Carnitine modulates crucial myocardial adenosine triphosphatases and acetylcholinesterase enzyme activities in choline-deprived rats

2014 ◽  
Vol 92 (1) ◽  
pp. 78-84 ◽  
Author(s):  
Athina A. Strilakou ◽  
Stylianos T. Tsakiris ◽  
Konstantinos G. Kalafatakis ◽  
Aikaterini T. Stylianaki ◽  
Petros L. Karkalousos ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Enzyme Activities ◽  
Cardiac Contraction ◽  
Carnitine Supplementation ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Adenosine Triphosphatases ◽  
Essential Nutrient ◽  
Acetylcholinesterase Enzyme ◽  
The Impact

Choline is an essential nutrient, and choline deficiency has been associated with cardiovascular morbidity. Choline is also the precursor of acetylcholine (cholinergic component of the heart’s autonomic nervous system), whose levels are regulated by acetylcholinesterase (AChE). Cardiac contraction–relaxation cycles depend on ion gradients established by pumps like the adenosine triphosphatases (ATPases) Na+/K+-ATPase and Mg2+-ATPase. This study aimed to investigate the impact of dietary choline deprivation on the activity of rat myocardial AChE (cholinergic marker), Na+/K+-ATPase, and Mg2+-ATPase, and the possible effects of carnitine supplementation (carnitine, structurally relevant to choline, is used as an adjunct in treating cardiac diseases). Adult male albino Wistar rats were distributed among 4 groups, and were fed a standard or choline-deficient diet for one month with or without carnitine in their drinking water (0.15% w/v). The enzyme activities were determined spectrophotometrically in the myocardium homogenate. Choline deficiency seems to affect the activity of the aforementioned parameters, but only the combination of choline deprivation and carnitine supplementation increased myocardial Na+/K+-ATPase activity along with a concomitant decrease in the activities of Mg2+-ATPase and AChE. The results suggest that carnitine, in the setting of choline deficiency, modulates cholinergic myocardial neurotransmission and the ATPase activity in favour of cardiac work efficiency.

Role of Iron Supplementation in Reducing Severity of Depression: A Review

2020 ◽  
pp. 67-76
Author(s):  
OJS Admin
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Iron Supplementation ◽  
Reproductive Age ◽  
Deficiency Anemia ◽  
Essential Nutrient ◽  
Severity Of Depression ◽  
The Impact ◽  
Clinical Problems

Depression is a public health disorder, ranking third after respiratory and cardiac diseases. There were many evidences that iron deficiency anemia (IDA) is one of the foremost causes regarding nutritional pointof view for depression. We reviewed these evidences that IDAlinking to depression. We identified seventeen studies in four databases including randomized-controlled trials (RCTs) and observational studies assessing the impact of IDAand iron supplementation on the risk of depression. We extracted data on the basis of sample size, geographical region, measures of depression, hemoglobin, iron levels and intake of iron supplementation and critically appraised the results from the studies. Eleven out of sixty one studies were experimental, which indicated that dietary supplementation particularly iron supplementation had an association (r − 0.19 to −0.43 and ORs 1.70–4.64) with severity of depression. Evidences showed that women of reproductive age were more vulnerable to iron deficiency anemia than other population. Low ferritin and low hemoglobin level were associated with severity of depression. Iron is an essential nutrient for all living creatures, as a cofactor of various enzymes and plays significant role in environmental stimulant for the articulation of numerous virulence factors. Many clinical problems are caused by iron deficiency. Therefore, this review intended to highlight the important role of iron supplementation in reducing the severity of depression.

Fluoxetine-induced changes in body weight and 5-HT1A receptor-mediated hormone secretion in rats on a tryptophan-deficient diet

2004 ◽  
Vol 286 (2) ◽  
pp. R390-R397 ◽  
Author(s):  
D. N. D'Souza ◽  
Y. Zhang ◽  
F. Garcia ◽  
G. Battaglia ◽  
L. D. Van de Kar
Keyword(s):  
Body Weight ◽  
Control Diet ◽  
Hormone Secretion ◽  
Significant Loss ◽  
Tryptophan Depletion ◽  
Deficient Diet ◽  
Hormone Responses ◽  
Plasma Hormones ◽  
Induced Changes ◽  
The Impact

Tryptophan depleting protocols are commonly used to study the role of serotonin in mood disorders. The present study examined the impact of a tryptophan-deficient diet and fluoxetine on the serotonergic regulation of neuroendocrine function and body weight. We hypothesized that the regulation of postsynaptic 5-HT1A receptors is dependent on the levels of 5-HT in the synapse. Rats on a control or a tryptophan-deficient diet received daily injections of saline or fluoxetine (5 or 10 mg·kg-1·day-1 ip) from day 7 to day 21. The tryptophan-deficient diet produced a 41% reduction in the level of 5-HT but no change in the density of [3H]paroxetine-labeled 5-HT transporters. Treatment with fluoxetine inhibited the gain in weight in rats maintained on the control diet. The tryptophan-deficient diet produced a significant loss in body weight that was not significantly altered by treatment with fluoxetine. Treatment with fluoxetine produced a dose-dependent desensitization of hormone responses to injection of the 5-HT1A receptor agonist (±)8-hydroxy-2-(di- n-propylamino)tetralin ((±)8-OH-DPAT). The tryptophan-deficient diet produced an increase in the basal levels of corticosterone but did not alter the basal levels of ACTH or oxytocin. Also, this diet inhibited the magnitude of 8-OH-DPAT-induced increase in plasma levels of ACTH and oxytocin but did not impair the ability of fluoxetine to desensitize the 5-HT1A receptor-mediated increase in plasma hormones. These data suggest that a reserve of 5-HT enables fluoxetine to desensitize postsynaptic 5-HT1A receptors in the hypothalamus. In conclusion, the profound physiological changes induced by tryptophan depletion may complicate the interpretation of studies using this experimental approach.

CHOLINE DEFICIENCY IN THE GUINEA PIG

1957 ◽  
Vol 35 (1) ◽  
pp. 1-6 ◽  
Author(s):  
R. J. Young ◽  
C. C. Lucas
Keyword(s):  
Guinea Pig ◽  
Body Fat ◽  
Guinea Pigs ◽  
Liver Fat ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Methyl Group ◽  
Complete Diet ◽  
Total Body Fat ◽  
Total Body

Young guinea pigs (4–6 days of age) fed a choline-deficient diet grew slowly and died within 3 to 4 weeks, at which time the livers showed only traces of stainable fat. Animals fed the diet supplemented with choline grew at the rate of 5.5 to 6.0 g. per day. Guinea pigs transferred from a complete diet to a choline-deficient diet after 3 to 4 weeks suffered an immediate retardation in growth but no mortality occurred (up to 6 weeks). A decrease in total body fat was noted. After 4 weeks, stainable fat was present in the liver. A small but definite increase in total liver fat occurred at 6 weeks. The guinea pig, like the chick, is unable to place the first methyl group on the ethanolamine moiety of choline, but betaine plus monomethylaminoethanol was as effective as choline in overcoming a deficiency of the latter.

The Impact of Soy Diets on Ecto-ATPase Activity in Obese Zucker Rats

2010 ◽  
Vol 42 ◽  
pp. 805
Author(s):  
Audrey J. Stone ◽  
Kirk W. Evanson ◽  
William C. Gilbert ◽  
Latha Devareddy ◽  
Heidi A. Kluess
Keyword(s):  
Atpase Activity ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
The Impact

scholarly journals Impact of Low Protein and Lysine-deficient Diets on Bone Metabolism (P08-072-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Daniel Tomé ◽  
Joanna Moro ◽  
Anne Blais ◽  
Catherine Chaumontet ◽  
Patrick Even ◽  
...  
Keyword(s):  
Body Weight ◽  
Bone Metabolism ◽  
Collagen Synthesis ◽  
Milk Protein ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Deficient Diet ◽  
Growing Rats ◽  
Low Protein ◽  
The Impact

Abstract Objectives Low protein diet and essential amino acid deficient-diet have an impact on body weight and growth and different studies also showed an impact of lysine intake on bone metabolism. Lysine has been shown to promote the absorption of intestinal calcium and to participate in the collagen synthesis through its involvement in the reticulation process of the tropocollagen beams. The assembly of tropocollagen bundle into mature collagen fibers is essential for bone formation and remodeling (civitelli et al, 1992; Fini et al, 2001). The objective of this study was to characterize the impact of low protein diet and lysine-deficient diet on bone metabolism of growing rats. Methods Study 1: 6 group of growing rats were fed for 3 weeks different diet with different content of milk protein at levels of 3%, 5%, 8%, 12%, 15% or 20% (% total energy). Study 2: 7 group of growing rats were fed diets with different lysine content (as % of lysine requirement), for 3 weeks: 15%, 25%, 40%, 60%, 75%, 100% or 170% (% Lysine requirement). Body weight was measured daily. At the end of the experiment, the body composition was analyzed and tissues were removed for measurements of the expression of genes involved in protein and bone metabolism. Statistical analysis was done by variance analysis. Results Rats fed low protein diet (3% and 5% of milk protein), compared to control have a lower growth, with a lower body weight and naso-anal length. This weak growth was associated with a lower lean body mass, and also had an impact on bone metabolism. There was a decrease in the bone mineral density, bone mineral content and femur size, associated with a decrease of markers of bone turnover and formation. The same results on bone metabolism were observed on rats fed the 85% lysine deficient diet. Conclusions Low protein diet and lysine-deficient diet reduce growth and bone metabolism. The impact of low protein diet could be related to the lysine deficiency, which have an impact on the calcium intestinal absorption and on collagen synthesis. Funding Sources INRA, AgroParisTech. Supporting Tables, Images and/or Graphs

Effect of phenobarbital on the development of fatty livers In choline-deficient rats

1970 ◽  
Vol 48 (11) ◽  
pp. 1284-1285 ◽  
Author(s):  
A. Chalvardjian
Keyword(s):  
Hepatic Cell ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Fatty Livers ◽  
Phenobarbital Administration ◽  
Phospholipid Pool

The increase in hepatic phospholipid pool induced by phenobarbital did not affect the hepatic accumulation of fat produced by feeding rats a choline-deficient diet for 4 days. This lack of effect suggests that phenobarbital administration does not increase the choline requirement of rats, and/or that phenobarbital and choline deficiency act on different loci within the hepatic cell independently of each other.

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