Persistence of diet‐induced obesity despite access to voluntary activity in mice lacking sarcolipin. Issue 9 (23rd September 2015)

• Record Type: Journal Article
• Authors: Gamu, Daniel; Trinh, Anton; Bombardier, Eric; Tupling, A. Russell
• Is Part Of: Physiological reports. Volume 3:Issue 9(2015:Sep.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2015-09-23
• Subjects: Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.12549
• Languages: English
• ISSNs: 2051-817X

Abstract

<abstract abstract-type="main" id="phy212549-abs-0001"> <title>Abstract</title> <p>Several rodent models of obesity have been shown to develop excessive adiposity only when voluntary cage ambulation is restricted. We have previously shown that mice lacking the sarco(endo)plasmic reticulum Ca<sup>2+</sup>‐ATPase pump regulatory protein sarcolipin (<italic>Sln</italic><sup><italic>−/−</italic></sup>), an uncoupler of Ca<sup>2+</sup> uptake, develop excessive diet‐induced obesity under standard housing conditions. However, it is unclear whether this phenotype is due, in part, to the sedentary housing environment in which these animals are kept. To address this, we allowed wild‐type and <italic>Sln</italic><sup><italic>−/−</italic></sup> animals ad libitum access to voluntary wheel running while consuming a standard chow or high‐fat diet for 8 weeks. During this period, wheel revolutions were monitored along with weekly mass gain. Postdiet glucose tolerance and visceral adiposity were also taken. The volume of wheel running completed was similar between genotype, regardless of diet. Although voluntary activity reduced mass gain relative to sedentary controls within each diet (<italic>P < </italic>0.05), visceral adiposity was surprisingly unaltered with activity. However, <italic>Sln</italic><sup><italic>−/−</italic></sup> mice developed excessive obesity (<italic>P </italic><<italic> </italic>0.05) and glucose intolerance (<italic>P < </italic>0.05) with high‐fat feeding relative to wild‐type controls. These findings indicate that the excessive diet‐induced obese phenotype previously observed in <italic>Sln</italic><sup><italic>−/−</italic></sup> mice is not the result of severely restricted daily ambulation, but in fact the inability to recruit uncoupling of the Ca<sup>2+</sup>‐ATPase pump.</p> </abstract>