Role of vitamin A in sulphate metabolism. Studies on the enzymic activation of sulphate by various tissue extracts of normal and vitamin A-deficient rats.
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ABSTRACT:
SUBMITTER: Mukherji B
PROVIDER: S-EPMC1270579 | biostudies-other | 1967 Jul
REPOSITORIES: biostudies-other
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Project description:1. Administration of propionate caused a twofold increase in the concentrations of lactate and pyruvate in the blood of vitamin B(12)-deficient rats, whereas there was a slight decrease in lactate and a 50% increase in pyruvate in normal rats. 2. Concentrations of total ketone bodies in the blood of normal rats were not significantly altered by propionate administration but the [3-hydroxybutyrate]/[acetoacetate] ratio decreased from 3.0 to 2.0. In the vitamin B(12)-deficient rats there was a 40% decrease in total ketone bodies and a change in the ratio from 3.4 to 1.2. 3. The changes in the concentration of ketone bodies in freeze-clamped liver preparations were similar in pattern to those observed in blood. 4. Propionate administration caused a decrease in the concentration of acetyl-CoA in the livers of both groups of animals, but the absolute decrease was greater in the vitamin B(12)-deficient group. The decrease in the concentration of CoA was similar in both groups. 5. As in blood, there were threefold increases in the concentrations of lactate and pyruvate in the livers of the vitamin B(12)-deficient rats after propionate administration, whereas there was no significant change in the concentrations of these metabolites in the normal rats. 6. There was a 50% inhibition of glucose synthesis in perfused livers from vitamin B(12)-deficient rats when lactate and propionate were substrates as compared with lactate alone. 7. It is concluded that the conversion of lactate into glucose is inhibited in vitamin B(12)-deficient rats after propionate administration, and that this effect is due to inhibition of the pyruvate carboxylase step resulting from a decrease in acetyl-CoA concentration and a postulated increase in methylmalonyl-CoA concentration.
| S-EPMC1177218 | biostudies-other
Project description:BackgroundVitamin D deficiency has been often observed in obese persons. One of the mechanisms suggested for low vitamin D status in obesity was decreased bioavailability of vitamin D (VD) due to sequestration in adipose tissue. However, only few studies have investigated this mechanism via quantifying vitamin D levels from tissues from the obese.MethodsSix-wk-old C57BL/6 mice were fed 10 or 45% kcal fat (CON or HFD) diets containing 50, 1000 or 25,000 IU vitamin D3/kg diet (LVd, CVd or HVd) for 13 wks. Serum 25-hydroxyvitamin D (25(OH)D) levels were determined by radioimmunoassay and liver and adipose tissue cholecalciferol (VD3) and 25-hydrocholecalciferol (25(OH)D3) levels were measured by LC-MS/MS. mRNA levels of jejunal Mttp, Cd36, Sr-b1, Npc1l1, and Abca1 and liver and adipose tissue 25-hydroxylases (Cyp2r1 and Cyp27a1) were determined by real-time PCR.ResultsSerum 25(OH)D levels were affected by dietary vitamin D content but differential effects were observed between HFD and CON groups. When vitamin D intake was at a supplementary level, the HFD-HVd group had lower serum 25(OH)D levels than the CON-HVd group, while there was no significant difference between the HFD and CON groups fed LVd or CVd. Total amount of VD3 in liver and adipose tissue were significantly higher in HFD-HVd group compared with the CON-HVd group. However, no difference in total amount of tissue VD3 was observed between the CON and HFD groups fed CVd. In jejunum, mRNA levels of Mttp and Abca1 were significantly higher in HFD groups than CON groups. There was no difference in mRNA levels of liver 25-hydroxylases by both dietary fat amount and vitamin D content.ConclusionA significant amount of VD3 seemed to be stored in the liver and adipose tissue when dietary vitamin D is at a supplementation level; thus excess body adiposity could contribute to relatively low serum 25(OH)D level when vitamin D was supplemented.
| S-EPMC7294642 | biostudies-literature
Project description:1. The effect of the administration of vitamin B(12) and biotin on the metabolic pattern of vitamin B(12) in biotin-deficient rats was studied. 2. No significant changes in the absorption and excretion of orally administered [(58)Co]vitamin B(12) were noted either in vitamin B(12)-treated and or in biotin-fed rats. A significant decrease of the uptake of orally given [(58)Co]vitamin B(12) was observed in the liver and kidneys of biotin-treated rats, whereas an increase of uptake in the kidneys of vitamin B(12)-treated rats was noted as compared with biotin-deficient animals. 3. No significant difference in the excretion of radioactivity was noted between biotin deficient and biotin-fed rats when [(58)Co]vitamin B(12) was administered by injection. A small decrease was observed in vitamin B(12)-treated rats. The retention of injected [(58)Co]vitamin B(12) by major organs of biotin-treated rats was lower than that of biotin-deficient rats. A lower content of [(58)Co]vitamin B(12) was also detected in the organs, with the exception of the kidneys, of vitamin B(12)-treated rats. 4. These results are discussed in terms of an interrelationship between biotin and vitamin B(12).
| S-EPMC1206903 | biostudies-other
Project description:1. The triglyceride, cholesterol ester and total phospholipid fractions were isolated from the livers and yolk sacs of normal and vitamin B(12)-deficient chick embryos after 13, 15, 17, 19 and 21 days of incubation, and the fatty acid compositions were determined. 2. At all stages of incubation, the concentration of cholesterol ester in the livers of the normal embryos were greater, and on days 15 and 17 the concentrations of triglyceride were considerably less, than the corresponding concentrations in the livers of the deficient embryos. 3. Between day 13 and day 21 of incubation the concentration of oleic acid in the liver triglycerides of the normal embryos increased, whereas the concentrations of palmitic acid and docosahexaenoic acid decreased. Vitamin B(12) deficiency resulted in higher concentrations of palmitic acid in the liver triglycerides on days 15, 17 and 19, higher concentrations of C(18) polyunsaturated acids on days 13 and 15 and lower concentrations of oleic acid on days 13, 15, 17 and 19. 4. At all stages of development, cholesterol oleate accounted for almost 80% of the total liver cholesterol esters in both normal and deficient embryos. 5. As development of the normal embryos progressed, the concentrations of palmitic acid and arachidonic acid in the liver phospholipid decreased, whereas the concentrations of stearic acid and docosahexaenoic acid increased. Vitamin B(12) deficiency resulted in markedly higher concentrations of stearic acid and palmitic acid and markedly lower concentrations of arachidonic acid and docosahexaenoic acid in the liver phospholipids. 6. Vitamin B(12) deficiency did not influence the fatty acid composition of the triglyceride, cholesterol ester and phospholipid fractions either in the yolks of fertile unincubated eggs or in the yolks obtained from eggs that had been incubated for 13, 15, 17, 19 and 21 days.
| S-EPMC1215187 | biostudies-other
Project description:In humans, dehydroepiandrosterone and its sulfate ester metabolite DHEA-S are secreted predominantly from the adrenal cortex, and dehydroepiandrosterone is converted to steroid hormones, including androgens and estrogens, and neurosteroid. Dehydroepiandrosterone exerts protective effects against several pathological conditions. Although there are reports on the association between dehydroepiandrosterone and vitamins, the exact relationship between dehydroepiandrosterone and vitamin E remains to be determined. Therefore, we attempted to elucidate the effect of dehydroepiandrosterone on vitamin E status and the expression of various vitamin E-related proteins, including binding proteins, transporters, and cytochrome P450, in vitamin E-deficient rats. Plasma α-tocopherol levels in vitamin E-deficient rats increased in response to dehydroepiandrosterone administration. The expression of hepatic α-tocopherol transfer protein was repressed in vitamin E-deficient rats compared to that in control rats; however, dehydroepiandrosterone administration significantly upregulated this expression. Hepatic expression of CYP4F2, an α-tocopherol metabolizing enzyme, in vitamin E-deficient rats was decreased by dehydroepiandrosterone administration, whereas hepatic expression of ATP-binding cassette transporter A1, an α-tocopherol transporter, was not altered following dehydroepiandrosterone administration. Dehydroepiandrosterone repressed lipid peroxidation in the liver of vitamin E-deficient rats. Therefore, adequate dehydroepiandrosterone supplementation may improve lipid peroxidation under several pathological conditions, and dehydroepiandrosterone may modulate α-tocopherol levels through altered expression of vitamin E-related proteins.
| S-EPMC4865594 | biostudies-literature
Project description:In vitamin B-12 (cobalamin) deficiency the metabolism of propionyl-CoA and methylmalonyl-CoA are inhibited secondarily to decreased L-methylmalonyl-CoA mutase activity. Production of acylcarnitines provides a mechanism for removing acyl groups and liberating CoA under conditions of impaired acyl-CoA utilization. Carnitine metabolism was studied in the vitamin B-12-deficient rat to define the relationship between alterations in acylcarnitine generation and the development of methylmalonic aciduria. Urinary excretion of methylmalonic acid was increased 200-fold in vitamin B-12-deficient rats as compared with controls. Urinary acylcarnitine excretion was increased in the vitamin B-12-deficient animals by 70%. This increase in urinary acylcarnitine excretion correlated with the degree of metabolic impairment as measured by the urinary methylmalonic acid elimination. Urinary propionylcarnitine excretion averaged 11 nmol/day in control rats and 120 nmol/day in the vitamin B-12-deficient group. The fraction of total carnitine present as short-chain acylcarnitines in the plasma and liver of vitamin B-12-deficient rats was increased as compared with controls. When the rats were fasted for 48 h, relative or absolute increases were seen in the urine, plasma, liver and skeletal-muscle acylcarnitine content of the vitamin B-12-deficient rats as compared with controls. Thus vitamin B-12 deficiency was associated with a redistribution of carnitine towards acylcarnitines. Propionylcarnitine was a significant constituent of the acylcarnitine pool in the vitamin B-12-deficient animals. The changes in carnitine metabolism were consistent with the changes in CoA metabolism known to occur with vitamin B-12 deficiency. The vitamin B-12-deficient rat provides a model system for studying carnitine metabolism in the methylmalonic acidurias.
| S-EPMC1135203 | biostudies-other
Project description:The activity of six hydrolytic enzymes-carboxyl esterase, acid phosphatase, alkaline phosphatase, ?-galactosidase, ?-glucosidase and ?-hexosaminidase, were studied in different regions of the normal human brain tissue obtained at autopsy. Protein estimation and activities of the hydrolytic enzymes with respective substrates were assayed by spectrophotometric and spectroflourometric methods. Amongst the eight regions of the brain-frontal, parietal, occipital, temporal, thalamus, cerebellum and hippocampus, the pineal gland showed highest activity for all hydrolytic enzymes studied except for carboxyl esterase. Among six hydrolases studied, hexosaminidase exhibited highest activity in all regions of the human brain while alkaline phosphatase activity was the least amongst all regions studied. A majority of the enzymes studied showed higher activity in gray matter as compared to the white matter except acid phosphatase and ?-glucosidase which exhibited higher activity in the white matter. The most significant finding in the present study was the high activity of all hydrolytic enzymes noted in the pineal gland as compared to all other regions of the human brain. Such a finding has not been hitherto reported earlier in human brain tissue samples. If the specific activities of these enzymes are to be considered as any functional index, then pineal gland may be more metabolically active tissue with respect to the hydrolytic function as compared to the other regions of the brain.
| S-EPMC3689325 | biostudies-literature
Project description:All-trans-retinoyl beta-glucuronide (RAG) was chemically synthesized in high yields (up to 79%) by a new procedure involving the reaction of the tetrabutylammonium salt of glucuronic acid with all-trans-retinoic acid (RA) via the imidazole or triazole derivative. When RAG was fed orally to vitamin A-deficient rats, RA was identified as the major metabolite in the serum within hours of administration of RAG. Very little or no RAG was detected in the serum. Thus RAG, which was not appreciably hydrolysed to RA in vitamin A-sufficient rats [Barua and Olson (1987) Biochem. J. 263, 403-409], was rapidly converted into RA in vitamin A-deficient rats.
| S-EPMC1217032 | biostudies-other
Project description:Vitamin D3 (VD3) plays an important role in the ovary and its deficiency is associated with ovarian pathologies, including polycystic ovary syndrome (PCOS). However, there is no data related to VD3 metabolism in the ovary during PCOS. Herein, we investigated differences in the expression of VD3 receptor (VDR) and key VD3 metabolic enzymes, 1α-hydroxylase (CYP27B1) and 24-hydroxylase (CYP24A1), in the ovary and periovarian adipose tissue (POAT) of control (proestrus and diestrus) and PCOS induced by letrozole rats. Vdr, Cyp27b1 and Cyp24a1 mRNA expression was determined, their protein abundance was examined and immunolocalized. Furthermore, VD3 metabolite concentrations in plasma (25OHD) and tissues (ovary and POAT; 1,25(OH)2D3), and plasma calcium level were determined. 25OHD concentration decreased markedly in letrozole-treated rats in comparison with controls, whereas calcium concentration did not vary among the examined groups. The amount of 1,25(OH)2D3 decreased in both ovary and POAT of PCOS rats. In the ovary, we found decreased Cyp27b1 and increased Vdr mRNA expression in letrozole-treated and diestrus control group. Corresponding protein abundances were down-regulated and up-regulated, respectively but only following letrozole treatment. In POAT, only Cyp27b1 transcript level and CYP27B1 protein abundance were decreased in letrozole-treated rats. VDR was immunolocalized in healthy and cystic follicles, while CYP27B1 and CYP24A1 were found exclusively in healthy ones. Concluding, our results provide the first evidence of disrupted VD3 metabolism in the ovary and POAT of PCOS rats. The reduced 1,25(OH)2D3 concentration in those tissues suggests their contribution to VD3 deficiency observed in PCOS and might implicate in PCOS pathogenesis.
| S-EPMC7847874 | biostudies-literature
Project description:1. Protein-calorie-depleted rats exhibit a decreased ability to oxidize leucine as compared with control animals. 2. The block in degradation of l-leucine is due to decreased activities of l-leucine transaminase and d-amino acid oxidase associated with liver mitochondria. 3. Cytoplasmic l-leucine transaminase in liver is not affected by the protein depletion. 4. The specific activities of the mitochondrial enzymes can be increased by a single oral dose of 1g. of Bacto-Peptone (meat hydrolysate). The effect of Bacto-Peptone can be inhibited by prior administration of dosages of 10mg. of puromycin/100g. body wt., suggesting that the increased enzyme specific activities may be due to new synthesis of enzyme protein.
| S-EPMC1187577 | biostudies-other