Olson Ann Louise, Humphries Kenneth
Biochemistry & Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Aging & Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
F1000Res. 2020 Jun 24;9. doi: 10.12688/f1000research.22237.1. eCollection 2020.
Deficient glucose transport and glucose disposal are key pathologies leading to impaired glucose tolerance and risk of type 2 diabetes. The cloning and identification of the family of facilitative glucose transporters have helped to identify that underlying mechanisms behind impaired glucose disposal, particularly in muscle and adipose tissue. There is much more than just transporter protein concentration that is needed to regulate whole body glucose uptake and disposal. The purpose of this review is to discuss recent findings in whole body glucose disposal. We hypothesize that impaired glucose uptake and disposal is a consequence of mismatched energy input and energy output. Decreasing the former while increasing the latter is key to normalizing glucose homeostasis.
葡萄糖转运和葡萄糖处置不足是导致葡萄糖耐量受损和2型糖尿病风险的关键病理因素。易化葡萄糖转运蛋白家族的克隆和鉴定有助于确定葡萄糖处置受损背后的潜在机制，特别是在肌肉和脂肪组织中。调节全身葡萄糖摄取和处置所需的不仅仅是转运蛋白浓度。本综述的目的是讨论全身葡萄糖处置的最新发现。我们假设葡萄糖摄取和处置受损是能量输入和能量输出不匹配的结果。减少前者同时增加后者是使葡萄糖稳态正常化的关键。
