Ckmt1 is Dispensable for Mitochondrial Bioenergetics Within White/Beige Adipose Tissue

Valerie Politis-Barber, Heather L. Petrick, Arthe Raajendiran, Genevieve J. Desormeaux, Henver S. Brunetta, Larissa M. Dos Reis, Marcelo A. Mori, David C. Wright, Matthew J. Watt, Graham P. Holloway

Research output: Contribution to journalArticleResearchpeer-review


Within brown adipose tissue (BAT), the brain isoform of creatine kinase (CKB) has been proposed to regulate the regeneration of ADP and phosphocreatine in a futile creatine cycle (FCC) that stimulates energy expenditure. However, the presence of FCC, and the specific creatine kinase isoforms regulating this theoretical model within white adipose tissue (WAT), remains to be fully elucidated. In the present study, creatine did not stimulate respiration in cultured adipocytes, isolated mitochondria or mouse permeabilized WAT. Additionally, while creatine kinase ubiquitous-type, mitochondrial (CKMT1) mRNA and protein were detected in human WAT, shRNA-mediated reductions in Ckmt1 did not decrease submaximal respiration in cultured adipocytes, and ablation of CKMT1 in mice did not alter energy expenditure, mitochondrial responses to pharmacological β3-adrenergic activation (CL 316, 243) or exacerbate the detrimental metabolic effects of consuming a high-fat diet. Taken together, these findings solidify CKMT1 as dispensable in the regulation of energy expenditure, and unlike in BAT, they do not support the presence of FCC within WAT.

Original languageEnglish
Article numberzqac037
Number of pages16
Issue number5
Publication statusPublished - 2022
Externally publishedYes


  • adipose tissue
  • beiging
  • browning
  • creatine
  • creatine kinase
  • energy expenditure
  • futile cycling
  • metabolism
  • mitochondria
  • mitochondrial bioenergetics

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