TRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.

Trpm8 (transient receptor potential cation channel, subfamily M, member 8) is expressed by sensory neurons and is involved in the detection of environmental cold temperatures. TRPM8 activity triggers an increase in uncoupling protein 1 (Ucp1)-dependent brown adipose tissue (BAT) thermogenesis. Bone...

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Autores principales:	Adriana Lelis Carvalho, Annika Treyball, Daniel J Brooks, Samantha Costa, Ryan J Neilson, Michaela R Reagan, Mary L Bouxsein, Katherine J Motyl
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/953e1edcb71d47958ff718fb0188a599
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spelling	oai:doaj.org-article:953e1edcb71d47958ff718fb0188a5992021-12-02T20:03:57ZTRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.1932-620310.1371/journal.pone.0231060https://doaj.org/article/953e1edcb71d47958ff718fb0188a5992021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0231060https://doaj.org/toc/1932-6203Trpm8 (transient receptor potential cation channel, subfamily M, member 8) is expressed by sensory neurons and is involved in the detection of environmental cold temperatures. TRPM8 activity triggers an increase in uncoupling protein 1 (Ucp1)-dependent brown adipose tissue (BAT) thermogenesis. Bone density and marrow adipose tissue are both influenced by rodent housing temperature and brown adipose tissue, but it is unknown if TRPM8 is involved in the co-regulation of thermogenesis and bone homeostasis. To address this, we examined the bone phenotypes of one-year-old Trpm8 knockout mice (Trpm8-KO) after a 4-week cold temperature challenge. Male Trpm8-KO mice had lower bone mineral density than WT, with smaller bone size (femur length and cross-sectional area) being the most striking finding, and exhibited a delayed cold acclimation with increased BAT expression of Dio2 and Cidea compared to WT. In contrast to males, female Trpm8-KO mice had low vertebral bone microarchitectural parameters, but no genotype-specific alterations in body temperature. Interestingly, Trpm8 was not required for cold-induced trabecular bone loss in either sex, but bone marrow adipose tissue in females was significantly suppressed by Trpm8 deletion. In summary, we identified sex differences in the role of TRPM8 in maintaining body temperature, bone microarchitecture and marrow adipose tissue. Identifying mechanisms through which cold temperature and BAT influence bone could help to ameliorate potential bone side effects of obesity treatments designed to stimulate thermogenesis.Adriana Lelis CarvalhoAnnika TreyballDaniel J BrooksSamantha CostaRyan J NeilsonMichaela R ReaganMary L BouxseinKatherine J MotylPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 6, p e0231060 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Adriana Lelis Carvalho Annika Treyball Daniel J Brooks Samantha Costa Ryan J Neilson Michaela R Reagan Mary L Bouxsein Katherine J Motyl TRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.
description	Trpm8 (transient receptor potential cation channel, subfamily M, member 8) is expressed by sensory neurons and is involved in the detection of environmental cold temperatures. TRPM8 activity triggers an increase in uncoupling protein 1 (Ucp1)-dependent brown adipose tissue (BAT) thermogenesis. Bone density and marrow adipose tissue are both influenced by rodent housing temperature and brown adipose tissue, but it is unknown if TRPM8 is involved in the co-regulation of thermogenesis and bone homeostasis. To address this, we examined the bone phenotypes of one-year-old Trpm8 knockout mice (Trpm8-KO) after a 4-week cold temperature challenge. Male Trpm8-KO mice had lower bone mineral density than WT, with smaller bone size (femur length and cross-sectional area) being the most striking finding, and exhibited a delayed cold acclimation with increased BAT expression of Dio2 and Cidea compared to WT. In contrast to males, female Trpm8-KO mice had low vertebral bone microarchitectural parameters, but no genotype-specific alterations in body temperature. Interestingly, Trpm8 was not required for cold-induced trabecular bone loss in either sex, but bone marrow adipose tissue in females was significantly suppressed by Trpm8 deletion. In summary, we identified sex differences in the role of TRPM8 in maintaining body temperature, bone microarchitecture and marrow adipose tissue. Identifying mechanisms through which cold temperature and BAT influence bone could help to ameliorate potential bone side effects of obesity treatments designed to stimulate thermogenesis.
format	article
author	Adriana Lelis Carvalho Annika Treyball Daniel J Brooks Samantha Costa Ryan J Neilson Michaela R Reagan Mary L Bouxsein Katherine J Motyl
author_facet	Adriana Lelis Carvalho Annika Treyball Daniel J Brooks Samantha Costa Ryan J Neilson Michaela R Reagan Mary L Bouxsein Katherine J Motyl
author_sort	Adriana Lelis Carvalho
title	TRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.
title_short	TRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.
title_full	TRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.
title_fullStr	TRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.
title_full_unstemmed	TRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.
title_sort	trpm8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/953e1edcb71d47958ff718fb0188a599
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TRPM8 modulates temperature regulation in a sex-dependent manner without affecting cold-induced bone loss.

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