Abstract
Frugivorous and nectarivorous bats are able to ingest large quantities of sugar in a short time span while avoiding the potentially adverse side-effects of elevated blood glucose. The glucose transporter 4 protein (GLUT4) encoded by the Slc2a4 gene plays a critical role in transmembrane skeletal muscle glucose uptake and thus glucose homeostasis. To test whether the Slc2a4 gene has undergone adaptive evolution in bats with carbohydrate-rich diets in relation to their insect-eating sister taxa, we sequenced the coding region of the Slc2a4 gene in a number of bat species, including four Old World fruit bats (Pteropodidae) and three New World fruit bats (Phyllostomidae). Our molecular evolutionary analyses revealed evidence that Slc2a4 has undergone a change in selection pressure in Old World fruit bats with 11 amino acid substitutions detected on the ancestral branch, whereas, no positive selection was detected in the New World fruit bats. We noted that in the former group, amino acid replacements were biased towards either Serine or Isoleucine, and, of the 11 changes, six were specific to Old World fruit bats (A133S, A164S, V377F, V386I, V441I and G459S). Our study presents preliminary evidence that the Slc2a4 gene has undergone adaptive changes in Old World fruit bats in relation to their ability to meet the demands of a high sugar diet.
Highlights
High acute blood glucose concentration causes severe physiological dysfunction and even death [1,2,3]
In the first of these regulatory mechanisms, it is skeletal muscle that contributes most to the removal of excess glucose from circulation [4,5], a process that is mediated by the transmembrane glucose transporter 4 protein (GLUT4) [5]
By comparing the Slc2a4 gene in frugivorous and nectarivorous bats to their insect-eating sister taxa, we provide some of the first data on molecular adaptation to a sugar rich diet in mammals [39]
Summary
High acute blood glucose concentration causes severe physiological dysfunction and even death [1,2,3]. Avoid potential toxicity, the blood glucose concentration is maintained within narrow limits by an inter-play between tissue glucose uptake, hepatic glucose production and insulin production [4]. In the first of these regulatory mechanisms, it is skeletal muscle that contributes most to the removal of excess glucose from circulation [4,5], a process that is mediated by the transmembrane glucose transporter 4 protein (GLUT4) [5]. In response to stimulation by insulin, exercise or contraction, GLUT4 is translocated from intracellular compartments to the plasma membrane of adipocytes and muscle, where it mediates glucose uptake [3,4,6]. Studies of transgenic mice revealed that GLUT4 plays a pivotal role in the regulation of skeletal muscle glucose uptake and maintenance of glucose homeostasis [7,8]
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