Hakam Hasan Alkhateeb
Yarmouk University, Irbid, Jordan
Biography
I did my PhD work at the University of Waterloo with Dr. Arend Bonen, who inspired me in the vast interface of how muscle utilizes substrates, more specifically the utilization of glucose and free fatty acids in health and diseases. My interests in muscle physiology and metabolism was further strengthened and evolved through my postdoctoral experiences at the University of Guelph, eventually focusing on using alternative strategies and approaches that regulate of carbohydrate and fat, and apply this knowledge to the study of various diseases like diabetes, cardiovascular disease and obesity.
Abstract
Eugenol, a polyphenolic compound present in many plant essential oils, is thought to have antidiabetic properties. However, the mechanisms underlying these effects are not fully understood. Therefore, in the present study, we examined the mechanisms by which Eugenol might ameliorate palmitate-induced insulin resistance in skeletal muscle. Soleus muscles were incubated for 12 h without or with palmitate (2 mM). Eugenol (100µM), in the presence of palmitate, was provided in the last 6 h of incubation. Insulin-stimulated glucose transport, plasmalemmal glucose transporter 4 (GLUT4), Akt substrate 160 (AS160) and AMP-activated protein kinase (AMPK) phosphorylations were examined at 12 h. Palmitate treatment for 12 h reduced insulin-stimulated glucose transport, GLUT4 translocation, and AS160 phosphorylation, but it has no effect on AMPK phosphorylation. Eugenol (6–12 h) fully rescued insulin-stimulated glucose transport, although Eugenol partially restored GLUT4 translocation, it fully rescued AS160 phosphorylation. Eugenol also increased AMPK phosphorylation. The restorative effects of Eugenol on insulin-stimulated glucose transportation, GLUT4 translocation and AS160 phosphorylation were not observed after the inhibition of AMPK with compound C (50 µM). Together, these findings indicate that Eugenol ameliorates palmitate-induced insulin resistance by activating AMPK/AS160 pathway involving partial restoration of GLUT4 translocation in skeletal muscle.