Halm Susan T, Bottomley Michael A, Almutairi Mohammed M, Di Fulvio Maurico, Halm Dan R
Department of Neuroscience, Cell Biology and Physiology, Wright State University Boonshoft School of Medicine, Dayton, Ohio.
Department of Mathematics and Statistics, Statistical Consulting Center, Wright State University, Dayton, Ohio.
Physiol Rep. 2017 Feb;5(4). doi: 10.14814/phy2.13137. Epub 2017 Feb 27.
Big conductance potassium (BK) channels contribute to K flow and electrical behavior in many cell types. Mice made null for the gene () producing the BK channel (BK) exhibit numerous deficits in physiological functions. Breeding mice lacking a single allele of (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 pup deaths (~P13) also were more numerous than Mendelian expectations. After weaning, weight gain was slower for BK mice compared with wild-type littermates: 5 g less for male BK mice and 4 g less for female BK 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 mice showed higher fat proportions than wild-type, with female BK mice exhibiting greater variation. Together, these results indicate that BK 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 mice, suggesting a diversion of energy supplies from growth to fat storage.
大电导钾（BK）通道在多种细胞类型中参与钾离子流动和电活动。使产生BK通道（BK）的基因（）无效的小鼠在生理功能上表现出众多缺陷。培育缺乏单个等位基因（C57BL/6J背景）的小鼠，其窝仔数约为8只幼崽。在母性照料期间（P0 - P21），幼崽死亡在P1达到峰值，在P13附近有第二个不太严重的死亡间隔峰值。与建筑停止后的静止期相比，在20个月的建筑施工期间，早期死亡的可能性是静止期的两倍。施工期间的出生情况不符合孟德尔预测，表明这种环境应激源会导致特定的不利影响。后期BK幼崽死亡（~P13）也比孟德尔预期的更多。断奶后，与野生型同窝幼崽相比，BK小鼠体重增加较慢：雄性BK小鼠少5克，雌性BK小鼠少4克。通过定量磁共振测定的身体成分表明，野生型雌性小鼠的脂肪比例高于雄性，且水合率更高。雄性和雌性BK小鼠的脂肪比例均高于野生型，雌性BK小鼠的差异更大。总之，这些结果表明BK小鼠存在导致产前和围产期死亡的不利因素。一种可能与葡萄糖处理相关的代谢差异导致BK小鼠体型较小且组成不同，这表明能量供应从生长转向了脂肪储存。
