scholarly journals Brain Susceptibility to Methyl Donor Deficiency: From Fetal Programming to Aging Outcome in Rats

2019 ◽  
Vol 20 (22) ◽  
pp. 5692 ◽  
Author(s):  
Ziad Hassan ◽  
David Coelho ◽  
Tunay Kokten ◽  
Jean-Marc Alberto ◽  
Rémy Umoret ◽  
...  
Keyword(s):  
Behavioral Outcomes ◽  
Normal Diet ◽  
Deficient Diet ◽  
Adult Rats ◽  
Learning Abilities ◽  
Methyl Donors ◽  
Functional Consequences ◽  
Folate And Vitamin B12 ◽  
Neuronal Layer ◽  
Sex And Age Differences

Deficiencies in methyl donors, folate, and vitamin B12 are known to lead to brain function defects. Fetal development is the most studied but data are also available for such an impact in elderly rats. To compare the functional consequences of nutritional deficiency in young versus adult rats, we monitored behavioral outcomes of cerebellum and hippocampus circuits in the offspring of deficient mother rats and in adult rats fed a deficient diet from 2 to 8 months-of-age. We present data showing that the main deleterious consequences are found in young ages compared to adult ones, in terms of movement coordination and learning abilities. Moreover, we obtained sex and age differences in the deleterious effects on these functions and on neuronal layer integrity in growing young rats, while deficient adults presented only slight functional alterations without tissue damage. Actually, the cerebellum and the hippocampus develop and maturate according to different time lap windows and we demonstrate that a switch to a normal diet can only rescue circuits that present a long permissive window of time, such as the cerebellum, whereas the hippocampus does not. Thus, we argue, as others have, for supplements or fortifications given over a longer time than the developmental period.

EFFECT OF CALCIUM DEPRIVATION ON PARATHYROID HORMONE-MEDIATED BONE AND KIDNEY CONTRIBUTIONS TO THE MAINTENANCE OF PLASMA CALCIUM IN RATS

1975 ◽  
Vol 64 (2) ◽  
pp. 299-304 ◽  
Author(s):  
D. N. KALU ◽  
A. HADJI-GEORGOPOULOS ◽  
G. V. FOSTER
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Calcium ◽  
Normal Diet ◽  
Plasma Calcium ◽  
Urinary Hydroxyproline ◽  
Deficient Diet ◽  
Adult Rats ◽  
Low Calcium Diet ◽  
Hydroxyproline Excretion ◽  
Plasma Calcium Level

SUMMARY This study was designed to investigate the roles of bone and kidney in the acute regulation of plasma calcium by parathyroid hormone (PTH) during prolonged calcium deprivation. The effect of PTH was assessed by gland ablation. Animals were thyroparathyroidectomized or sham-operated and their urine was collected for 3 h. Subsequently they were anaesthetized and bled from the abdominal aorta. In rats fed on a low calcium diet, urinary hydroxyproline excretion was enhanced and, unlike animals fed on a normal diet, decreased 3 h after thyroparathyroidectomy (TPTX). In addition TPTX decreased plasma calcium by 0·45 mg/100 ml in normal rats compared with 1·94 mg/100 ml in animals fed on a calcium-deficient diet. Urinary calcium increased by 161 and 12 μg and accounted for 82 and 1·4% of the fall in plasma calcium in normal and calcium-deprived animals respectively. The corresponding contributions of bone were 18 and 98·6%. These findings support the view that with prolonged calcium deprivation in adult rats, the relative contributions of bone and kidney to the acute regulation of the plasma calcium level by PTH are reversed. As a result, bone rather than kidney becomes the more important organ. At the same time non-PTH-mediated kidney reabsorption of calcium is increased.

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 A Folate- and Vitamin B12-Deficient Diet Decreases the Latency and Increases the Incidence of Mammary Tumors in MMTV-ErbB2 Transgenic Mice

2021 ◽  
Author(s):  
Zhengzheng Xiao ◽  
Guoliang Yao ◽  
Yongxuan Liu ◽  
Chunling Zhao
Keyword(s):  
Breast Cancer ◽  
Tyrosine Kinase ◽  
Vitamin B12 ◽  
Signaling Pathways ◽  
Mammary Tumor ◽  
Receptor Tyrosine Kinase ◽  
Tumor Development ◽  
Deficient Diet ◽  
Tyrosine Kinase 2 ◽  
Folate And Vitamin B12

Abstract There has been controversy regarding folate- and vitamin B12-deficient diet (FVD)-induced hyperhomocysteinemia (HHcy) associated with breast cancer risk in most published epidemiological studies. Thus, the present study designed experiments to assess the causal association between FVD-induced HHcy and mammary tumor risk, as well as to identify the relative underlying mechanism. In this study, mammary tumor development was examined in mouse mammary tumor virus (MMTV)-erb-b2 receptor tyrosine kinase 2 (ErbB2) mice fed with a control AIN-93G diet or a FVD diet. MMTV-ErbB2 mice fed with the FVD diet displayed elevated blood levels of the amino acid homocysteine, a shorter tumor latency and an increased tumor multiplicity compared with the controls. The expression levels of key markers in the receptor tyrosine kinase and estrogen receptor (ER) signaling pathways, including phosphorylated (p)-Akt, p-Erk, p-ERα and Cyclin D1, were elevated in mammary tissues from MMTV-ErbB2 mice fed the FVD diet compared with mice fed with control diet. These data suggested that FVD-induced HHcy may promote mammary tumor development and decrease tumor latency, possibly by activating the epidermal growth factor receptor/ErbB2 and ERα signaling pathways. Therefore, examining the signaling mechanisms and identifying the relative metabolic pathways underlying mammary tumor promotion following FVD-induced HHcy may provide a novel strategy for breast cancer prevention and treatment.

Relationship between brain zinc and transient learning impairment of adult rats fed zinc-deficient diet

2000 ◽  
Vol 859 (2) ◽  
pp. 352-357 ◽  
Author(s):  
Atsushi Takeda ◽  
Sachiyo Takefuta ◽  
Shoji Okada ◽  
Naoto Oku
Keyword(s):  
Deficient Diet ◽  
Adult Rats ◽  
Zinc Deficient Diet ◽  
Learning Impairment

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

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.

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