title: Survival and growth of C57BL/6J mice lacking the BK channel,Kcnma1: lower adult body weight occurs together with higher body fat.
abstract: Big conductance potassium (BK) channels contribute to K+flow and electrical behavior in many cell types. Mice made null for the gene (Kcnma1) producing the BK channel (BKKO) exhibit numerous deficits in physiological functions. Breeding mice lacking a single allele ofKcnma1(C57BL/6J background) had litter sizes of approximately eight pups. For the period of maternal care (P0-P21), pup deaths peaked at P1 with a second less severe interval of death peaking near P13. Early deaths were twice as likely during a 20-month period of building construction compared with the quiescent period after cessation of construction. Births during construction were not consistent with Mendelian predictions indicating the likelihood of a specific disadvantage induced by this environmental stressor. Later BKKOpup deaths (~P13) also were more numerous than Mendelian expectations. After weaning, weight gain was slower for BKKOmice compared with wild-type littermates: 5 g less for male BKKOmice and 4 g less for female BKKOmice. Body composition determined by quantitative magnetic resonance indicated a higher fat proportion for wild-type female mice compared with males, as well as a higher hydration ratio. Both male and female BKKOmice showed higher fat proportions than wild-type, with female BKKOmice exhibiting greater variation. Together, these results indicate that BKKOmice suffered disadvantages that lead to prenatal and perinatal death. A metabolic difference likely related to glucose handling led to the smaller body size and distinct composition for BKKOmice, suggesting a diversion of energy supplies from growth to fat storage.
authors.affiliation: Department of Neuroscience, Cell Biology and Physiology, Wright State University Boonshoft School of Medicine, Dayton, Ohio.
authors.forename: Susan T
authors.initials: ST
authors.lastname: Halm
authors.affiliation: Department of Mathematics and Statistics, Statistical Consulting Center, Wright State University, Dayton, Ohio.
authors.forename: Michael A
authors.initials: MA
authors.lastname: Bottomley
authors.affiliation: Department of Pharmacology and Toxicology, Wright State University Boonshoft School of Medicine, Dayton, Ohio.
authors.forename: Mohammed M
authors.initials: MM
authors.lastname: Almutairi
authors.affiliation: Department of Pharmacology and Toxicology, Wright State University Boonshoft School of Medicine, Dayton, Ohio.
authors.forename: Maurico
authors.initials: M
authors.lastname: Di Fulvio
authors.affiliation: Department of Neuroscience, Cell Biology and Physiology, Wright State University Boonshoft School of Medicine, Dayton, Ohio dan.halm@wright.edu.
authors.forename: Dan R
authors.initials: DR
authors.lastname: Halm
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001823:Body Composition / Q000235:genetics*; D001835:Body Weight / Q000235:genetics*; D051037:Large-Conductance Calcium-Activated Potassium Channel alpha Subunits / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout
chemical_list: C465449:Kcnma1 protein, mouse; D051037:Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
keywords: Body composition; breeding success; environmental stress; glucose tolerance; mouse development; quantitative magnetic resonance