الفهرس 
Introduction And RationaleOnly 14 pages are availabe for public view
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Abstract
Asprosin is a newly discovered fasting induced protein hormone that promotes glucose production from the liver. It is the C-terminal cleavage product of profibrillin (encoded by FBN-1). Various tissues produce it across the body but the WAT seems to contribute to this production with the largest proportion. Asprosin is a gluconeogenic hormone that exerts its action by binding to GPCR receptor and activates PKA-cAMP axis to induce hepatic glucose production and release. Glucose is a powerful and potent negative regulator of asprosin as concluded from acute DROP in serum asprosin levels in mice after feeding (Romere et al., 2016).
DM is a metabolic disorder characterized by chronic hyperglycemia with disturbances of carbohydrate, protein and fat metabolism resulting from defects in insulin secretion, insulin action, or both (Ghosh and Collier, 2012). In Egypt, diabetes crude prevalence in 2017 was 15.1% (International Diabetes Federation, 2017). Type 2 diabetes is a subtype of DM that developed due to progressive loss of β-cell insulin secretion frequently on the background of insulin resistance and accounts for 90 – 95% of all diabetes cases (American Diabetes Association., 2014).
Insulin resistance and hyperinsulinemia are major contributors to the pathogenesis T2DM (DeFronzo, 2004). Increased body fat is associated with the development of insulin resistance in muscle and in the liver particularly if excess fat is deposited in these tissues. Pancreas is able to overcome this insulin resistance initially by producing more insulin. Hyperinsulinemia is also provoked by decreased sensitivity of pancreas to the negative feedback mechanism from the increased insulin produced by it. The terminal stage is failure of β-cell output (Wilding, 2014).