LIVER VITAMIN A MOBILIZATION DURING ZINC DEFICIENCY AND RESTRICTED FOOD INTAKE

Six 9-month-old female Dutch Friesian cattle were given hay and pelleted concentrates with added 130 g CaCO3 or 100 g Na2HPO4 daily for periods of 50 days each. The supplements did not significantly influence growth or vitamin A, Cu or Mn in liver or blood plasma, although more P tended to retard growth. Liver vitamin A, Cu and Mn generally decreased significantly with time. Cu was more closely related to growth than vitamin A or Mn. A fall of Cu in blood plasma and liver was associated with a fall in the vitamin A in liver and with an increase of vitamin A in plasma.-V. J. B. (Abstract retrieved from CAB Abstracts by CABI’s permission)

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Vitamin A Status and Hepatic Drug Metabolism in the Rat

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y73-002 ◽

1973 ◽

Vol 51 (1) ◽

pp. 6-11 ◽

Cited By ~ 51

Author(s):

G. C. Becking

Keyword(s):

Vitamin A ◽

Drug Metabolism ◽

Vitamin A Deficiency ◽

Hepatic Drug Metabolism ◽

Deficient Diet ◽

Hepatic Drug ◽

Vitamin A Status ◽

Cytochrome P 450 ◽

Liver Vitamin

The effect of vitamin A status on hepatic drug metabolism was studied in rats. Animals were fed diets with and without vitamin A for 20 and 25 days. Weight gains of control and deficient animals were not significantly different, whereas liver vitamin A levels had decreased to less than 10% of control animals after 20 days and were essentially zero after eating the deficient diet for 25 days. Aniline metabolism in vitro and aminopyrine metabolism in vitro and in vivo were significantly lower in male weanling rats fed a vitamin A deficient diet for 20 days. No alteration in in vitro p-nitrobenzoic acid metabolism was noted after 25 days on the test. Vitamin A deficiency did not alter microsomal protein levels or cytochrome c reductase activity but deficient animals did have a lower microsomal cytochrome P-450 content. Hepatic enzyme activities and cytochrome P-450 levels were restored to values approaching those found in control animals by feeding vitamin A deficient rats the vitamin A containing diet for 21 days. Liver vitamin A levels were markedly increased after re-feeding studies but were still significantly lower than control animals.

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Effects of food or nutrient restriction on milk vitamin A transfer and neonatal vitamin A stores in the rat

British Journal Of Nutrition ◽

10.1079/bjn19900121 ◽

1990 ◽

Vol 63 (2) ◽

pp. 351-362 ◽

Cited By ~ 8

Author(s):

Ana Maria ◽

G. Pasatiempo ◽

A. Catharine Ross

Keyword(s):

Vitamin A ◽

Maternal Diet ◽

Control Diet ◽

Serum Vitamin ◽

Liver Weight ◽

Retinol Binding Protein ◽

Serum Retinol ◽

Total Food Intake ◽

Affect Transfer ◽

Liver Vitamin

We have investigated the effects of maternal diets low in fat or protein, or restricted in total food intake on vitamin A transfer from the dam to her pups. When animals were fed on diets moderately restricted in fat or protein, minimal differences in milk, serum, and liver vitamin A concentrations were observed compared with animals fed on a control diet. In a second study, dams were fed on diets more severely restricted in protein, or fat, or both, or were fed on a control diet equal to 50% of the intake of control rats but containing an equal amount of vitamin A. The quantity of milk obtained from these more severely restricted dams' nipples or the pups' stomachs was greatly reduced; however, there were no differences in milk vitamin A concentration. Body-weight, liver weight, and total liver vitamin A stores of undernourished pups were just half those measured for control pups, although serum vitamin A and serum retinol-binding protein were nearly normal in concentration. We conclude that (a) moderate restrictions in fat or protein in the maternal diet are insufficient to affect transfer of vitamin A to the suckling pup; (b) further dietary restrictions could cause decreased milk production with little change in milk vitamin A concentration and, hence, (c) the neonates' hepatic retinol accumulation during the suckling period is markedly reduced when maternal diets are severely deficient in fat or protein or of normal composition but restricted in amount.

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Androgen excess increases food intake in a rat polycystic ovary syndrome model by down-regulating hypothalamus insulin and leptin signaling pathways preceding weight gain

Neuroendocrinology ◽

10.1159/000521236 ◽

2021 ◽

Author(s):

Ying Liu ◽

Yu-chen Xu ◽

Yu-gui Cui ◽

Shi-wen Jiang ◽

Fei-yang Diao ◽

...

Keyword(s):

Weight Gain ◽

Food Intake ◽

Polycystic Ovary Syndrome ◽

Polycystic Ovary ◽

Androgen Excess ◽

Ovary Syndrome ◽

Leptin Signaling ◽

Leptin Sensitivity ◽

Androgen Levels ◽

Restricted Food Intake

Background Polycystic ovary syndrome (PCOS) is a common reproductive and metabolic disorder characterized by high androgen levels. The aim of this study was to evaluate the effects of hyperandrogenism on the hypothalamus, and subsequently on the food intake and obesity in females. Methods A dihydroxy testosterone (DHT)-induced rat model was established to recapitulate the hyperandrogenism features of PCOS patients. Body weight and food intake of the rats were recorded. The food intake of DHT-induced rats was restricted by pair feeding to exclude possible effects of weight gain on the hypothalamus. The expression levels of relevant proteins and mRNAs in the hypothalamus, primary hypothalamic neurons exposed to DHT were analyzed by Western blotting and RT-PCR respectively. The leptin levels in serum and cerebrospinal fluid (CSF) were measured, and leptin was injected via the intracerebroventricular (ICV) route to test the leptin sensitivity of hypothalamus. Results The excessive pre-puberty androgen levels in the DHT-induced rats markedly elevated food intake prior to weight gain. Consistent with this, the expression of NPY and Agouti-related peptide (Agrp) mRNAs were up-regulated, which occurred prior to obesity and even with restricted food intake. In addition, the hypothalamic sensitivity to insulin and leptin was also impaired in the DHT-induced rats before obesity and with restricted food intake. DHT significantly reduced the leptin levels in the CSF, and ICV injection of leptin inhibited the DHT-induced increase in food intake. Conclusions Androgen excess increased food intake in rats and promoted obesity by down-regulating insulin and leptin signaling in the hypothalamus, most likely by suppressing leptin levels in the CSF.

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