for 10 weeks. Bone specimens were cyclically loaded in three-point bending under load control for 2000 cycles. Humeri were then monotonically loaded to failure. The load-displacement curve of thein vitrocyclically loaded humerus was compared to the contralateral noncyclically loaded humerus and the influence of both protein diets. Material level properties were also evaluated through a nanoindentation test. Cyclic loading decreased postyield load and plastic deflection in rats fed a low protein diet, but not in those on a regular diet. Bone material level properties were altered in rats fed a low protein diet. This suggests that bone biomechanical alterations consequent to cyclic loading are more likely to occur in rats fed a low protein diet than in control animals subjected to the samein vitrocyclic loading regimen.

scholarly journals Metabolic activation of acetylenic substituents to derivatives in the rat causing the loss of hepatic cytochrome P-450 and haem

1978 ◽  
Vol 174 (3) ◽  
pp. 853-861 ◽  
Author(s):  
Ian N. H. White
Keyword(s):  
Covalent Binding ◽  
Metabolic Activation ◽  
Microsomal Protein ◽  
Significant Loss ◽  
Microsomal Cytochrome ◽  
Rf Values ◽  
Green Pigments ◽  
Cytochrome P 450

1. A number of acetylenic-substituted steroidal and non-steroidal compounds, including 2,2-dipropargylacetamide, pregna-2,4-dien-20-yno[2,3-d]isoxazol-17-ol (Danazol) and acetylene gas, when administered to rats in vivo brought about a decrease in the concentrations of hepatic microsomal cytochrome P-450 and haem. Abnormal haem-breakdown products, ‘green pigments’, and porphyrins accumulated in the livers of these animals. 2. For loss of microsomal cytochrome P-450 to occur in vitro, metabolic activation of the acetylenic substituent was necessary. The enzyme system responsible required NADPH and air, and was induced by pretreatment of rats with phenobarbitone; these are characteristics typical of the microsomal mixed-function oxidases. 3. When rats were dosed with 17α-ethynyl-17β-hydroxyandrost-4-en-3-one (ethynyltestosterone, 1mmol/kg) the pattern of green pigments extracted from the liver 4h after dosing and separated by t.l.c. was quite different from that in rats given 17β-hydroxy-17α-vinylandrost-4-en-3-one (vinyltestosterone), suggesting that reduction of the unsaturated triple bond to a double bond is not normally part of the metabolic activation pathway of the acetylenic substituent. 4. The green pigments extracted from the livers of rats 4h after the administration of the acetylenic-substituted compounds (1mmol/kg) when separated by silica-gel t.l.c. had variable RF values. The number and distribution of green pigments was characteristic for each compound examined. There was little correlation between the total loss of hepatic microsomal haem and the apparent intensity of the green pigments seen on the thin-layer chromatograms. 5. After incubation of [14C]acetylene in vitro with microsomal preparations from phenobarbitone-pretreated rats and a NADPH-generating system, no significant covalent binding to microsomal protein was detected over a 30min incubation period, although under similar conditions there was a significant loss of cytochrome P-450.

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.

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