Genetic lineage, bone mass, and physical activity in mice
Identifieur interne : 003F67 ( Main/Exploration ); précédent : 003F66; suivant : 003F68Genetic lineage, bone mass, and physical activity in mice
Auteurs : Michael Kaye [Canada] ; Robert P. Kusy [États-Unis]Source :
- Bone [ 8756-3282 ] ; 1995.
Abstract
Five strains of inbred mice were found to have variations in bone mass although they were similar in body weight. Two of these strains, C57BL/6J and A/J, were studied in greater detail and the former had more bone in both femur and tibia. The increased bone mass was associated with larger quadriceps muscles in the C57BL/6J animals when measured at 18 weeks of age. Activities of animals from these two strains were studied over 24 h periods using a cage with an ultrasonic movement detector and automatic counter. The C57BL/6J animals were more active than the A/J mice. The male C57BL/6J mice tended to have larger testicles and higher testosterone levels than the A/J animals, whereas the female A/J animals had larger ovaries and higher oestradiol levels. As both male and female C57BL/6J animals were more active, it was concluded that the sex hormone differences between the two strains was not responsible for either the changes in bone mass or physical activity. These findings indicate that in the mouse, activity is in part genetically determined. We have hypothesized that this, in turn, could affect muscle mass and secondarily, bone size and strength. If these results can be applied to humans, it would suggest that differences at birth between individuals are important for bone mass in later life and that muscle mass and activity are in part genetically influenced. If this was the case, then muscle mass and strength could be a factor in bone mass and one of the goals in the prevention and treatment of osteoporosis should be directed toward preservation and/or augmentation of muscle strength. (Bone 17:131–135; 1995)
Url:
DOI: 10.1016/S8756-3282(00)00164-2
Affiliations:
- Canada, États-Unis
- Caroline du Nord, Québec
- Chapel Hill (Caroline du Nord), Montréal
- Université de Caroline du Nord à Chapel Hill
Links toward previous steps (curation, corpus...)
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- to stream Istex, to step Curation: 001D31
- to stream Istex, to step Checkpoint: 001941
- to stream Main, to step Merge: 004689
- to stream Main, to step Curation: 003F67
Le document en format XML
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Kusy</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F0E84C5DBCED142BCBF53CEE757E8BA7AA2D9417</idno><date when="1995" year="1995">1995</date><idno type="doi">10.1016/S8756-3282(00)00164-2</idno><idno type="url">https://api-v5.istex.fr/document/F0E84C5DBCED142BCBF53CEE757E8BA7AA2D9417/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001D31</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001D31</idno><idno type="wicri:Area/Istex/Curation">001D31</idno><idno type="wicri:Area/Istex/Checkpoint">001941</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">001941</idno><idno type="wicri:doubleKey">8756-3282:1995:Kaye M:genetic:lineage:bone</idno><idno type="wicri:Area/Main/Merge">004689</idno><idno type="wicri:Area/Main/Curation">003F67</idno><idno type="wicri:Area/Main/Exploration">003F67</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Genetic lineage, bone mass, and physical activity in mice</title><author><name sortKey="Kaye, Michael" sort="Kaye, Michael" uniqKey="Kaye M" first="Michael" last="Kaye">Michael Kaye</name><affiliation wicri:level="3"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Nephrology and Geriatric Medicine, The Montreal General Hospital, Montreal</wicri:regionArea><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Kusy, Robert P" sort="Kusy, Robert P" uniqKey="Kusy R" first="Robert P." last="Kusy">Robert P. Kusy</name><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Dental Research Center, University of North Carolina at Chapel Hill, Chapel Hill, NC</wicri:regionArea><placeName><region type="state">Caroline du Nord</region><settlement type="city">Chapel Hill (Caroline du Nord)</settlement></placeName><orgName type="university">Université de Caroline du Nord à Chapel Hill</orgName></affiliation></author></analytic><monogr></monogr><series><title level="j">Bone</title><title level="j" type="abbrev">BON</title><idno type="ISSN">8756-3282</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995">1995</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="131">131</biblScope><biblScope unit="page" to="135">135</biblScope></imprint><idno type="ISSN">8756-3282</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">8756-3282</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Five strains of inbred mice were found to have variations in bone mass although they were similar in body weight. Two of these strains, C57BL/6J and A/J, were studied in greater detail and the former had more bone in both femur and tibia. The increased bone mass was associated with larger quadriceps muscles in the C57BL/6J animals when measured at 18 weeks of age. Activities of animals from these two strains were studied over 24 h periods using a cage with an ultrasonic movement detector and automatic counter. The C57BL/6J animals were more active than the A/J mice. The male C57BL/6J mice tended to have larger testicles and higher testosterone levels than the A/J animals, whereas the female A/J animals had larger ovaries and higher oestradiol levels. As both male and female C57BL/6J animals were more active, it was concluded that the sex hormone differences between the two strains was not responsible for either the changes in bone mass or physical activity. These findings indicate that in the mouse, activity is in part genetically determined. We have hypothesized that this, in turn, could affect muscle mass and secondarily, bone size and strength. If these results can be applied to humans, it would suggest that differences at birth between individuals are important for bone mass in later life and that muscle mass and activity are in part genetically influenced. If this was the case, then muscle mass and strength could be a factor in bone mass and one of the goals in the prevention and treatment of osteoporosis should be directed toward preservation and/or augmentation of muscle strength. (Bone 17:131–135; 1995)</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>Caroline du Nord</li><li>Québec</li></region><settlement><li>Chapel Hill (Caroline du Nord)</li><li>Montréal</li></settlement><orgName><li>Université de Caroline du Nord à Chapel Hill</li></orgName></list><tree><country name="Canada"><region name="Québec"><name sortKey="Kaye, Michael" sort="Kaye, Michael" uniqKey="Kaye M" first="Michael" last="Kaye">Michael Kaye</name></region></country><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Kusy, Robert P" sort="Kusy, Robert P" uniqKey="Kusy R" first="Robert P." last="Kusy">Robert P. Kusy</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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