Emiglitate (BAY o 1248) is a potent, selective and competitive inhibitor of α-glucoside hydrolase.
Emiglitate greatly suppresses the glucose-stimulated insulin release in parallel with an inhibitory effect on the activities of acid glucan-1,4-α-glucosidase and acid α-glucosidase. In contrast, the activities of acid phosphatase and N-acetyl-β-D-glucosaminidase tend to increase in the presence of the α-glucoside hydrolase inhibitor. The CO-induced amplification of the glucose-stimulated insulin release as well as of the increased activities of the acid α-glucoside hydrolases are abrogated by emiglitate and displayed the same levels as in the absence of CO. The CO-induced rise in the activities of acid phosphatase and acid N-acetyl-β-D-glucosaminidase is not appreciably affected by emiglitate[1].
In fasted rats, emiglitate inducec a significant, dose-dependent increase of hepatic glycogen concentrations. The increase in hepatic glycogen is due to lysosomal storage of glycogen only. Emiglitate in the amount of 5 mg/kg b.wt. does not induce significant changes either of glycogen concentrations or at the EM-level[2].
[1]. Mosén H, et al. Nitric oxide inhibits, and carbon monoxide activates, islet acid alpha-glucoside hydrolase activitiesin parallel with glucose-stimulated insulin secretion. J Endocrinol. 2006 Sep;190(3):681-93. [2]. Lembcke B, et al. Lysosomal storage of glycogen as a sequel of alpha-glucosidase inhibition by the absorbed deoxynojirimycin derivative emiglitate (BAYo1248). A drug-induced pattern of hepatic glycogen storage mimicking Pompe's disease (glycogenosis type II). Res Exp Med (Berl). 1991;191(6):389-404.