Skeletal sensitivity to dietary calcium deficiency is increased in the female compared with the male rat

2001 ◽  
Vol 79 (5) ◽  
pp. 379-385 ◽  
Author(s):  
W Geng ◽  
G L Wright
Keyword(s):  
Bone Resorption ◽  
Bone Mass ◽  
Dietary Calcium ◽  
Calcium Deficiency ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Calcium Diet ◽  
Dietary Calcium Deficiency ◽  
Body Bone

We investigated potential sex differences in bone resorption and the conservation of whole body bone mass in 24-week-old Sprague-Dawley rats maintained on a 1.0% calcium diet and then fed diets containing 0.02, 0.5, 1.0, or 1.75% calcium for 31 days. Lowering dietary calcium from 1.00% to 0.02% doubled whole skeleton bone resorption (urinary 3H-tetracycline loss). Female rats were more sensitive to calcium stress, exhibiting the maximal resorptive response when fed the 0.5% calcium diet, whereas the 0.02% calcium diet was required to elicit this response in males. Despite the evidence of increased bone resorption, whole skeleton mass was unchanged in females and was significantly increased in males, indicating that switching to even the 0.02% calcium diet did not result in an overt loss of total body bone mass. Compared with controls, the skeleton mass of females (97 ± 1.4%) maintained on the 0.02% calcium diet was significantly lower than males (107 ± 2.4%), again suggesting a greater impact of calcium deficiency in females. The calculation of the average percentage growth of selected individual bones in male rats indicated a proportional increase in bone mass between the axial and appendicular skeleton of approximately +4% and +18% in animals maintained on 0.02 and 1.75% diets, respectively. By comparison, female rats consuming the 0.02% calcium diet showed an average 14% loss in axial bone and 7.5% gain in appendicular bone mass. The results indicate increased sensitivity to dietary calcium deficiency in female rats which involves a significant loss in axial bone mass not observed in male rats maintained under similar dietary conditions.Key words: skeleton bone mass, calcium diet, 3H-tetracycline, axial, appendicular, gender, sex.

Effect of Oophorectomy and Calcium Deprivation on Bone Mass in the Rat

1978 ◽  
Vol 54 (4) ◽  
pp. 439-446 ◽  
Author(s):  
A. Hodgkinson ◽  
Jean E. Aaron ◽  
A. Horsman ◽  
M. S. F. McLachlan ◽  
B. E. C. Nordin
Keyword(s):  
Bone Mass ◽  
Trabecular Bone ◽  
Dry Weight ◽  
Calcium Deficiency ◽  
Normal Diet ◽  
Female Rats ◽  
Cross Sectional ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium

1. The effects of a low calcium diet and of oophorectomy, separately and together, on cortical and trabecular bone mass, have been examined in mature female rats. 2. Calcium deprivation caused a significant decrease of weight, cortical cross-sectional area and ratio of cortical to total area in the femur, it significantly reduced the volume of trabecular bone and increased the percentage of osteoid surface in the tail vertebrae, and in addition increased the urinary excretion of phosphate and, initially, of hydroxyproline. 3. Oophorectomy caused similar though smaller changes in trabecular bone and urine, whereas the effects of oophorectomy on cortical bone were greater on a low calcium intake than on a normal intake. 4. The ash weight of the femora, expressed as a percentage of the total dry weight, was unaffected by calcium deprivation or oophorectomy alone but was significantly reduced when the two occurred together. 5. The percentage of resorption surfaces in the vertebrae tended to increase on the low calcium diet and after oophorectomy on the normal diet but decreased after oophorectomy on a low calcium diet. 6. It is concluded that oophorectomy and calcium deficiency each reduce bone mass in the adult rat but the greatest effect is seen when they are combined.

scholarly journals The RANKL Distal Control Region Is Required for the Increase in RANKL Expression, But Not the Bone Loss, Associated with Hyperparathyroidism or Lactation in Adult Mice

2012 ◽  
Vol 26 (2) ◽  
pp. 341-348 ◽  
Author(s):  
Melda Onal ◽  
Carlo Galli ◽  
Qiang Fu ◽  
Jinhu Xiong ◽  
Robert S. Weinstein ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Control Region ◽  
Dominant Role ◽  
Dietary Calcium ◽  
Calcium Deficiency ◽  
Wild Type ◽  
Rankl Expression ◽  
Adult Mice ◽  
Dietary Calcium Deficiency

Abstract Osteoclast-mediated bone resorption plays an essential role in calcium homeostasis and lactation. The cytokine receptor activator of nuclear factor κB ligand (RANKL) is one of a number of factors that controls the production, survival, and activity of osteoclasts. Calciotropic hormones, such as PTH, control RANKL transcription in part via an enhancer known as the distal control region (DCR), and mice lacking this enhancer have fewer osteoclasts under normal physiological conditions. Here, we have addressed the role of the DCR in situations in which activation of the PTH receptor is thought to stimulate bone resorption via elevation of RANKL expression. Dietary calcium deficiency stimulated RANKL expression in the bone of young (1 month old) wild-type, but not DCR knockout (KO), mice. Consistent with this, the cancellous bone loss and the increase in osteoclasts caused by dietary calcium deficiency were blunted in young KO mice. DCR deletion also prevented the increase in RANKL expression caused by dietary calcium deficiency in 6-month-old mice. However, the diet-induced bone loss was similar in wild-type and KO mice at this age. The increase in RANKL expression caused by lactation was also blunted in DCR KO mice, but lactation-induced bone loss was similar in both genotypes. These results demonstrate that, even though the DCR is required for the increase in RANKL expression associated with hyperparathyroidism or lactation, this increase is not required for the bone loss caused by these conditions in adult mice, suggesting that changes in other factors, such as osteoprotegerin or estrogen levels, play a dominant role.

scholarly journals THE EFFECT OF EXPERIMENTAL REDUCTION OF KIDNEY SUBSTANCE UPON THE PARATHYROID GLANDS AND SKELETAL TISSUE

1936 ◽  
Vol 64 (6) ◽  
pp. 965-980 ◽  
Author(s):  
Alwin M. Pappenheimer ◽  
Keyword(s):  
Dietary Calcium ◽  
Calcium Deficiency ◽  
Renal Tissue ◽  
Parathyroid Glands ◽  
Skeletal Tissue ◽  
Young Rats ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Dietary Calcium Deficiency

Reduction of renal tissue in young rats regularly leads to a marked increase in the volume of the parathyroid glands. If partially nephrectomized rats are maintained on a low calcium diet, growth is stunted, and skeletal lesions are produced, of far greater severity than can be ascribed to the dietary calcium deficiency alone. The picture closely resembles that found in cases of renal rickets in children.

scholarly journals Accelerated Bone Resorption, Due to Dietary Calcium Deficiency, Promotes Breast Cancer Tumor Growth in Bone

2007 ◽  
Vol 67 (19) ◽  
pp. 9542-9548 ◽  
Author(s):  
Yu Zheng ◽  
Hong Zhou ◽  
James R.K. Modzelewski ◽  
Robert Kalak ◽  
Julie M. Blair ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Resorption ◽  
Tumor Growth ◽  
Dietary Calcium ◽  
Calcium Deficiency ◽  
Cancer Tumor ◽  
Dietary Calcium Deficiency

scholarly journals Osteocyte-derived RANKL is a critical mediator of the increased bone resorption caused by dietary calcium deficiency

Bone ◽  
2014 ◽  
Vol 66 ◽  
pp. 146-154 ◽  
Author(s):  
Jinhu Xiong ◽  
Marilina Piemontese ◽  
Jeff D. Thostenson ◽  
Robert S. Weinstein ◽  
Stavros C. Manolagas ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Dietary Calcium ◽  
Calcium Deficiency ◽  
Dietary Calcium Deficiency

scholarly journals Efficacy of Supplemental Natural Zeolite in Broiler Chickens Subjected to Dietary Calcium Deficiency

2014 ◽  
Vol 13 (2) ◽  
pp. 3141 ◽  
Author(s):  
Erol Bintaş ◽  
Mehmet Bozkurt ◽  
Kamil Küçükyılmaz ◽  
Ramazan Konak ◽  
Mustafa Çınar ◽  
...  
Keyword(s):  
Natural Zeolite ◽  
Broiler Chickens ◽  
Dietary Calcium ◽  
Calcium Deficiency ◽  
Dietary Calcium Deficiency

scholarly journals Increased bioactivation of dihaloalkanes in rat liver due to induction of class Theta glutathione S-transferase T1-1

1998 ◽  
Vol 335 (3) ◽  
pp. 619-630 ◽  
Author(s):  
Philip J. SHERRATT ◽  
Margaret M. MANSON ◽  
Anne M. THOMSON ◽  
Erna A. M. HISSINK ◽  
Gordon E. NEAL ◽  
...  
Keyword(s):  
Western Blotting ◽  
Rat Liver ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Female Rat ◽  
Glutathione S Transferase ◽  
Chemopreventive Agents ◽  
Cytoplasmic Staining ◽  
Potent Inducer

A characteristic feature of the class Theta glutathione S-transferase (GST) T1-1 is its ability to activate dichloromethane and dibromoethane by catalysing the formation of mutagenic conjugates. The level of the GSTT1 subunit within tissues is an important determinant of susceptibility to the carcinogenic effects of these dihaloalkanes. In the present study it is demonstrated that hepatic GST activity towards these compounds can be elevated significantly in female and male Fischer-344 rats by feeding these animals on diets supplemented with cancer chemopreventive agents. Immunoblotting experiments showed that increased activity towards the dihaloalkanes is associated with elevated levels of the GSTT1 subunit in rat liver. Sex-specific effects were observed in the induction of GSTT1 protein. Amongst the chemopreventive agents tested, indole-3-carbinol proved to be the most potent inducer of hepatic GSTT1 in male rats (6.2-fold), whereas coumarin was the most potent inducer of this subunit in the livers of female rats (3.5-fold). Phenobarbital showed significant induction of GSTT1 only in male rat liver and had little effect in female rat liver. Western blotting showed that class Alpha, Mu and Pi GST subunits are not co-ordinately induced with GSTT1, indicating that the expression of GSTT1 is determined, at least in part, by mechanisms distinct from those that regulate levels of other transferases. The increase in amount of hepatic GSTT1 protein was also reflected by an increase in the steady-state level of mRNA in response to treatment with chemopreventive agents and model inducers. Immunohistochemical detection of GSTT1 in rat liver supported the Western blotting data, but showed, in addition to cytoplasmic staining, significant nuclear localization of the enzyme in hepatocytes from some treated animals, including those fed on an oltipraz-containing diet. Significantly, the hepatic level of cytochrome P-450 2E1, an enzyme which offers a detoxification pathway for dihaloalkanes, was unchanged by the various inducing agents studied. It is concluded that the induction of GSTT1 by dietary components and its localization within cells are important factors that should be considered when assessing the risk dihaloalkanes pose to human health.

scholarly journals EFFECT OF YOHIMBINE ON CLOMIPRAMINE-INDUCED SEXUAL DYSFUNCTION IN MALE RATS

2017 ◽  
Vol 10 (2) ◽  
pp. 92
Author(s):  
Devangam Sheshadri Shekar
Keyword(s):  
Sexual Behavior ◽  
Sexual Dysfunction ◽  
Histopathological Examination ◽  
Red Light ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Testicular Damage

Object: The present investigation has been carried out to find out the effect of yohimbine on clomipramine-induced sexual dysfunction in male rats.Methods: The male rats were treated with clomipramine and yohimbine simultaneously for 60 days. During the treatment, all the male rats werechallenged with the female rats which are in estrous phase and their sexual behavior was observed under dim red light. Half of the animals in each group and remaining on 60 day were sacrificed, blood was collected and serum separated. Testis was collected and preserved in 10% formalin forsubsequent histopathological examination. thResults: The study reveals that yohimbine failed to antagonize the clomipramine-induced sexual dysfunction in male rats in all aspects, except thepartial improvement in the sexual behavior.Conclusion: Yohimbine a well-known aphrodisiac failed to antagonize the clomipramine-induced sexual dysfunction in male rats. The decrease intestosterone levels, a decrease in spermatozoa count were continued even in the presence of yohimbine except improvement in the sexual behaviorparameters. Hence, yohimbine could not be a safe antidote against clomipramine-induced sexual dysfunction in male rats.Keywords: Yohimbine, Clomipramine, Testosterone, Male rat sexual competence, Testicular damage.

scholarly journals Negligible Effect of Estrogen Deficiency on Development of Skeletal Changes Induced by Type 1 Diabetes in Experimental Rat Models

2020 ◽  
Vol 2020 ◽  
pp. 1-21
Author(s):  
Aleksandra Janas ◽  
Ewa Kruczek ◽  
Piotr Londzin ◽  
Sławomir Borymski ◽  
Zenon P. Czuba ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Bone Resorption ◽  
Bone Mass ◽  
Cancellous Bone ◽  
Maximum Load ◽  
Estrogen Deficiency ◽  
Female Rats ◽  
Skeletal System ◽  
Tibial Metaphysis ◽  
Ovx Rats

Although postmenopausal osteoporosis often occurs concurrently with diabetes, little is known about interactions between estrogen deficiency and hyperglycemia in the skeletal system. In the present study, the effects of estrogen deficiency on the development of biochemical, microstructural, and mechanical changes induced by streptozotocin-induced diabetes mellitus (DM) in the rat skeletal system were investigated. The experiments were carried out on nonovariectomized (NOVX) and ovariectomized (OVX) control and diabetic mature female Wistar rats. Serum levels of bone turnover markers (CTX-I and osteocalcin) and 23 cytokines, bone mass and mineralization, histomorphometric parameters, and mechanical properties of cancellous and compact bone were determined. The results were subjected to two-way ANOVA and principal component analysis (PCA). Estrogen deficiency induced osteoporotic changes, with increased bone resorption and formation, and worsening of microstructure (femoral metaphyseal BV/TV decreased by 13.0%) and mechanical properties of cancellous bone (the maximum load in the proximal tibial metaphysis decreased by 34.2%). DM in both the NOVX and OVX rats decreased bone mass, increased bone resorption and decreased bone formation, and worsened cancellous bone microarchitecture (for example, the femoral metaphyseal BV/TV decreased by 17.3% and 18.1%, respectively, in relation to the NOVX controls) and strength (the maximum load in the proximal tibial metaphysis decreased by 35.4% and 48.1%, respectively, in relation to the NOVX controls). Only in the diabetic rats, profound increases in some cytokine levels were noted. In conclusion, the changes induced by DM in female rats were only slightly intensified by estrogen deficiency. Despite similar effects on bone microstructure and strength, the influence of DM on the skeletal system was based on more profound systemic homeostasis changes than those induced by estrogen deficiency.

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