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Ablation of CKMT1 Does Not Affect Energy Expenditure, Adipose Tissue Mitochondrial Respiration or Susceptibility to High-fat Diet-induced Obesity

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Title: Ablation of CKMT1 Does Not Affect Energy Expenditure, Adipose Tissue Mitochondrial Respiration or Susceptibility to High-fat Diet-induced Obesity
Author: Politis-Barber, Valerie
Department: Department of Human Health and Nutritional Sciences
Program: Human Health and Nutritional Sciences
Advisor: Holloway, Graham
Abstract: Thermogenic adipose tissues are studied as a prospective anti-obesity target for their ability to increase energy expenditure (EE) by dissipating chemical energy through non-shivering thermogenesis (NST). A novel effector of NST has been identified in vitro, whereby creatine stimulates mitochondrial respiration when ADP is limiting. The mechanism is proposed to be mediated in part by a creatine kinase enzyme, however the specific isoform remains elusive. Since creatine kinase ubiquitous-type, mitochondrial (CKMT1) is a candidate, we utilized Ckmt1 knockout (KO) mice to assess its biological contribution to EE and mitochondrial respiration in iWAT and gWAT. Interestingly, we could not recapitulate the stimulatory effects of creatine ex vivo, and Ckmt1 KO mice did not display altered responses to pharmacological adrenergic activation or a high-fat diet. Taken together, these findings challenge the direct stimulatory nature of creatine beyond an in vitro model and suggest that CKMT1 is not a primary contributor of EE.
URI: https://hdl.handle.net/10214/26331
Date: 2021-07
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Embargoed Until: 2022-07-22


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