title: Female mice target deleted for the neuromedin B receptor have partial resistance to diet-induced obesity.
abstract: Previous studies have proposed a role for neuromedin B (NB), a bombesin-like peptide, in the control of body weight homeostasis. However, the nature of this role is unclear. The actions of NB are mediated preferentially by NB-preferring receptors (NBRs). Here we examined the consequences of targeted deletion of NBRs in female mice on body weight homeostasis in mice fed a normolipid diet (ND) or a high-fat diet (HFD) for 13 weeks. Body weight and food ingestion of neuromedin B receptor knockout (NBR-KO) mice fed a normolipid diet showed no difference in relation to wild-type (WT). However, the high-fat diet induced an 8.9- and 4.8-fold increase in body weight of WT and NBR-KO, respectively, compared to their controls maintained with a normolipid diet, even though the mice ingested the same amount of calories, regardless of genotype. Comparing mice fed the high-fat diet, NBR-KO mice accumulated approximately 45% less fat depot mass than WT, exhibited a lower percentage of fat in their carcasses (19.2 vs. 31.3%), and their adipocytes were less hypertrophied. Serum leptin and leptin mRNA in inguinal and perigonadal fat were lower in HFD NBR-KO than HFD WT, and serum adiponectin was similar among HFD groups and unaltered in comparison to ND-fed mice. HFD-fed WT mice developed glucose intolerance but not the HFD-fed NBR-KO mice, although they had similar glycaemia and insulinaemia. NBR-KO and WT mice on the normolipid diet showed no differences in any parameters, except for a trend to lower insulin levels. Therefore, disruption of the neuromedin B receptor pathway did not change body weight homeostasis in female mice fed a normolipid diet; however, it did result in partial resistance to diet-induced obesity.
authors.affiliation: Laboratório de Endocrinologia Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS, bloco G, Ilha do Fundão, Rio de Janeiro, 21949-900, Brazil.
authors.forename: Gabriela Silva Monteiro
authors.initials: GS
authors.lastname: Paula
authors.forename: Luana Lopes
authors.initials: LL
authors.lastname: Souza
authors.forename: Adriana
authors.initials: A
authors.lastname: Cabanelas
authors.forename: Flavia Fonseca
authors.initials: FF
authors.lastname: Bloise
authors.forename: Valéria
authors.initials: V
authors.lastname: Mello-Coelho
authors.forename: Etsuko
authors.initials: E
authors.lastname: Wada
authors.forename: Tania Maria
authors.initials: TM
authors.lastname: Ortiga-Carvalho
authors.forename: Karen Jesus
authors.initials: KJ
authors.lastname: Oliveira
authors.forename: Carmen Cabanelas
authors.initials: CC
authors.lastname: Pazos-Moura
mesh_terms: D052436:Adipose Tissue, White / Q000033:anatomy & histology; D000818:Animals; D001391:Azo Compounds; D001823:Body Composition / Q000235:genetics / Q000502:physiology; D001835:Body Weight / Q000235:genetics / Q000502:physiology; D004396:Coloring Agents; D004032:Diet; D004041:Dietary Fats / Q000494:pharmacology; D002149:Energy Intake; D004734:Energy Metabolism / Q000235:genetics / Q000502:physiology; D005260:Female; D005951:Glucose Tolerance Test; D006706:Homeostasis / Q000235:genetics / Q000502:physiology; D006728:Hormones / Q000097:blood; D020738:Leptin / Q000096:biosynthesis / Q000235:genetics; D008055:Lipids / Q000097:blood; D008099:Liver / Q000737:chemistry / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009765:Obesity / Q000235:genetics*; D018004:Receptors, Bombesin / Q000235:genetics / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology
chemical_list: D001391:Azo Compounds; D004396:Coloring Agents; D004041:Dietary Fats; D006728:Hormones; D020738:Leptin; D008055:Lipids; D018004:Receptors, Bombesin; C011049:oil red O