Newly Identified Protein CDP138 Controls Metabolism and Insulin Sensitivity

Researchers have brought new insight that newly discovered protein CDP138 is a possible way for controlling body fat metabolism, energy balance and insulin sensitivity through stress signaling pathways.

BUSM faculty created a model removing CDP138, a protein responsible for energy balance and insulin sensitivity through catecholamine release from adrenal glands and sympathetic nervous terminals in adipose tissue.

The creation of the model lacking CDP138 blocks catecholamine release allowing for better understanding of how physiologic metabolic process are controlled in response to stress.

Decreased metabolic rates from poor stress responses are associated with decreased energy balance which can lead to obesity and metabolic syndromes like insulin resistance.

Researchers at BUSM accomplished this by comparing CDP138 knockouts with controls and noticed that the CDP138 knockouts had substantial decrease in the release of catecholamine which resulted in energy imbalance from impaired metabolic pathways like decreased thermogenesis, fat browning, lipolysis, cAMP signaling and altered hepatic glucose utilization resulting in increased rates of obesity and insulin resistance.

These findings appear in the journal Molecular and Cellular Biology.

The research was led by Zhen Jiang, PhD, Associate Professor of Pharmacology and Qiong Lin Zhou, PhD, Assistant Professor of Pharmacology.

Submitted by Mitchell Wice, MD.