Does phosphorylation of GSK-3β mediate intralipid-induced cardioprotection against ischemia/reperfusion injury?
Postischemic treatment with Intralipid inhibits the opening of mitochondiral permeability transition pore and protects the heart through glycogen synthase kinase-3β via PI3K/Akt/ERK pathways.
Long segment IT shows a rapid rise in GLP-1 and PYY levels, thus leading to early amelioration of glucose control.