Morphological studies of hypomineralized enamel of rat pups on calcium-deficient diet, and of its changes after return to normal diet

1994 ◽  
Vol 239 (4) ◽  
pp. 379-395 ◽  
Author(s):  
Ermanno Bonucci ◽  
Enrico Lozupone ◽  
Giuliana Silvestrini ◽  
Angela Favia ◽  
Patrizia Mocetti
Keyword(s):  
Normal Diet ◽  
Deficient Diet ◽  
Rat Pups ◽  
Morphological Studies

Liver Histological Improvement After Administration of High-Dose Vitamin C in Guinea Pig with Nonalcoholic Steatohepatitis

2018 ◽  
Vol 88 (5-6) ◽  
pp. 263-269
Author(s):  
Seong-Hoon Park ◽  
A Lum Han ◽  
Na-Hyung Kim ◽  
Sae-Ron Shin
Keyword(s):  
Liver Biopsy ◽  
Vitamin C ◽  
Nonalcoholic Steatohepatitis ◽  
Guinea Pigs ◽  
Normal Diet ◽  
High Dose ◽  
Biochemical Tests ◽  
Deficient Diet ◽  
Histological Improvement ◽  
Vit C

Abstract. Background: Vitamin C is a strong antioxidant, and the health effects of vitamin C megadoses have not been validated despite the apparent health benefits. Therefore, the present study sought to confirm the effects of vitamin C megadoses. Materials and Methods : Four groups of six guinea pigs were used. Each group was fed one of the following diets for three weeks: normal diet, methionine choline-deficient diet, methionine choline-deficient diet + vitamin C megadose (MCD + vit C 2.5 g/kg/day), and methionine-choline deficient diet + ursodeoxycholic acid (MCD + UDCA 30 mg/kg/day). The MCD diet was given to induce nonalcoholic steatohepatitis, and UDCA was used to treat nonalcoholic steatohepatitis. Three weeks after initial diet administration, the results of biochemical tests and liver biopsy were compared between the groups. Results: The cytoplasm state was similar in the MCD + vit C and MCD + UDCA groups, exhibiting clearing of the cytoplasm and ballooning degeneration. However, macrovesicular steatosis was not observed in the MCD + vit C group. Aspartate transaminase and alanine transaminase were elevated significantly following vitamin C administration. Conclusions: The present study confirmed that alone vitamin C megadoses are potential remedies for nonalcoholic steatohepatitis, based on the liver biopsy results of guinea pigs that were unable to synthesize vitamin C.

Biochemical Basis of Heart Function. IV. Energy Metabolism and Calcium Transport in Hearts of Vitamin E Deficient Rats

1971 ◽  
Vol 49 (10) ◽  
pp. 909-918 ◽  
Author(s):  
Margaret Fedelesova ◽  
Prakash V. Sulakhe ◽  
John C. Yates ◽  
Naranjan S. Dhalla
Keyword(s):  
Vitamin E ◽  
Sarcoplasmic Reticulum ◽  
Heart Function ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Normal Diet ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Biochemical Basis

Feeding a vitamin E deficient diet to rats for 10 weeks was found to decrease myocardial creatine phosphate, ATP, ATP/ADP ratio, NAD+, NADP+, and NADPH, whereas the level of ADP was increased without any changes in the levels of AMP, total adenine nucleotides, NADH, and ATP/AMP ratio. The levels of ATP and pyridine nucleotides were restored fully, whereas creatine phosphate was restored partially on feeding a normal diet for 4 weeks to animals previously on the vitamin E deficient diet for 10 weeks. Vitamin E deficiency was found to increase cardiac lactate, pyruvate, and lactate/pyruvate ratio and decrease the activities of lactate dehydrogenase and malate dehydrogenase. The activity of Na+–K+-stimulated, ouabain-sensitive ATPase was markedly elevated in the hearts of animals on the vitamin E deficient diet. The ATP-dependent calcium accumulation by the sarcoplasmic reticular fraction in the absence and presence of P1 or oxalate was greater in the vitamin E deficient heart. Vitamin E deficiency also increased the Ca2+-stimulated ATPase activity of the cardiac sarcoplasmic reticulum. Although myocardial contractility of the hearts from vitamin E deficient rats was depressed, no damage to the ultrastructures of mitochondria and sarcoplasmic reticulum was apparent. These results indicate marked alterations in myocardial metabolism due to vitamin E deficiency and it is suggested that such changes are due to abnormalities in the processes of both energy production and utilization.

scholarly journals Maternal Melatonin Therapy Attenuates Methyl-Donor Diet-Induced Programmed Hypertension in Male Adult Rat Offspring

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1407 ◽  
Author(s):  
You-Lin Tain ◽  
Julie Chan ◽  
Chien-Te Lee ◽  
Chien-Ning Hsu
Keyword(s):  
Methylation Status ◽  
Normal Diet ◽  
Male Offspring ◽  
Adult Offspring ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Male Adult ◽  
Methyl Donor ◽  
Adult Rat

Although pregnant women are advised to consume methyl-donor food, some reports suggest an adverse outcome. We investigated whether maternal melatonin therapy can prevent hypertension induced by a high methyl-donor diet. Female Sprague-Dawley rats received either a normal diet, a methyl-deficient diet (L-MD), or a high methyl-donor diet (H-MD) during gestation and lactation. Male offspring were assigned to four groups (n = 7–8/group): control, L-MD, H-MD, and H-MD rats were given melatonin (100 mg/L) with their drinking water throughout the period of pregnancy and lactation (H-MD+M). At 12 weeks of age, male offspring exposed to a L-MD or a H-MD diet developed programmed hypertension. Maternal melatonin therapy attenuated high methyl-donor diet-induced programmed hypertension. A maternal L-MD diet and H-MD diet caused respectively 938 and 806 renal transcripts to be modified in adult offspring. The protective effects of melatonin against programmed hypertension relate to reduced oxidative stress, increased urinary NO2− level, and reduced renal expression of sodium transporters. A H-MD or L-MD diet may upset the balance of methylation status, leading to alterations of renal transcriptome and programmed hypertension. A better understanding of reprogramming effects of melatonin might aid in developing a therapeutic strategy for the prevention of hypertension in adult offspring exposed to an excessive maternal methyl-supplemented diet.

scholarly journals Rat pups from dams fed a partial tryptophan‐deficient diet exhibit a decreased ventilatory response to hypercapnia and slower heart rates

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Eliana Mori Penatti ◽  
Alexis E Barina ◽  
Alexandra Harris ◽  
Sharat Raju ◽  
Aihua Li ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Deficient Diet ◽  
Heart Rates ◽  
Rat Pups

A maternal defect is responsible for growth failure in vitamin D-deficient rat pups

1984 ◽  
Vol 246 (3) ◽  
pp. E216-E220
Author(s):  
R. Brommage ◽  
H. F. DeLuca
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Vitamin D3 ◽  
High Performance ◽  
Growth Failure ◽  
Female Rats ◽  
Deficient Diet ◽  
Rat Pups ◽  
Undetectable Plasma ◽  
Pup Growth

Vitamin D deficiency was induced in lactating rats and their pups by placing female rats on a vitamin D-deficient diet immediately after mating. Evidence of vitamin D deficiency included undetectable plasma levels of 25-hydroxyvitamin D3 in the dams, maternal hypocalcemia, the lack of pup growth, and pup hypocalcemia following starvation. This method of producing vitamin D-deficient pups was then used to determine whether the failure of vitamin D-deficient pups to grow properly results from a maternal or neonatal defect. Vitamin D-deficient dams and pups were injected with either vitamin D3 or the ethanol vehicle, and pup growth was monitored over the subsequent 6 days. Providing vitamin D3 to the pups directly had no effect on their growth, but administering vitamin D3 to the dams resulted in a tripling of the pup growth rate. The failure of vitamin D3 to promote pup growth when given directly to the pups was not the result of their inability to metabolize the vitamin because these pups converted [3H]-vitamin D3 to 25(OH)D3, 24,25(OH)2D3, and 1,25(OH)2D3 as determined by comigration with standards on both straight and reverse phase high-performance liquid chromatography systems. These results demonstrate that a maternal defect is responsible for the growth failure observed in vitamin D-deficient rat pups.

Growth of Normal and Thyroidectomized Rats on Iodine-Deficient Diet

1958 ◽  
Vol 195 (2) ◽  
pp. 381-384 ◽  
Author(s):  
Chalmers L. Gemmill
Keyword(s):  
Normal Diet ◽  
Considerable Time ◽  
Deficient Diet ◽  
Organic Iodine ◽  
Retarded Growth

Thyroidectomized rats on an iodine-deficient diet have little or no growth. Inorganic iodide, 3,5-diiodothyronine and inorganic iodide with 3,5-diiodothyronine do not promote growth in these animals. On a normal diet, thyroidectomized rats have retarded growth. After considerable time of cessation of growth on the iodine-deficient diet, 3,3',5-triiodo-l-thyronine restores growth in the thyroidectomized animal. The cessation of growth in the thyroidectomized rats on iodine-deficient diet is considered due to the absence of metabolically active organic iodine which is present in the normal diet.

EFFECT OF ADRENOCORTICOTROPHIC AND GROWTH HORMONES ON ALDOSTERONE PRODUCTION AND PLASMA RENIN ACTIVITY IN CHRONICALLY HYPOPHYSECTOMIZED SODIUM-DEFICIENT RATS

1970 ◽  
Vol 47 (2) ◽  
pp. 243-250 ◽  
Author(s):  
M. PALKOVITS ◽  
W. DE JONG ◽  
B. VAN DER WAL ◽  
D. DE WIED
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Normal Diet ◽  
Secretory Response ◽  
Renin Activity ◽  
Deficient Diet ◽  
Sodium Deficiency ◽  
Long Term Treatment ◽  
Aldosterone Production ◽  
Hypophysectomized Rats

SUMMARY Hypophysectomy abolishes the aldosterone secretory response to sodium deficiency in rats. Sodium deficiency causes a significant increase in plasma renin activity in chronically hypophysectomized rats which is of the same order as that found in intact animals. Long-term treatment with either adrenal maintenance doses of corticotrophin (ACTH) or with growth hormone (STH) did not affect the low rate of aldosterone production of hypophysectomized rats on a sodium-deficient diet. However, ACTH and STH given simultaneously restored the aldosterone secretory response to sodium deficiency in chronically hypophysectomized rats. The plasma renin activity of hypophysectomized rats on a sodium-deficient or a normal diet remained unaltered during treatment with either ACTH or STH or with the two hormones given simultaneously. This was also reflected in the systolic blood pressure of rats which, under the conditions used, did not change when the animals were sodium-deficient, or after hypophysectomy or hormone treatment. These results indicate that the effect of STH, in restoring the aldosterone secretory response to sodium deficiency in the presence of adrenal maintenance doses of ACTH in chronically hypophysectomized rats, is independent of changes in the renin-angiotensin system.

scholarly journals Levels of polyunsaturated fatty acids in lymphocytes of rats fed on diets varying in polyunsaturated fatty acid content

1980 ◽  
Vol 43 (2) ◽  
pp. 367-373 ◽  
Author(s):  
W. M. Tsagn ◽  
J. Belin ◽  
A. D. Smith
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acid ◽  
Fatty Acid Content ◽  
Inverse Correlation ◽  
Normal Diet ◽  
Deficient Diet ◽  
Polyunsaturated Fatty Acid Content ◽  
Weanling Rats ◽  
Total Fatty Acids

1. When weanling rats were fed on a diet containing 0.1 g/kg of the diet as polyunsaturated fatty acid, it was found that after 2 weeks the level of linoleate in the lymphocyte total lipids was 56 mg/ g total fatty acids, as compared with a level of 138 mg/ g in rats on a normal diet (P < 0.005). Similar levels were obtained from rats which had been fed for up to 16 weeks on the deficient diet, but in a group killed after 28 weeks on the diet the level was found to be only 20 mg/ g total fatty acids. The arachidonate level was found to be approximately 220 mg/ g total fatty acids, regardless of whether the rats were fed on a diet deficient in linoleate for up to 16 weeks or on a normal diet. In the group of rats killed after 28 weeks on the linoleate deficient diet, however, the arachidonate level was only 60 mg/ g total fatty acids.2. Percentage values for total fatty acids are given for plasma, adipose tissue, and lymphocytes for rats on normal and experimental diets.3. Scatter diagrams of the levels of linoleate v. arachidonate in the lymphocyte total fatty acids showed no correlation between the levels of the two acids (r 0.05), but similar plots of linoleate and oleate levels showed an inverse correlation (r – 0.68).

scholarly journals Pharmacokinetics, Biodistribution, and Toxicity of Folic Acid-Coated Antiretroviral Nanoformulations

2014 ◽  
Vol 58 (12) ◽  
pp. 7510-7519 ◽  
Author(s):  
Nagsen Gautam ◽  
Pavan Puligujja ◽  
Shantanu Balkundi ◽  
Rhishikesh Thakare ◽  
Xin-Ming Liu ◽  
...  
Keyword(s):  
Folic Acid ◽  
Plasma Concentrations ◽  
Pharmacokinetic Profile ◽  
Antiretroviral Drugs ◽  
Normal Diet ◽  
Poloxamer 407 ◽  
Deficient Diet ◽  
Drug Concentrations ◽  
Immunodeficiency Virus ◽  
Delivery Platform

ABSTRACTThe drug delivery platform for folic acid (FA)-coated nanoformulated ritonavir (RTV)-boosted atazanavir (FA-nanoATV/r) using poloxamer 407 was developed to enhance cell and tissue targeting for a range of antiretroviral drugs. Such formulations would serve to extend the drug half-life while improving the pharmacokinetic profile and biodistribution to reservoirs of human immunodeficiency virus (HIV) infection. To this end, we now report enhanced pharmacokinetics and drug biodistribution with limited local and systemic toxicities of this novel nanoformulation. The use of FA as a targeting ligand for nanoATV/r resulted in plasma and tissue drug concentrations up to 200-fold higher compared to equimolar doses of native drug. In addition, ATV and RTV concentrations in plasma from mice on a folate-deficient diet were up to 23-fold higher for mice administered FA-nanoATV/r than for mice on a normal diet. Compared to earlier nanoATV/r formulations, FA-nanoATV/r resulted in enhanced and sustained plasma and tissue ATV concentrations. In a drug interaction study, ATV plasma and tissue concentrations were up to 5-fold higher in mice treated with FA-nanoATV/r than in mice treated with FA-nanoATV alone. As observed in mice, enhanced and sustained plasma concentrations of ATV were observed in monkeys. NanoATV/r was associated with transient local inflammation at the site of injection. There were no systemic adverse reactions associated with up to 10 weeks of chronic exposure of mice or monkeys to FA-nanoATV/r.

Nutrition

1936 ◽  
Vol 9 (4) ◽  
pp. 272-296
Keyword(s):  
Spinal Cord ◽  
Vitamin A ◽  
Medical Research ◽  
Nervous Tissue ◽  
Normal Diet ◽  
Cod Liver Oil ◽  
Tyrode Solution ◽  
Deficient Diet ◽  
Rat Embryos ◽  
Indian Journal

The Growth of Embryonic Nervous Tissue in Plasma taken from Vitamin A deficient Fowls and Rats. W. R. Aykroyd and G. Sankaran. Indian Journal of Medical Research. Vol. 23, 1936, p. 929. (Ref. Nutrition Abstracts, Vol. 6, 1936, p. 318.)Fragments of spinal cord or cerebrum from fowl embryos incubated for 7 to 9 days were cultivated in a mixture of Tyrode solution with the plasma of young fowls which had been exposed to sunlight and fed on a diet deficient in vitamin A, on the same diet with cod liver oil added, and on a normal diet. Fragments of cerebrum from rat embryos 19 to 21 days old were similarly cultured in plasma from rats on corresponding diets. In both series the growth of the explanted tissue was markedly inferior in the plasma from deficient animals, was best in that from normally fed animals, and was intermediate in that from animals on the deficient diet with vitamin A as cod liver oil.

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