Adipocyte CAMK2 deficiency improves obesity-associated glucose intolerance.

ABSTRACT:

Objective

Obesity-related adipose tissue dysfunction has been linked to the development of insulin resistance, type 2 diabetes, and cardiovascular disease. Impaired calcium homeostasis is associated with altered adipose tissue metabolism; however, the molecular mechanisms that link disrupted calcium signaling to metabolic regulation are largely unknown. Here, we investigated the contribution of a calcium-sensing enzyme, calcium/calmodulin-dependent protein kinase II (CAMK2), to adipocyte function, obesity-associated insulin resistance, and glucose intolerance.

Methods

To determine the impact of adipocyte CAMK2 deficiency on metabolic regulation, we generated a conditional knockout mouse model and acutely deleted CAMK2 in mature adipocytes. We further used in vitro differenti

SUBMITTER: Dai W 

PROVIDER: S-EPMC8365526 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature