AMPK and CaMKII are protein kinases in skeletal muscle cells that can activate glucose uptake without insulin's influence. They are elevated during exercise when muscles contract actively. Managing and preventing type 2 diabetes through AMPK and CaMKII could avoid insulin dependency and beta cell destruction, as insulin resistance progresses and damages pancreatic beta cells over time. Unlike current pharmacological treatments relying on optimizing insulin function, targeting AMPK and CaMKII could provide an alternative pathway for muscle glucose uptake without insulin's involvement.
AMPK and CaMKII are protein kinases in skeletal muscle cells that can activate glucose uptake without insulin's influence. They are elevated during exercise when muscles contract actively. Managing and preventing type 2 diabetes through AMPK and CaMKII could avoid insulin dependency and beta cell destruction, as insulin resistance progresses and damages pancreatic beta cells over time. Unlike current pharmacological treatments relying on optimizing insulin function, targeting AMPK and CaMKII could provide an alternative pathway for muscle glucose uptake without insulin's involvement.
AMPK and CaMKII are protein kinases in skeletal muscle cells that can activate glucose uptake without insulin's influence. They are elevated during exercise when muscles contract actively. Managing and preventing type 2 diabetes through AMPK and CaMKII could avoid insulin dependency and beta cell destruction, as insulin resistance progresses and damages pancreatic beta cells over time. Unlike current pharmacological treatments relying on optimizing insulin function, targeting AMPK and CaMKII could provide an alternative pathway for muscle glucose uptake without insulin's involvement.
AMPK and CaMKII are protein kinases in skeletal muscle cells that can activate glucose uptake without insulin's influence. They are elevated during exercise when muscles contract actively. Managing and preventing type 2 diabetes through AMPK and CaMKII could avoid insulin dependency and beta cell destruction, as insulin resistance progresses and damages pancreatic beta cells over time. Unlike current pharmacological treatments relying on optimizing insulin function, targeting AMPK and CaMKII could provide an alternative pathway for muscle glucose uptake without insulin's involvement.
The Potention of AMPK and CaMK II as Alternative Muscle Glucose
Uptake Pathway on Management and Prevention of Type 2 Diabetes Abstrak :
Untill nowadays, management and prevention in type 2 diabetes mellitus are still rely on pharmacological modality which optimilized the function of insulin to trigger the muscle glucose uptake. Insulin and OAD can cause insulin dependency and fastened the irreversible diabetic phase. AMPK and CaMKII are protein kinases existing in skeletal muscle cytoplasm, which activated the uptake of muscle glucose without the influence of insulin. The expression and activity of AMPK and CaMKII are elevated in the actively contracted muscle, such as in exercise. The use of transduction signal without the influence of insulin can avoid the destruction of beta cell. AMPK and CaMKII are very potential in management and prevention type 2 diabetes mellitus, viewed from the insulin resistence progressivity and the pancreatic beta cell destruction. Keyword : AMPK, CaMKII, Glucose, diabetes
