Deletion of Nhlh2 Results in a Defective Torpor Response and Reduced Beta Adrenergic Receptor Expression in Adipose Tissue
dc.contributor.author | Wankhade, U. D. | en |
dc.contributor.author | Vella, K. R. | en |
dc.contributor.author | Fox, D. L. | en |
dc.contributor.author | Good, Deborah J. | en |
dc.contributor.department | Human Nutrition, Foods, and Exercise | en |
dc.date.accessioned | 2017-02-08T13:15:06Z | en |
dc.date.available | 2017-02-08T13:15:06Z | en |
dc.date.issued | 2010-08-23 | en |
dc.description.abstract | Background: Mice with a targeted deletion of the basic helix-loop-helix transcription factor, Nescient Helix-Loop-Helix 2 (Nhlh2), display adult-onset obesity with significant increases in their fat depots, abnormal responses to cold exposure, and reduced spontaneous physical activity levels. These phenotypes, accompanied by the hypothalamic expression of Nhlh2, make the Nhlh2 knockout (N2KO) mouse a useful model to study the role of central nervous system (CNS) control on peripheral tissue such as adipose tissue. Methodology: Differences in body temperature and serum analysis of leptin were performed in fasted and ad lib fed wildtype (WT) and N2KO mice. Histological analysis of white (WAT) and brown adipose tissue (BAT) was performed. Gene and protein level expression of inflammatory and metabolic markers were compared between the two genotypes. Principal Findings: We report significant differences in serum leptin levels and body temperature in N2KO mice compared with WT mice exposed to a 24-hour fast, suggestive of a defect in both white (WAT) and brown adipose tissue (BAT) function. As compared to WT mice, N2KO mice showed increased serum IL-6 protein and WAT IL-6 mRNA levels. This was accompanied by slight elevations of mRNA for several macrophage markers, including expression of macrophage specific protein F4/80 in adipose, suggestive of macrophage infiltration of WAT in the mutant animals. The mRNAs for β3-adrenergic receptors (β3-AR), β2-AR and uncoupling proteins were significantly reduced in WAT and BAT from N2KO mice compared with WT mice. Conclusions: These studies implicate Nhlh2 in the central control of WAT and BAT function, with lack of Nhlh2 leading to adipose inflammation and altered gene expression, impaired leptin response to fasting, all suggestive of a deficient torpor response in mutant animals. | en |
dc.description.version | Published version | en |
dc.format.extent | 9 pages | en |
dc.format.mimetype | application/pdf | en |
dc.identifier.doi | https://doi.org/10.1371/journal.pone.0012324 | en |
dc.identifier.issn | 1932-6203 | en |
dc.identifier.issue | 8 | en |
dc.identifier.uri | http://hdl.handle.net/10919/74962 | en |
dc.identifier.volume | 5 | en |
dc.language.iso | en | en |
dc.publisher | PLOS | en |
dc.relation.uri | http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000281153500010&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=930d57c9ac61a043676db62af60056c1 | en |
dc.rights | Creative Commons Attribution 4.0 International | en |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | en |
dc.subject | beta-3-adrenergic receptor | en |
dc.subject | cold-exposure | en |
dc.subject | adult humans | en |
dc.subject | molecular characterization | en |
dc.subject | gene-expression | en |
dc.subject | obese gene | en |
dc.subject | brown | en |
dc.subject | mice | en |
dc.subject | transcription | en |
dc.subject | fat | en |
dc.title | Deletion of Nhlh2 Results in a Defective Torpor Response and Reduced Beta Adrenergic Receptor Expression in Adipose Tissue | en |
dc.title.serial | PLOS ONE | en |
dc.type | Article - Refereed | en |
dc.type.dcmitype | Text | en |
pubs.organisational-group | /Virginia Tech | en |
pubs.organisational-group | /Virginia Tech/Agriculture & Life Sciences | en |
pubs.organisational-group | /Virginia Tech/Agriculture & Life Sciences/CALS T&R Faculty | en |
pubs.organisational-group | /Virginia Tech/Agriculture & Life Sciences/Human Nutrition, Foods, & Exercise | en |
pubs.organisational-group | /Virginia Tech/All T&R Faculty | en |
pubs.organisational-group | /Virginia Tech/Faculty of Health Sciences | en |
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