Survival and growth of C57BL/6J mice lacking the BK channel, Kcnma1: lower adult body weight occurs together with higher body fat

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 (BK(KO)) exhibit numerous deficits in physiological functions. Breeding mice lacking a single allele of Kcnma1 (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 BK(KO) pup deaths (~P13) also were more numerous than Mendelian expectations. After weaning, weight gain was slower for BK(KO) mice compared with wild‐type littermates: 5 g less for male BK(KO) mice and 4 g less for female BK(KO) mice. 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 BK(KO) mice showed higher fat proportions than wild‐type, with female BK(KO) mice exhibiting greater variation. Together, these results indicate that BK(KO) mice 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 BK(KO) mice, suggesting a diversion of energy supplies from growth to fat storage.