[Nicotinamide inhibition of 2-14C acetate incorporation into free fatty acids and lipids of rat tissues]. / Ingibirovanie nikotinamidom vkliucheniia 2-14C atsetata v svobodnye zhirnye kisloty i lipidy tkanei krys.

The synthesis of fatty acids and lipids in the rat tissues is inhibited to a considerable extent during fasting and is activated when feeding highly carobhydrate ration to rats after fasting. Nicotinamide (50 mg/100 g of weight) causes a decrease in intensity of 14C incorporation into free fatty acids and lipids of blood, liver, epididimal and perienal fatty tissues. The degree of nicotinamide inhibition of fatty acids and lipids sythesis is in direct dependence on lipogenesis intensity.

[Hypoglycemic effect of nicotinamide in rats with alloxan diabetes]. / Gipoglikemicheskii effekt nikotinamida pri alloksanovom diabete u krys.

Experimentally-induced alloxan diabetes was characterized in rats by a marked increase in the blood glucose level and by a number of disturbances in the concentration of metabolites and the activity of the enzymes of carbohydrate metabolism in the liver. Stimulation of gluconeogenesis in diabetes was judged by reduction of the redox condition of free NAD- and NADP-couples, by the increase in the concentration of phosphoenolpyruvate, malic oxaloacetate and phosphoenolpyruvate carboxykinase activity of the liver. Nicotinamide in a dose of 50 mg per 100 g of body weight caused a marked reduction in the blood glucose level of diabetic rats. An increase of the [NAD+]/[NADN], [NADP+]/[NADPN] ratio, a reduction of the concentration of phosphoenolpyruvate, malate and phosphoenolpyruvate carboxylase activity pointed to the inhibition of gluconeogenesis and stimulation of glycolysis in the liver of diabetic rats given nicotinamide.

[Stimulation of gluconeogenesis with 1,3-butanediol in the perfused rat liver]. / Stimuliatsiia gliukoneogenezu 1,3-butandiolom u perfuzovanii pechintsi shchuriv.

An intensified synthesis of glucose is observed in gluconeogenesis from endogenous precursor only for the first 30 min of perfusion. Pyruvate introduction into the medium raises phosphoenolpyruvate carboxykinase and fructose-1,6-diphosphatase activities in the liver and determines maintenance of the glucose formation high rate for 90 min of perfusion. 1,3-butanediol is found to have a stimulating effect on gluconeogenesis from pyruvate. Introduction of 1,3 bytanediol into perfusate decreases the redox state of free NAD-pairs, increases the content of phosphoenolpyruvate, malate. ATP and the phosphoenolpyruvate carboxykinase and fructose-1.6-diphosphatase activity in the perfused liver.

[Dynamics of the intake and utilization of orally administered 1,2-propanediol in glycogen synthesis in the rat liver]. / Dinamika postupleniia i ispol'zovaniia oral'no vvedennogo 1,2-propandiola v sinteze glikogena pecheni krys

The possibility of an isocaloric substitution of 1,2-propandiol for carbohydrates in the food ration of rats was investigated. The inclusion of propandiol as a synthetic source of food energy in the alimentation in an amount comprising 20 per cent of the overall calorific value of carbohydrates does not affect adversely the growth intensity, nor does it produce any materials upsets in the metabolism of test animals. With its oral introduction in a dose of 1 g per 100 g of weight 1,2-propandiol is quickly absorbed, its level reaching the maximum in the blood and liver after a lapse of 1 hour with complete metabolization in the organism over a period of 12 hours. In fasting rats 1,2-propandiol is utilized as a precurser in the synthesis of glycogen and when introduced by the intraperitoneal route it does not influence the rate of the liver glycogen synthesis from glucose. Daily oral introduction of 2 g of 1,2-propandiol per 100 g of body weight for a space of three and seven days, superimposed upon a carbohydrate-rich diet, brings about a fall of the liver reserve glycogen level.