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Publication
The E3 ubiquitin ligase parkin is dispensable for metabolic homeostasis in
murine pancreatic ß cells and adipocytes.
Authors Corsa CAS, Pearson GL, Renberg A, Askar MM, Vozheiko T, MacDougald OA,
Soleimanpour SA
Submitted By Submitted Externally on 12/5/2019
Status Published
Journal The Journal of biological chemistry
Year 2019
Date Published 5/1/2019
Volume : Pages 294 : 7296 - 7307
PubMed Reference 30877201
Abstract The E3 ubiquitin ligase parkin is a critical regulator of mitophagy and has been
identified as a susceptibility gene for type 2 diabetes (T2D). However, its role
in metabolically active tissues that precipitate T2D development is unknown.
Specifically, pancreatic ß cells and adipocytes both rely heavily on
mitochondrial function in the regulation of optimal glycemic control to prevent
T2D, but parkin's role in preserving quality control of ß cell or adipocyte
mitochondria is unclear. Although parkin has been reported previously to control
mitophagy, here we show that, surprisingly, parkin is dispensable for glucose
homeostasis in both ß cells and adipocytes during diet-induced insulin
resistance in mice. We observed that insulin secretion, ß cell formation, and
islet architecture were preserved in parkin-deficient ß cells and islets,
suggesting that parkin is not necessary for control of ß cell function and islet
compensation for diet-induced obesity. Although transient parkin deficiency
mildly impaired mitochondrial turnover in ß cell lines, parkin deletion in
primary ß cells yielded no deficits in mitochondrial clearance. In
adipocyte-specific deletion models, lipid uptake and ß-oxidation were increased
in cultured cells, whereas adipose tissue morphology, glucose homeostasis, and
beige-to-white adipocyte transition were unaffected in vivo In key metabolic
tissues where mitochondrial dysfunction has been implicated in T2D development,
our experiments unexpectedly revealed that parkin is not an essential regulator
of glucose tolerance, whole-body energy metabolism, or mitochondrial quality
control. These findings highlight that parkin-independent processes maintain ß
cell and adipocyte mitochondrial quality control in diet-induced obesity.




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