Abstract
High altitude hypoxia adaptation can improve glucose tolerance in people with metabolic syndrome and type 2 diabetes (T2D). Apelin is an endogenous ligand of the G protein‐coupled receptor APJ and has possible roles in energy metabolism. Apelin‐null mice have been reported to exhibit impaired insulin sensitivity, which can be reversed by supplementation of exogenous apelin. Here, we examined the effects of 4 weeks’ intermittent hypoxia exposure on physiological and biochemical variables in apelin knockout (KO) mice. Apelin KO mice exhibited decreased expression of substrate metabolism‐associated genes/proteins, impaired glucose tolerance, and reduced exercise capacity compared to wild‐type mice, and all of these effects were rescued by hypoxia. These findings suggest that hypoxia intervention may possibly be able to alleviate metabolic conditions caused by genetic defects.
Highlights
High altitude hypoxia adaptation can improve glucose tolerance in people with metabolic syndrome and type 2 diabetes (T2D)
Effect of hypoxia exposure on glucose and insulin tolerance During the glucose tolerance test (GTT), the blood glucose levels were significantly higher in the KO–Normoxia group compared with the WT–Normoxia group, whereas the blood glucose levels were significantly lower in the KO–Hypoxia group compared with the KO–Normoxia group
No significant difference in blood glucose levels was found between apelin KO and WT mice after hypoxia exposure
Summary
High altitude hypoxia adaptation can improve glucose tolerance in people with metabolic syndrome and type 2 diabetes (T2D). Apelin KO mice exhibited decreased expression of substrate metabolism-associated genes/proteins, impaired glucose tolerance, and reduced exercise capacity compared to wild-type mice, and all of these effects were rescued by hypoxia. These findings suggest that hypoxia intervention may possibly be able to alleviate metabolic conditions caused by genetic defects. 4 weeks’ intermittent hypobaric hypoxia exposure has been demonstrated to improve the impaired glucose tolerance in diabetic rats [4], and decrease fasting blood glucose and insulin resistance in fructose-induced metabolic syndrome rats [5].
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