scholarly journals Protective effect of dietary long-chainn-3 polyunsaturated fatty acids on bone loss in gonad-intact middle-aged male rats

2006 ◽  
Vol 95 (3) ◽  
pp. 462-468 ◽  
Author(s):  
Chwan-Li Shen ◽  
James K. Yeh ◽  
Jahan Rasty ◽  
Yong Li ◽  
Bruce A. Watkins
Keyword(s):  
Bone Loss ◽  
Bone Mineral ◽  
Male Rats ◽  
Prostaglandin E ◽  
No Production ◽  
Safflower Oil ◽  
Menhaden Oil ◽  
Middle Aged ◽  
Mineral Density ◽  
Middle Aged Male

This study evaluated the effect of a fat blend containing long-chain (LC)n-3 PUFA on bone mineral density (BMD) and bone metabolism in gonad-intact middle-aged male rats (12 months old,n28). Seven rats were killed on day 0 of dietary intervention to determine the baseline BMD. The remaining rats (seven per group) were fed a diet with one of the following dietary lipid treatments (g/kg diet): 167g safflower oil+33g menhaden oil (N6+N3 diet, control), 200g safflower oil (N6 diet, almost devoid of LCn-3 PUFA), or 190g menhaden oil+10g corn oil (N3 diet, rich in LCn-3 PUFA) for 20 weeks. After 20 weeks, all dietary treatment groups had a lower BMD compared with the baseline reference. However, rats fed the N3 diet had the highest bone mineral content and cortical+subcortical BMD compared with those fed the N6 and control N6+N3 diet. Compared with the control (N6+N3) group, rats fed the N3 diet had higher values for serum insulin-like growth factor-I, parathyroid hormone, 1, 25-(OH)2vitamin D3and bone-specific alkaline phosphatase activity, but lower bone NO production and urinary Ca, whereas rats fed the N6 diet had higher bone prostaglandin E2production and serum pyridinoline. These findings indicate a protective action of LCn-3 PUFA on ageing-induced bone loss in gonad-intact middle-aged male rats through a modulation of local factors and systemic calcitrophic hormones.

scholarly journals Prospective evaluation of bone mineral density among middle-aged HIV-infected and uninfected women: Association between methadone use and bone loss

Maturitas ◽  
2011 ◽  
Vol 70 (3) ◽  
pp. 295-301 ◽  
Author(s):  
Anjali Sharma ◽  
Hillel W. Cohen ◽  
Ruth Freeman ◽  
Nanette Santoro ◽  
Ellie E. Schoenbaum
Keyword(s):  
Bone Mineral Density ◽  
Bone Loss ◽  
Bone Mineral ◽  
Prospective Evaluation ◽  
Middle Aged ◽  
Mineral Density

scholarly journals Plasma nitrate+nitrite levels are regulated by ovarian steroids but do not correlate with trabecular bone mineral density in rats

1998 ◽  
Vol 159 (1) ◽  
pp. 27-34 ◽  
Author(s):  
RL van Bezooijen ◽  
I Que ◽  
AG Ederveen ◽  
HJ Kloosterboer ◽  
SE Papapoulos ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Loss ◽  
Trabecular Bone ◽  
Bone Mineral ◽  
Ovariectomized Rats ◽  
No Production ◽  
Mineral Density ◽  
Trabecular Bone Mineral Density ◽  
Oestrogen Treatment ◽  
Plasma Nitrate

Nitric oxide (NO) is a mediator of bone metabolism and its production is under the control of gender hormones in several cell types or tissues. Changes in endogenous NO production, measured as plasma nitrate+nitrite levels, may therefore contribute to ovariectomy (OVX)-induced bone loss. We studied plasma nitrate+nitrite levels and trabecular bone mineral density (TBMD) 4 weeks after sham-operation or OVX in rats receiving various hormonal treatments. OVX decreased plasma nitrate+nitrite levels significantly and this was accompanied by a significant decrease in TBMD. Treatment with oral ethinyl oestradiol (EE) and subcutaneous 17beta-oestradiol dose-dependently prevented the decrease in plasma nitrate+nitrite levels after OVX, but treatment with oral 17beta-oestradiol did not. Oestrogen treatment, 17beta-oestradiol (s. c. or orally) or EE (orally), prevented the OVX-induced decrease in TBMD. Treatment of sham-operated rats with the anti-oestrogen ICI164, 384 induced a significant decrease in TBMD that corresponded to 54% of the decrease observed after OVX, but did not affect plasma nitrate+nitrite levels. Treatment of ovariectomized rats with Org 2058, a pure progestagen, did not prevent bone loss, but prevented the decrease in plasma nitrate+nitrite levels dose-dependently. Treatment with tibolone, a synthetic steroid with combined weak oestrogenic, progestagenic, and androgenic properties, or with progestagen in combination with EE completely prevented bone loss after OVX. These treatments, however, only partly prevented the OVX-induced decrease in plasma nitrate+nitrite levels. In conclusion, OVX decreased both TBMD and plasma nitrate+nitrite levels. Although plasma nitrate+nitrite levels were under the control of both oestrogen and progesterone, TBMD was affected by oestrogen only. Decreased systemic production of NO is, therefore, not involved in OVX-induced bone loss in rats.

scholarly journals The Effect of Chronic Alcohol Administration on Bone Mineral Content and Bone Strength in Male Rats

2010 ◽  
pp. 599-604
Author(s):  
PD Broulík ◽  
J Rosenkrancová ◽  
P Růžička ◽  
R Sedláček ◽  
T Zíma
Keyword(s):  
Risk Factor ◽  
Bone Loss ◽  
Mechanical Strength ◽  
Bone Mineral ◽  
Male Rats ◽  
Bending Test ◽  
Mineral Density ◽  
Term Administration ◽  
Male Wistar Rats ◽  
And Control

Alcohol use has been identified as a risk factor for the development of osteoporosis. Eight male Wistar rats at two months of age were alcoho-fed (7.6 g 95 % ethanol/kg b.w. per day) to evaluate the effects of long-term administration (three months) of alcohol in drinking water. We have used a dose which is considered to be comparable to a dose of 1 liter of wine or 2.5 liters of 12° beer used in male adults daily. The bones were tested mechanically by a three-point bending test in a Mini Bionix (MTS) testing system. The bones from alcohol-fed rats were characterized by a reduction in bone density as well as in ash, calcium and phosphate content. In alcohol-fed rats the reduction in bone mineral density (10 %) was reflected by about 12 % reduction of mechanical strength of femur (158±5.5 vs. 178±3.2 N/mm2 ). Alcohol significantly altered femoral cortical thickness. In our experiment alcohol itself did not exert any antiandrogenic effect and it did not produce changes in the weight of seminal vesicles. Liver function test (GGT, ALP, AST) did not differ between alcohol-fed rats and control rats. Alcohol-induced bone loss is associated with increased bone resorption and decreased bone formation. These results document the efficacy of alcohol at the dose of 7.6 g 95 % ethanol/kg b.w. to cause bone loss and loss of bone mechanical strength in intact rats. The results of the present study may be interpreted as supporting the hypothesis of alcohol as a risk factor for osteoporosis.

Genistein Increase Thyroid Hormone and 7 alpha-hydroxycholesterol concentrations in the liver of middle-aged male rats

2018 ◽  
Author(s):  
Branka Sosic-Jurjevic ◽  
Dieter Lutjohann ◽  
Dragana Miljic ◽  
Jasmina Ciric ◽  
Svetlana Trifunovic ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Male Rats ◽  
Middle Aged ◽  
Middle Aged Male

Impaired Estrogen Sensitivity in Bone by Inhibiting Both Estrogen Receptor a and b Pathways*

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Bone Mineral Density ◽  
Estrogen Receptor ◽  
Bone Loss ◽  
Bone Turnover ◽  
Bone Mineral ◽  
Female Rats ◽  
Wild Type ◽  
Mineral Density ◽  
Transgenic Rats ◽  
Estrogen Sensitivity

Although it is well established that estrogen deficiencycauses osteoporosis among the postmenopausalwomen, the involvement of estrogen receptor (ER) in itspathogenesis still remains uncertain. In the presentstudy, we have generated rats harboring a dominantnegative ERa, which inhibits the actions of not only ERabut also recently identified ERb. Contrary to our expectation,the bone mineral density (BMD) of the resultingtransgenic female rats was maintained at the same levelwith that of the wild-type littermates when sham-operated.In addition, ovariectomy-induced bone loss wasobserved almost equally in both groups. Strikingly, however,the BMD of the transgenic female rats, after ovariectomized,remained decreased even if 17b-estradiol(E2) was administrated, whereas, in contrast, the decreaseof littermate BMD was completely prevented byE2. Moreover, bone histomorphometrical analysis ofovariectomized transgenic rats revealed that the higherrates of bone turnover still remained after treatmentwith E2. These results demonstrate that the preventionfrom the ovariectomy-induced bone loss by estrogen ismediated by ER pathways and that the maintenanceof BMD before ovariectomy might be compensatedby other mechanisms distinct from ERa and ERbpathways.

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