Noopept (N-phenylacetyl-L-prolylglycine ethyl ester) revealed wide spectrum of neuroprotective effects (Seredenin et al, Patent USA 5.439.930; Gudasheva et al., Eur. J. Med. Chem. 1996, 31, 151 - 157). One of mechanism underlying this neuroprotection is the increase of NGF and BDNF expression in hippocampus and hypothalamus. Features of neurons and pancreatic beta-cells similarity (Scharfmann. Horm. Metab. Res. 1997, 29, 294—296) as well as data on neurotrophines insufficiency in diabetes (Krabbe et al., Diabetologia. 2007, 50, 431-438) prompted us to study the effects of Noopept 0.5 mg/kg i.p. for 14 days, before streptocotozine 40 mg/kg i.p. on rats. Besides of well-known STZ ability to produce hyperglycemia and weight loss, we revealed pronounced decrease of NGF and BDNF content in pancreatic and hepatic tissues. Noopept was firstly shown to ameliorate hyperglycemia, weight loss as well as to overcome NGF and BDNF deficits in these organs. Recent study of Vahitova et al. (Acta Naturae 2016, 8, 1, 90-98) revealed Noopept ability to increase the content of HIF-1. Involvement of HIF-1 deficiency in pathogenesis of diabetes combined with HIF ability to increase neurotrophines expression (Girgis et al. Trends in Endocrinology and Metabolism, 2012, 23, 372-380) allow to consider HIF-positve effects of Noopept as one of the mechanism underlying above-listed anti-diabetic effect of Noopept.rnrn