(1) In addition, the marked hepatic accumulation of glucogenic precursors, observed in parallel, indicates that the elevated tryptophan levels may also block hepatic glucogenesis.
(2) The lack of clear synchronous changes in the activity of glucogenesis key enzymes in the liver and kidneys indicates that the cells of these organs do not provide the united operon for phosphoenolpyruvate carboxinase, fructoso-1,6-diphosphatase and glucoso-6-phosphatase with common regulation mechanism.
(3) The relationship of glucogenesis and other energy-requiring functions of the liver to the proteolysis which is characteristic of trauma and sepsis was studied in conscious pigs following laporotomy and after the induction of intraperitoneal sepsis.
(4) The activity of glucogenesis key enzymes (phosphoenolpyruvate carboxinase, fructoso-1,6-siphosphatase, glucoso-6-phosphatase) of the rat liver and kidneys was studied simultaneously under the effect of extreme and subextreme factors on the organism.
(5) It is suggested that the phenomenon is based on glucogenesis taking place in the brain from non-carbohydrate glucose precursors, which is phylogenetically predetermined and biologically expedient.
(6) into the femoral vein provoked no glucogenesis or systemic hypotension.
(7) By means of appropriately placed thermal dilution catheters, portal and hepatic arterial blood flows, hepatic oxygen consumption, glucogenesis, and uptake of the fuel, substrates were measured.
(8) Increased maternal supply of fetal glucose during exercise substitutes for rather than adds to fetal endogenous glucogenesis.
(9) Skeletal muscle can oxidize only branch chain aminoacids; other aminoacids, including alanine, are transported to the liver for glucogenesis or other purposed.
(10) Since no detectible change in hepatic glycogen distribution and in the contents of liver and muscle glycogen accompanied glucogenesis, glycogen catabolism and deposition are postulated to proceed simultaneously and at equivalent rates by 60 min following the experimental induction of endotoxemia.
(11) The streptodecase effect is particularly marked and may be connected with the inhibition of endogenous substrate induction of glucogenesis as well as the inhibition of key enzymes.
(12) The augmented protein catabolism and glucogenesis that accompany diabetic ketoacidosis cannot be explained primarily on the basis of hyperglucagonemia.
(13) The former seems to be due to an increased glucogenesis, whereas the latter may be attributed to an insulin resistance in contrast to the high anaerobic glucose utilization observed in the neoplastic tissue.
(14) Aspartate aminotransferase activity, an enzyme participating in renal glucogenesis, increased transiently in the control but remained unchanged in the experimental group.
(15) There is evidence for the involvement of peptides in liver nitrogen exchanges and amino acids in peptides represent a potential source of carbon for glucogenesis and nitrogen for ureagenesis.
(16) This implies that under normal conditions in sheep, substrate supply has a much greater impact on hepatic glucogenesis than do hormones.
(17) The rate of glucogenesis was proportional (r equals 0.71) to the sum of the glucogenic precursors (lactate, pyruvate, glycerol, and alanine) taken up by the liver.
(18) Thus it is concluded that in sepsis the release of glucogenic substrates because of altered metabolism in peripheral tissues determines the rate of hepatic glucogenesis.
(19) In every group the change in the alanine oxidation rate was reciprocal to that in the alanine-derived glucogenesis rate.
(20) Congenital enzymopathic hyperlactacidemia results from a defect of utilisation of pyruvate either at the level of the pyruvate junction (pyruvate-carboxylase, pyruvate-dehydrogenase and Kreb's cycle), or at the level of the unidirectional enzymes on neo-glucogenesis and of neo-glycogenogenesis, e.g.
Glycogenesis
Definition:
(n.) The production or formation of sugar from gycogen, as in the liver.
Example Sentences:
(1) Glucose deprivation had opposite effects on the contributions of [14C]galactose (decreased) and [14C]fructose (increased) to glycogenesis, which occurred independently of insulin and were reversed by glucose concentrations as low as 30-100 microM.
(2) Insulin-dependent glycogenesis evidenced a much slower rate of glycogen deposition and was accompanied by a near tripling of glycogen synthase activity.
(3) In the present study hepatic glycogenesis by the direct versus indirect pathway was determined as a function of the glucose infusion rate.
(4) Glycogenesis and serum glucose levels were unaffected during obesity.
(5) In studies conducted with isolated rat hepatocytes, LY177507 inhibited net glucose production from a variety of substrates, inhibited glycolysis from exogenous glucose and endogenous glycogen, inhibited glycogenolysis, and stimulated glycogenesis.
(6) Pathologic and point count-morphometric studies of ribs, vertebrae, and iliac crests of 7 patients with Von Gierke's glycogenesis type Ia aged 5 months to 30 years were performed.
(7) Insulin at 10(-8) M activated glycolysis (X1.40) and glycogenesis (X1.34), and glucagon at 10(-9) M stimulated gluconeogenesis (X1.35) and glycogenolysis (X2.18).
(8) We have performed an in vivo study to test the hypothesis that induction of fetal hepatic glycogenesis is stimulated by insulin and involves activation of protein phosphatase type-1.
(9) Therefore, acute exercise provokes increments in glycogenesis, whereas training increases glycolysis, in the presence of insulin, for some time after exercise.
(10) These studies demonstrate that oPL acutely inhibits glycogen degradation in fetal rat hepatocytes and suggest that oPL promotes glycogen storage in fetal liver both by antagonizing the glycogenolytic effects of glucagon and by stimulating fetal hepatic glycogenesis.
(11) However, they were mostly, if not totally, abolished by adrenalectomy, which suppressed gluconeogenesis and glycogenesis.
(12) We examined the effects of selected hormones and pH on the rates of glyconeogenesis (L-[U-14C]-lactate----glycogen) and glycogenesis (D-[U-14C]glucose----glycogen) in mouse fast-twitch (FT) and slow-twitch muscles incubated in vitro (37 degrees C).
(13) Staining techniques for demonstration of various stored materials include: 1) toluidine blue at pH 2.8 for acid mucopolysaccharide in skeletal muscle fibers in Pompe's glycogenesis 2, 2) one-step trichrome stain for nemaline myopathy and for abnormal mitochondria in X-linked infantile cardiomyopathy, 3) periodic acid-methenamine silver stain for glycolipid-containing lysosomes in I-cell disease (mucolipidosis 2), 4) Sudan black B stain for lipid in skeletal muscle fibers in Reye's syndrome, infantile lactic acidosis, Leigh's infantile subacute necrotizing encephalopathy and Jansky-Bielschowsky late infantile ceroid lipofuscinosis, 5) iron stain for iron in cardiac and skeletal muscle fibers in thalassemia with advanced hemosiderosis, and 6) autofluorescence for "ceroid" in skeletal muscle fibers in Jansky-Bielschowsky disease.
(14) Insulin-stimulated glycogenesis was not induced in 17-day fetal rat hepatocytes in control or methylamine-treated cultures.
(15) The effects of dichloroacetate and phenazine methosulphate on the content of fructose-2,6-bisphosphate and glycogenesis in incubated epididymal adipose tissue were examined.
(16) Conversely, access to sucrose for a few days led to a pronounced glycogenesis (up to 509%) and lipogenesis (up to 450% of the teneral values), depending on the species.
(17) It is suggested that the reduction of liver glycogen induced by GH1 resulted from its obvious increase of cAMP which promoted glycogenolysis and decreased glycogenesis.
(18) Azaguanine does not alter liver glycogenesis, but prevents both liver triglyceride accumulation and the overshoot of lipogenic enzymes.
(19) Mifepristone (RU 486) had an antagonistic effect on the action of P. These results suggest that early P-dependent glycogenesis in the endometrial glandular cells of the rabbit may play an important role in the increased rate of mitosis and cellular proliferation that are necessary events in preparing the endometrium for implantation.
(20) We have therefore examined liver PDH activities during the light and dark phases of the feeding cycle in the adult rat in relation to hepatic glycogenesis, fatty acid synthesis and cholesterogenesis.