Biphasic Roles of a Small G-Protein, RAC1 in Pancreatic Β-Cell
Diabetes is a metabolic disorder with multiple etiologies characterized by chronic
hyperglycemia.
This results from dysregulated insulin secretion and/or from the resistance to
insulin action in peripheral tissues.
In the settings of the metabolic disorder, disturbances in carbohydrate,
fat and protein metabolism results in a diverse set of complications associated
with pancreas, liver, kidney, heart and other vital organs.
As per the National Diabetes Statistics Report, 2014, in 2012, 29.1 million Americans
have diabetes, which include 1.25 million type 1 diabetic children and adults.
Further, 86 million people of age 20 and above are pre-diabetic, and are at increased risk for developing type 2 diabetes.
This is mediated through fluctuations in the intracellular calcium,
and interplay of soluble secondary messengers like reactive oxygen species,
cyclic nucleotides and hydrolytic products
generated from the phospholipases A2, C and D.
In addition, adenine nucleotides and guanine nucleotides regulate physiological
insulin secretion.
Even though many studies have shown the underlying mechanism
involved in stimulus-secretion coupling of glucose stimulated insulin
secretion (GSIS), the precise molecular and cellular mechanism still remains unknown.
However, role of guanine nucleotide-binding protein (G-protein)
has been highly researched for their role in insulin release.
Gastro Open J. 2015; 1(3): 79-88. doi: 10.17140/GOJ-1-114
