Aberrant behaviors, unaltered sensory, cognitive functions and hedonic responses in vitamin D receptor mutant mice

2007 ◽  
Author(s):  
A. Minasyan ◽  
T. Keisala ◽  
Y.-R. Lou ◽  
A. V. Kalueff ◽  
P. Tuohimaa
2007 ◽  
Vol 104 (3-5) ◽  
pp. 274-280 ◽  
Author(s):  
Anna Minasyan ◽  
Tiina Keisala ◽  
Yan-Ru Lou ◽  
Allan V. Kalueff ◽  
Pentti Tuohimaa

2007 ◽  
Vol 104 (3-5) ◽  
pp. 269-273 ◽  
Author(s):  
Tiina Keisala ◽  
Anna Minasyan ◽  
Ulla Järvelin ◽  
Jinghuan Wang ◽  
Tuula Hämäläinen ◽  
...  

2009 ◽  
Vol 114 (3-5) ◽  
pp. 161-166 ◽  
Author(s):  
Anna Minasyan ◽  
Tiina Keisala ◽  
Jing Zou ◽  
Ya Zhang ◽  
Esko Toppila ◽  
...  

2009 ◽  
Vol 115 (3-5) ◽  
pp. 91-97 ◽  
Author(s):  
Tiina Keisala ◽  
Anna Minasyan ◽  
Yan-Ru Lou ◽  
Jing Zou ◽  
Allan V. Kalueff ◽  
...  

Author(s):  
Maheen Shahid ◽  
Syeda Amrah Hashmi ◽  
Rehana Rehman ◽  
Admin

Dear Madam, Infertility is a known source of distress among couples worldwide. This agony significantly stems from the concern of not having an identifiable cause leading to infertility. With male factors accounting for 20-30% of the total causes of infertility (1), a thorough evaluation of both the partners is done. Upon evaluation, Vitamin D deficiency was noticed significantly in males coming to infertility centres. However, its functions and how it impacted reproduction was not known until the research led to the discovery of Vitamin D Receptor (VDR) in many organs of the male reproductive tract. It is now known that vitamin D deficiency decreases male fertility by contributing to oxidative stress and gonadal insufficiency, disrupting spermatogenesis, affecting sperm morphology and normal calcium haemostasis. (2) Oxidative stress, caused by an imbalance between oxidative and antioxidative mechanisms, is believed to be a well-known mechanism underlying idiopathic male infertility. Reproductive health professionals and researchers fittingly started searching for antioxidants to combat this imbalance. A study concluded that adding vitamin D to a cryopreserved semen sample reduced oxidative stress and resulted in better fertility outcomes (3). Animal trials have shown that Vitamin D supplementation reduced oxidative stress and improved semen DNA integrity (4). As Vitamin D exerts its effects by binding to Vitamin D receptors, it was noted that vitamin D receptor null mutant mice had a significant reduction in successful reproductive outcomes due to gonadal insufficiencies. Reduced levels of oestrogen and testosterone were seen along with low sperm count, reduced motility, abnormal spermatogenesis and histological abnormalities in testes of mutant mice. These insufficiencies were attributed to a decreased CYP2R1, CYP27B1 and CYP24A1 expression, lower aromatase activity, secondary to suppression of CYP19 gene and calcium supplementation improved fertility in such cases. (5) There is limited human data available on how Vitamin D deficiency causes gonadal insufficiency, which is important to maintain normal reproductive physiology. More studied are needed to clarify the role of vitamin D in gonadal physiology. Considering the importance of Vitamin D on reproductive functions, its role in causing Oxidative stress and gonadal dysfunction, we suggest randomized control trials in pre-pubertal phase. Continuous....


2011 ◽  
Vol 125 (3-5) ◽  
pp. 202-210 ◽  
Author(s):  
Amanda M. Ousley ◽  
Hilda S. Castillo ◽  
Anna Duraj-Thatte ◽  
Donald F. Doyle ◽  
Bahareh Azizi

2002 ◽  
Vol 4 (22) ◽  
pp. 3863-3866 ◽  
Author(s):  
Steve L. Swann ◽  
Joel J. Bergh ◽  
M. Cindy Farach-Carson ◽  
John T. Koh

2009 ◽  
Vol 296 (4) ◽  
pp. E820-E828 ◽  
Author(s):  
Kari E. Wong ◽  
Frances L. Szeto ◽  
Wenshuo Zhang ◽  
Honggang Ye ◽  
Juan Kong ◽  
...  

Recent studies have established that vitamin D plays multiple biological roles beyond calcium metabolism; however, whether vitamin D is involved in energy metabolism is unknown. To address this question, we characterized the metabolic phenotypes of vitamin D receptor (VDR)-null mutant mice. Under a normocalcemic condition, VDR-null mice displayed less body fat mass and lower plasma triglyceride and cholesterol levels compared with wild-type (WT) mice; when placed on a high-fat diet, VDR-null mice showed a slower growth rate and accumulated less fat mass globally than WT mice, even though their food intake and intestinal lipid transport capacity were the same as WT mice. Consistent with the lower adipose mass, plasma leptin levels were lower and white adipocytes were histologically smaller in VDR-null mice than WT mice. The rate of fatty acid β-oxidation in the white adipose tissue was higher, and the expression of uncoupling protein (UCP) 1, UCP2 and UCP3 was markedly upregulated in VDR-null mice, suggesting a higher energy expenditure in the mutant mice. Experiments using primary brown fat culture confirmed that 1,25-dihydroxyvitamin D3 directly suppressed the expression of the UCPs. Consistently, the energy expenditure, oxygen consumption, and CO2 production in VDR-null mice were markedly higher than in WT mice. These data indicate that vitamin D is involved in energy metabolism and adipocyte biology in vivo in part through regulation of β-oxidation and UCP expression.


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