title: Leanness of Lou/C rats does not require higher thermogenic capacity of brown adipose tissue.
abstract: Lou/C rats, an inbred strain of Wistar origin, remain lean throughout life and therefore represent a remarkable model of obesity resistance. To date, the exact mechanisms responsible for the leanness of Lou/C rats remain unknown. The aim of the present study was to investigate whether the leanness of Lou/C rats relies on increased thermogenic capacities in brown adipose tissue (BAT). Results showed that although daily energy expenditure was higher in Lou/C than in Wistar rats, BAT thermogenic capacity was not enhanced in Lou/C rats kept at thermoneutrality as demonstrated by reduced thermogenic response to norepinephrine in vivo, similar oxidative activity of BAT isolated mitochondria in vitro, similar levels of UCP1 mRNA and lower abundance of UCP1 protein in interscapular BAT depots. Relative abundance of β3-adrenergic receptor mRNA was lower in Lou/C BAT while that of GLUT4, FABP or CPT1 was not altered. Activity-related energy expenditure was however considerably increased at thermoneutrality as Lou/C rats demonstrated an impressively high spontaneous running activity in voluntary running wheels. Prolonged cold-exposure (4 °C) depressed the spontaneous running activity of Lou/C rats while BAT thermogenic capacity was increased as reflected by rises in BAT mass, oxidative activity and UCP1 expression. It is concluded that the leanness of Lou/C rats cannot be ascribed to higher thermogenic capacity of brown fat but rather to, at least in part, increased locomotor activity. BAT is not deficient in this rat strain as it can be stimulated by cold exposure when locomotor activity is reduced suggesting some substitution between these thermogenic processes.
authors.affiliation: Laboratoire de Physiologie, Université de Lyon, CNRS, 43 Bvd 11 Novembre 1918, F-69622 Villeurbanne Cedex, France.
authors.forename: Maud
authors.initials: M
authors.lastname: Belouze
authors.forename: Brigitte
authors.initials: B
authors.lastname: Sibille
authors.forename: Benjamin
authors.initials: B
authors.lastname: Rey
authors.forename: Damien
authors.initials: D
authors.lastname: Roussel
authors.forename: Caroline
authors.initials: C
authors.lastname: Romestaing
authors.forename: Loïc
authors.initials: L
authors.lastname: Teulier
authors.forename: Delphine
authors.initials: D
authors.lastname: Baetz
authors.forename: Harry
authors.initials: H
authors.lastname: Koubi
authors.forename: Stéphane
authors.initials: S
authors.lastname: Servais
authors.forename: Claude
authors.initials: C
authors.lastname: Duchamp
mesh_terms: D002001:Adipose Tissue, Brown / Q000378:metabolism* / Q000648:ultrastructure; D000704:Analysis of Variance; D000818:Animals; D001833:Body Temperature Regulation / Q000187:drug effects / Q000502:physiology*; D001835:Body Weight; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000187:drug effects; D005106:Exploratory Behavior; D005786:Gene Expression Regulation / Q000187:drug effects; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D008297:Male; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D009765:Obesity / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D011922:Rats, Mutant Strains; D017208:Rats, Wistar; D013696:Temperature; D013851:Thinness / Q000378:metabolism* / Q000473:pathology*; D013997:Time Factors; D000071256:Uncoupling Protein 1
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; C000604373:Ucp1 protein, rat; D000071256:Uncoupling Protein 1; D009638:Norepinephrine