The results demonstrate that examined plant extracts contain flavonoids with insulinotropic and antihyperglycemic effects.

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Heat preconditioning (HP) is a powerful adaptive and protective phenomenon and the heat stress proteins (HSPs) it produces are an important determinant for the development of diabetic complications. Aspirin has been reported to modulate heat shock response in different organisms through increased induction of HSPs and is also known to exert antioxidative and radical scavenging effects in diabetes. We estimated the effect of physiological (heat stress: 45 min at 41 ± 0.5 °C) and pharmacological (aspirin treatment) induction of HSP70 on several parameters of oxidative state in the pancreas and liver of diabetic rats. Diabetes increased HSP70 level and decreased poly(ADP) ribose polymerase (PARP), glutathione (GSH), and glutathione peroxidase (GPx) activities in the pancreas. In the liver, there was reduction of HSP70 level, GSH concentration, and CAT activity, while GPx and GR activity were enhanced. HP of diabetic rats caused an additional increase of HSP70, GSH, and antioxidant enzymes in both organs. Pre-treatment of HP-diabetic animals with aspirin led to an additional increase of PARP and HSP70. Both HP and aspirin, as physiological and pharmacological inductors of HSP70, respectively, enhanced the antioxidative defense mechanisms of the liver and pancreas in diabetic rats.

Aspirin (ASA), as a multifunctional drug has been used as a hypoglycaemic agent in the treatment of diabetes and severe hyperglycaemia and has been established as a secondary strategy which may prevent many cardiovascular events. In this study we investigated high dose (100 mg/kg b.w./i.p) and time-dependent (2, 7 and 14 days) effects of ASA on the heart key enzymes and substrates from glycogen/glucose metabolism in control and diabetic rats. The results accomplished demonstrated that ASA significantly potentiates glycogen accumulation, as well as decreased blood glucose level and heart glycolytic potential in control rats. The treatment of diabetic rats with ASA caused moderation of the diabetic complication-significant inhibition of glycogen accumulation, lowering of blood glucose, as well as elevation of glycolytic potential. In conclusion, we propose that use of high-dose of ASA has anabolic effects in control rats and reduces heart glycogen glucose complications in diabetic rats. The moderation of diabetes-induced changes is time-dependent and involves reduction of glycogenogenesis and inhibited depression of glycolysis, with a tendency to maintenance control values.

We studied the influence of heat acclimation (1 to 48 h and 4 to 60 d at 35 +/- 1 degrees C) on certain hepatic carbohydrate-related enzymes and substrates in rats. The results showed a decrease of liver glycogen content and GPho-ase a activity during the period of short-term exposure, followed by normalization to the control level and stabilization to the new level in the period of long-term heat acclimation. Conversely, G-6-P-ase and F-1,6-BP-ase activities increased during the short-term period, followed by a decrease and stabilization to a new, lower level in the prolonged acclimation. The blood glucose level decreased during whole period of acclimation, whereas intermediate substrates increased during the short-term and stabilized at a new, higher level during prolonged acclimation. The time-dependent changes of duration of heat acclimation could be summarized in three phases: short-term heat exposure (1 to 24 h) with intensive glycogenolysis and gluconeogenesis to glucose; a period with temporary changes (24 h to 7 d) with tendency of normalization to control level, and prolonged heat acclimation (7 d to 60 d), which favors both direct and indirect glycogen synthesis.

Based on the observation that heat acclimation is a slowly developing response, evoked by continuous exposure to moderate heat, we investigated the time-dependent acclimatory changes of heart glycogen metabolism. Cardiac levels of key carbohydrate-related enzymes and substrates were studied in the function of the duration of short-term (STHA; 6, 12, 24 and 48 h) and long-term heat acclimation (LTHA; 7, 14, 21 and 30 days) to high environmental temperature (35 ± 1°C). The changes in heart glycogen metabolism during STHA could be separated in two phases: up to 12 h exposure, where significant decrease of the heart glycogen (Glk), glucose-6-phosphate (G6P), hexokinase (HK) activity as well as increase of heart glucose was observed; and from 24 to 48 h exposure, manifested with elevation of Glk, Glu, glycogen phosphorylase a (GPa), phosphofructokinase (PFK) and HK activities. The metabolic changes in the period of LTHA could also be seen as separate phases: in a period of 7-14 days of heat exposure there was an increase of heart Glk, Glu, G6P, HK, as well as a decrease of GPa and PFK, while in the period of 21-28 days there was more intensive rebound of Glk and G6P, increase of GPa activity and non-significant changes of Glu, HK and PFK. The results obtained have showed that acclimation to moderate hyperthermic environment has caused significant changes in examined parameters which differ depending on duration to the exposure: intensive stress-induced glycogenolytic and glycolytic processes in the period of STHA and intensive energy sparing, manifested by Glk deposition in the period of LTHA.