Role of PDE3B and PRKACA genes through Insulin-Independent Pathways in Alternative Glucose Metabolism under Stress

Abstract

PDE3B is an important energy homeostasis regulator. Alterations in the expression of the PDE3B gene have been shown to affect various metabolic pathways in the body. In the liver, PDE3B is involved in the lipolysis and glycogenolysis pathway. PDE3B is a regulator of cAMP-activated PKA gene that is involved in lipolysis metabolism. Many chemicals and different substances have been perceived as controllers of lipolysis, however, insulin and catecholamines seem, by all accounts, to be the most significant. In this paper, we subjected normal C57-type mice to emotional stress for 14 consecutive days and isolated the liver of these mice to study the in vivo expression of PDE3B and the catalytic subunit of cAMP-mediated PKA. Observations showed that PDE3B expression is upregulated, while PKA expression is downregulated under stress, therefore, down regulating lipolysis in the liver. Due to reduced lipolysis, lipotoxicity increases in the liver, which prompts aggregation of fats causing cirrhosis or fatty liver disease. Moreover, the glucose level is increased twice the amount in treated group as compared with the control study group. This will hinder the normal mechanism of the feed fast cycle and mechanistically restrains insulin activity, ultimately leading to type 2 diabetes(T2D).