Somayeh Alsadat Hosseini Khorami - Department of Nutrition and dietetic, Faculty of Medicine & Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia
Ariyo Movahedi - Department of Nutrition and dietetic, Faculty of Medicine & Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia- Department of Public Health Nutrition, Faculty of Medicine, Science & Research Branch, Islamic Azad University, Teh
Khaza ai Huzwah - Department of Nutrition and dietetic, Faculty of Medicine & Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia
Abd Mutalib Mohd Sokhiri - Department of Nutrition and dietetic, Faculty of Medicine & Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia

The prevalence of type II diabetes is rapidly increasing worldwide which the primary causes of it is the insulin resistance in peripheral tissues. Tightly coordinated control of both insulin function and secretion is required to maintain glucose homeostasis. Phosphatidyl Inositol 3-Kinase pathway (PI3K) is crucial in mediating insulin’s metabolic effects. A key downstream effector is AKT/protein kinase B (PKB), which in activated/ phosphorylated form, regulates the activity of numerous targets, including kinases, transcription factors and other regulatory molecules. On the other hand, studies have been performed to realize the role of negative modulators (specially the role of PTEN and SHIP2) of insulin signal transduction, in order to find therapeutic targets for reducing insulin resistance. In this article, the current understanding of involved molecular mechanisms in impaired insulin signaling pathway that cause Type II diabetes mellitus is reviewed.

AKT; Diabetes; GLUT4; GSK3; Insulin signaling; PI3K; PKC; PDK; PTEN; SHIP2