Unknown

Dataset Information

0

CK2 modulates adipocyte insulin-signaling and is up-regulated in human obesity.


ABSTRACT: Insulin plays a major role in glucose metabolism and insulin-signaling defects are present in obesity and diabetes. CK2 is a pleiotropic protein kinase implicated in fundamental cellular pathways and abnormally elevated in tumors. Here we report that in human and murine adipocytes CK2-inhibition decreases the insulin-induced glucose-uptake by counteracting Akt-signaling and GLUT4-translocation to the plasma membrane. In mice CK2 acts on insulin-signaling in adipose tissue, liver and skeletal muscle and its acute inhibition impairs glucose tolerance. Notably, CK2 protein-level and activity are greatly up-regulated in white adipose tissue from ob/ob and db/db mice as well as from obese patients, regardless the severity of their insulin-resistance and the presence of pre-diabetes or overt type 2 diabetes. Weight loss obtained by both bariatric surgery or hypocaloric diet reverts CK2 hyper-activation to normal level. Our data suggest a central role of CK2 in insulin-sensitivity, glucose homeostasis and adipose tissue remodeling. CK2 up-regulation is identified as a hallmark of adipose tissue pathological expansion, suggesting a new potential therapeutic target for human obesity.

SUBMITTER: Borgo C 

PROVIDER: S-EPMC5730587 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

altmetric image

Publications


Insulin plays a major role in glucose metabolism and insulin-signaling defects are present in obesity and diabetes. CK2 is a pleiotropic protein kinase implicated in fundamental cellular pathways and abnormally elevated in tumors. Here we report that in human and murine adipocytes CK2-inhibition decreases the insulin-induced glucose-uptake by counteracting Akt-signaling and GLUT4-translocation to the plasma membrane. In mice CK2 acts on insulin-signaling in adipose tissue, liver and skeletal mus  ...[more]

Similar Datasets

| S-EPMC11199588 | biostudies-literature
| S-EPMC6308911 | biostudies-literature
| S-EPMC2730923 | biostudies-literature
| S-EPMC4985653 | biostudies-literature
| S-EPMC5193405 | biostudies-literature
| S-EPMC5816206 | biostudies-literature
| S-EPMC9205899 | biostudies-literature
| S-EPMC4441322 | biostudies-literature
| S-EPMC7968520 | biostudies-literature
| S-EPMC3745423 | biostudies-literature