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Creatine kinase B controls futile creatine cycling in thermogenic fat
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Journal Article
Creatine kinase B controls futile creatine cycling in thermogenic fat
2021
Overview
Obesity increases the risk of mortality because of metabolic sequelae such as type 2 diabetes and cardiovascular disease
1
. Thermogenesis by adipocytes can counteract obesity and metabolic diseases
2
,
3
. In thermogenic fat, creatine liberates a molar excess of mitochondrial ADP—purportedly via a phosphorylation cycle
4
—to drive thermogenic respiration. However, the proteins that control this futile creatine cycle are unknown. Here we show that creatine kinase B (CKB) is indispensable for thermogenesis resulting from the futile creatine cycle, during which it traffics to mitochondria using an internal mitochondrial targeting sequence. CKB is powerfully induced by thermogenic stimuli in both mouse and human adipocytes. Adipocyte-selective inactivation of
Ckb
in mice diminishes thermogenic capacity, increases predisposition to obesity, and disrupts glucose homeostasis. CKB is therefore a key effector of the futile creatine cycle.
Upon induction by thermogenic stimuli, creatine kinase B traffics to mitochondria to trigger the futile creatine cycle in thermogenic fat.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
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/ 38/1
/ 38/23
/ 38/39
/ 38/77
/ 38/89
/ 38/90
/ 42/35
/ 631/443
/ 631/45
/ 64/60
/ 82
/ 82/29
/ 82/80
/ Analysis
/ Animals
/ Cold
/ Creatine
/ Creatine Kinase, BB Form - deficiency
/ Creatine Kinase, BB Form - genetics
/ Creatine Kinase, BB Form - metabolism
/ Diabetes mellitus (non-insulin dependent)
/ Energy Metabolism - genetics
/ Female
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Male
/ Mice
/ Obesity
/ Proteins
/ Science
