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PubMed1988

Effects of diabetes on development of small intestinal enzymes of infant rats.

The effect of streptozotocin (SZ) on the development of small intestinal enzymes in postnatal rat pups was studied. SZ was injected ip on Day 10 and, if necessary, again on Day 12. On Days 15, 18, and 21, one pup from each group (including a vehicle-injected control (C) group) was decapitated under conditions which minimized stress. Plasma glucose, insulin (IRI), and corticosterone were measured, as were pancreatic IRI, liver glycogen, and liver membrane binding of IRI. Small intestinal segments were processed and analyzed for sucrase, lactase, maltase, and ileal acid beta-galactosidase activities. Our results indicate that plasma glucocorticoid levels remained virtually constant in both SZ and C groups, while the ontogenic profiles of sucrase and maltase in SZ rats were shifted toward an earlier appearance and a precocious maturation. Circulating levels of IRI were not reduced significantly by SZ despite the fact that pancreatic IRI was decreased 95%. Jejunal lactase, unlike data reported for diabetic rats, was not affected by SZ diabetes. Also, acid beta-galactosidase was unaltered in the SZ rat pups. It is concluded that possibly the elevated disaccharidases seen in diabetic postnatal rat pups are the direct effect of elevated blood glucose. If so, the SZ rat pup model may be a useful tool with which to study effects of glucose on intestinal enzymes in the absence of changes in plasma insulin.

Animals↗
PubMed2003

Normal hepatic glycogen storage after fasting and feeding in children and adolescents with type 1 diabetes.

OBJECTIVE: Hypoglycemia is the most important acute complication in patients with type 1 diabetes. Liver glycogen is an important storage form of glucose and thus important for maintaining glucose homeostasis. To test the hypothesis whether abnormal storage of glycogen in the liver is contributing to the risk of hypoglycemia in type 1 diabetic children and adolescents, liver glycogen was measured. STUDY DESIGN: Hepatic glycogen concentrations were measured in 19 type 1 diabetic children and adolescents as well as in 19 age-matched controls, following overnight fasting and 4 h after two standardized meals. Hepatic glycogen was assessed by natural abundance 13C nuclear magnetic resonance spectroscopy (MRS). RESULTS: Mean (+/- SEM) fasting hepatic glycogen concentrations measured in arbitrary units (au) were similar in type 1 diabetic subjects and controls (4.98 +/- 0.36 vs. 4.48 +/- 0.33 au; p = 0.31). Both groups presented with an increase in liver glycogen concentrations 4 h after the standardized meals (diabetic subjects 5.70 +/- 0.37 au, p = 0.01; controls 5.78 +/- 0.47 au, p < 0.01). Hepatic glycogen accumulation after feeding was 19.1% in diabetic children and adolescents compared with 35.8% in controls, but this difference did not reach significance. CONCLUSION: In children and adolescents with moderately controlled type 1 diabetes, hepatic glycogen stores after fasting and feeding are comparable to those of matched controls.

Adolescent↗
PubMed2003

Feed deprivation of channel catfish, Ictalurus punctatus (Rafinesque), influences organosomatic indices, chemical composition and susceptibility to Flavobacterium columnare.

Withholding feed has been suggested as a strategy to manage infectious disease of channel catfish, Ictalurus punctatus (Rafinesque). In a previous study, we demonstrated that deprivation of feed for as little as 7 days reduced innate resistance of catfish to Flavobacterium columnare. This study was conducted to evaluate the effect of feeding regimens [no feeding (NF), fed once every other day to satiation (FEOD) and fed once daily to satiation (FD)] on organosomatic indices, physiological changes and susceptibility of channel catfish to F. columnare. Fish that were not fed for 2 and 4 weeks had a significant increase (P < 0.05) in gutted weight:-wet weight ratio and decrease in other organosomatic indices [gut index (GI), mesenteric fat index (MFI) and hepatosomatic index (HSI)]. Haematology was not effected by feeding regimen except at week 4, when a significantly higher haemoglobin level was observed in the NF fish. Serum protein did not differ at week 2, but the level at week 4 of the NF fish (35.91 mg mL(-1)) was significantly lower than that of the FD fish (41.77 mg mL(-1)). Significantly lower (P < 0.05) blood glucose (39.5 and 40.3 mg dL(-1)) and liver glycogen (1.7 and 1.8 mg g(-1)) were seen in the NF fish at weeks 2 and 4, respectively, as compared with blood glucose and liver glycogen levels of FD fish (67.5 and 92.8 mg dL(-1) and 46.5 and 52.6 mg g(-1) at weeks 2 and 4, respectively) and FEOD (82.8 and 85.5 mg dL(-1) and 45.1 and 51.4 mg g(-1) at weeks 2 and 4, respectively). Mortality in the NF fish caused by F. columnare (78%) was significantly higher (P < 0.05) than mortality in the FD and FEOD treatments (0.0 and 1.7%, respectively). Blood glucose and liver glycogen showed the same trend of low values for NF fish following challenge (week 6). Blood glucose, liver glycogen, GI and HSI are sensitive indicators for channel catfish deprived of feed (NF) for 4 weeks. Blood glucose and liver glycogen levels around 40 mg dL(-1) and 2 mg g(-1), respectively, are indicative of starvation in juvenile channel catfish. Moreover, NF fish were susceptible to F. columnare infection. Thus, it is suggested that in the absence of natural food, juvenile channel catfish should be fed at least once every other day to apparent satiation to maintain normal physiological function and improve resistance to F. columnare.

Animals↗
PubMed1982

"In vivo" effects of insulin on carbohydrate metabolism of catfish (Ictalurus melas).

The effect of insulin was studied on blood glucose, and on the glycogen level of liver, muscles and heart in fed and in starved catfish (Ictalurus melas). Fish received intraperitoneally 60 iu/kg body weight of bovine insulin, or physiological saline and were sacrificed after 2, 4, 8, 24, 72 hr from injection. Insulin caused a decrease of blood glucose level, both in fed and in fasted animals, and the effect is more evident in fed animals. After insulin treatment, liver glycogen shows a decrease which is significant at the 8th and 24th hr in fasted and in fed animals respectively; after 72 hr the glycogen level in livers of fed and fasted animals is still very low. Insulin increases the glycogen level both in white and in dark muscle, both in fed and in fasted fish, although with different characteristics, but at the 72nd hr in all animals, the increases are significant. Hormone treatment does not change heart glycogen levels in fed catfish till the 24th hr, then there is a net decrease; in starved animals the decrease begins at the 2nd hr, but only at the 48th hr is it significant. The role of insulin was discussed in relation to the lowering of glycogen concentration in liver, in connection with the fact that many authors found different and even opposite effects of this hormone in various fish. It is possible that the glycogen depletion observed in liver after insulin injection is not due to a direct action of this hormone, but depends on the stimulated production of other specific glycogenolytic hormones, such as epinephrine and/or glucagon.

Animals↗
PubMedDate not supplied

[Effect of prednisolone, hyperbaric oxygenation and their combination on the glucose content of the blood and glycogen in the organs of white rats].

A single injection of prednisolone in doses of 10, 30, 80 and 100 mg/kg provoked different shifts in blood glucose concentration and glycogen content in the heart, liver, and skeletal muscles. Prednisolone increased liver glycogen content almost in all the doses. Administered in doses of 10 and 30 mg/kg the drug reduced blood glucose level and glycogen content in the myocardium and skeletal muscles. Administered in doses of 80 and 100 mg/kg the drug produced almost no effect on the characteristics under consideration or increased them. Oxygen raised glycogen liver content, blood glucose level, reduced the content of the polysaccharide in the skeletal muscles at a pressure of 3039 Pa (3 at. abs). Combined use of prednisolone and oxygen at an elevated pressure led, depending on the drug dose, to the occurrence of the phenomena of either synergism or antagonism.

Animals↗
PubMed1995

Glycogen concentration and regulation of synthase activity in rat liver in vivo.

The proportion of liver glycogen synthase in the active (R+I) forms is lower in the fed than in the fasted state. This has been attributed to inhibition of synthase phosphatase by the accumulated hepatic glycogen. We observed that after oral administration of glucose or galactose to fasted rats, hepatic synthase R+I activity first increased, as expected, but then decreased to a nadir significantly below the control level regardless of the maximal glycogen concentration reached. Therefore, we investigated further the relationship of hepatic synthase R+I activity and glycogen concentration in vivo in fasted rats given increasing oral glucose loads. Male rats fasted 24 h were given glucose doses of 0.1-4.0 g/kg by oral gavage (n > or = 8). Liver synthase R+I, total synthase, phosphorylase a, glucose, glycogen, glucose-6-P, and UDP glucose were measured at intervals over 20-240 min after gavage. Even the smallest glucose load elicited rapid glycogen synthesis. The maximum glycogen concentration increased linearly with the size of the glucose load, although the proportion of administered glucose accounted for by liver glycogen decreased as the glucose load increased. The proportion of synthase in the active (R+I) forms peaked at 20 min after all doses and then declined. By the time the glycogen concentration was maximal, synthase R+I activity had decreased to the control value, regardless of the glucose dose administered or the maximum glycogen concentration reached. Although the decrease in synthase R+I at the time of the glycogen peak was correlated with the increase in glycogen concentration, synthase R+I continued to decrease for another 1-2 h even though liver glycogen was stable or decreasing. The nadir reached was independent of the maximal glycogen concentration. The synthase R+I nadir also did not correlate with hepatic glucose or glucose-6-P concentrations or phosphorylase a activity. Overall, there was not a straightforward temporal or quantitative relationship between the glycogen concentration and synthase R+I activity. These data suggest a more complex mechanism than simply direct inhibition of synthase phosphatase by glycogen.

Animals↗
PubMed1983

Coordinated feedback regulation of muscle glycogen metabolism: inhibition of purified phosphorylase phosphatase by glycogen.

An assay method was devised for accurately measuring the activity of phosphorylase phosphatase in the presence of glycogen. Both oyster glycogen and rabbit liver glycogen inhibited the activity of purified phosphorylase phosphatase catalytic subunit in a concentration-dependent manner. In the presence of 120 mM KCl, micromolar AMP increased the sensitivity of the phosphatase to glycogen inhibition. The present studies suggest that glycogen feedback inhibition may be a coordinated mechanism producing a decrease in phosphorylase phosphatase activity as well as glycogen synthase phosphatase activity.

Adenosine Monophosphate↗
PubMed1976

Glycogen levels and peripheral mechanisms of glucose-induced spppression of feeding.

Rabbits deprived of food for 0, 2, 4, 6, 8, 16, and 24 h were assessed for glucose-induced feeding suppression, refeeding after deprivation, and liver glycogen. In previous research, we hypothesized a relationship between liver glycogen and the transition from duodenal to hepatic glucose suppression. In duodenally cannulated rabbits, the infusion of 10 ml of isotonic glucose in awake, free-feeding animals significantly suppressed food intake but did not do so in those food deprived for 2, 4, 6, 8, or 24 h. In hepatic-cannulated rabbits, similar amounts of glucose significantly suppressed food intake in 4-, 6-, 16-, and 24-h-deprived animals. Also, refeeding after deprivation increased as a function of continued deprivation until 6 or 8 h, when refeeding reached asymptote, or decreased through 24-h deprivations. In agreement with these observations, liver glycogen showed a sharp decline between 4, 6, and 8 h of deprivation (depending on circadian cycle). It is proposed that liver glycogen depletion, or some correlate, alters liver glucostatic regulation and determines refeeding after deprivation.

Animals↗
PubMed1967

Studies on glycogen synthesis in pigeon liver homogenates. Incorporation of hexose into glycogen.

Liver homogenates of avian species, but not of mammals, form glycogen from glucose, mannose, fructose and galactose. Incorporation of labelled glucose, fructose and mannose, but not of labelled galactose, into glycogen is diluted isotopically by unlabelled glucose. Except for fructose, glycogen formation from other substrates by pigeon liver homogenates compares favourably with that from the same substrates in pigeon liver slices. Optimum conditions for glycogen synthesis from glucose by pigeon liver homogenate are: medium of incubation, 0.175m-sucrose-45mm-potassium chloride-15mm-glycylglycine buffer, pH7.5; concentration of substrate, 15mm; concentration of tissue, less than 120mg./ml.; temperature of incubation, 37-43 degrees ; atmosphere, oxygen. Uncouplers of oxidative phosphorylation, Ca(2+), EDTA, PP(i), 2-deoxyglucose 6-phosphate and microsomal fraction of rat liver are inhibitory to glycogen synthesis from glucose. Starvation of pigeons for 24 and 48hr. leads to a slight stimulation of glycogen synthesis in their liver homogenates as compared with fed controls. Pigeon liver homogenates can be separated into subcellular fractions that on reconstitution can synthesize glycogen. All the enzymes of the glycogen pathway except soluble high-K(m) glucokinase are present in pigeon liver.

Animals↗
PubMed1989

Effect of hepatic vagotomy on postexercise substrate levels in food-restricted rats.

The metabolic effects of a selective hepatic vagotomy (HV) were investigated at rest and immediately after a 50-min exercise period (26 m/min, 0% grade) in rats subjected to an overnight 50% food restriction. This dietary restriction reduced liver glycogen content to 50% of normal resting concentrations (2.2-2.8 g/100 g). No significant differences between HV and sham-operated rats were found in resting and exercising beta-hydroxybutyrate, glucose, glycerol, and insulin concentrations. Postexercise liver glycogen concentrations were reduced to approximately 1.0 g/100 g in both HV and sham-operated groups. This decrease was associated with significantly (P less than 0.01) lower postexercise glycogen levels in the soleus muscle of HV rats (2.6 times) along with higher plasma free fatty acid concentrations (P less than 0.01). These data provide evidence that HV combined with a progressive decrease in liver glycogen content may influence substrate regulation during exercise. They also support the concept of the existence of hepatic glucoreceptors responsive to a decrease in liver glycogen content.

Animals↗
PubMed1986

Influence of diet on the storage, mobilization and utilization of energy reserves in trained and untrained rats.

The effect of the major dietary energy source (fat or carbohydrate) on some of the adaptations to physical training, particularly body composition and tissue glycogen concentrations, were studied in growing male Wistar rats. Resting liver glycogen concentrations were lower in both trained and sedentary rats fed a high fat diet compared to corresponding rats fed a high carbohydrate (low fat) diet. Trained rats on both diets had higher liver glycogen levels than corresponding sedentary controls. Resting gastrocnemius muscle glycogen concentrations were not influenced by diet or training. Rates of liver and muscle glycogen depletion during a 60-min swim were lower in trained rats but were not influenced by diet. Significant interactions were noted between the dietary energy source and exercise training with respect to body weight gain, body fat content, liver weight and liver glycogen concentrations.

Animals↗
PubMed1989

Survival and postweaning performance of pigs from sows fed fat during late gestation and lactation.

Sows were fed a control corn-soybean meal gestation diet to d 80 of gestation. One group of sows (n = 25) continued receiving the control diet until the end of lactation, whereas two groups were placed on other treatments. One group (n = 27) was fed a diet containing 5% added solid fat pellets from gestation d 80 through lactation, whereas another group (n = 25) was fed a diet with 10% added solid fat pellet from gestation d 100 through d 14 of lactation. Feed supply was 2.27 kg/d during gestation and to appetite during lactation. Pigs from sows fed the control diet or 5% solid fat pellet diet were weaned with an age range of 22 to 28 d and immediately allotted in a 2 x 3 factorially designed 4-wk feeding trial. Pigs from these two sow groups were fed diets 1) without fat, 2) with 4.5% choice white grease or 3) with 5% solid fat pellet. Sow weight loss, backfat change and pig weights were not different at weaning among treatments. Survival rates of all pigs to 21 d averaged 90% with no significant differences between treatments. Pigs from fat-fed sows had more (P less than .05) glycogen per gram of liver, 41% more total liver glycogen and 16% more serum glucose at birth. Weanling pigs from fat-fed sows grew slower (P less than .05) than pigs from control sows. Supplemental fat during gestation increased liver glycogen of pigs, which should help survival, but the feeding of fat throughout lactation had a negative effect on ADG during a 4-wk postweaning period.

Animal Feed↗
PubMed2005

Glucose production in response to glucagon is comparable in preterm AGA and SGA infants.

BACKGROUND AND AIMS: Low plasma glucose concentrations are more often detected in small-for-gestational-age (SGA) than in appropriate-for-gestational-age (AGA) infants. This is ascribed to impaired glucose production due to presumed lower liver glycogen stores in SGA infants. The change in glucose production induced by glucagon is considered to be an indicator of liver glycogen content. We compared the effect of glucagon on glucose kinetics in preterm AGA and SGA infants. METHODS: In 5 AGA and 5 SGA preterm infants (postnatal age: 3-6 days) glucose production and gluconeogenesis were measured using stable isotopes immediately before and for 1 h after a bolus of glucagon. RESULTS: After glucagon the plasma glucose concentration and glucose production increased significantly over time (P<0.05 and P<0.0001, respectively). The changes were comparable between AGA and SGA infants. Glycogenolysis contributed 75-80% to the increase in glucose production. CONCLUSION: The increase in glucose production after glucagon was similar in preterm AGA and SGA infants, and mainly due to an increase in glycogenolysis. Based on the assumption that glycogenolysis is an indicator of liver glycogen content, our data do not support the hypothesis that liver glycogen content is lower in preterm SGA compared to AGA infants after the first postnatal day.

Area Under Curve↗
PubMed1977

[Isolation and properties of glycogen phosphorylase b from rabbit liver].

Purification of dephosphorylated form of rabbit liver glycogen phosphorylase (phosphorylase b) has been carried out. The purification procedure included 3 steps:sedimentation of protein-glycogen pellet by centrifugation at 62 000 x g during 2 hours, chromathography on omega-amino-hexyl-Sepharose column and isoelectric focusing. The yield of the enzyme is about 60%, the specific activity at glucose-1-phosphate concentration 100mM is 35 mkmol of Pi/mg protein-min. The final preparation revealed apparent homogeneity during ultracentrifugation and polyacrylamide gel electrophoresis. The subunit molecular weight of 100 000 was determined by disc-electrophoresis in the presence of sodium dodecyl sulfate. The absorption spectrum of liver phosphorylase b shows a protein maximum at 280 nm and a second peak at 333 nm produced by bound PLP. A kinetic analysis of initial rates with variable concentrations of the substrate revealed the homotropic cooperativity of glucose-1-phosphate binding sites. This cooperative effect is more pronounced in the presence of inhibitors, glucose and ATP and less pronounced in the presence of AMP.

Adenosine Monophosphate↗
PubMed1980

Photoperiod effects on carbohydrate metabolites in the goldfish, Carassius auratus: role of the pineal and retinal pathways.

The effects of exposure to various photoregimes or to constant darkness on liver glycogen and plasma glucose levels in the goldfish were examined during different seasons. In addition, pinealectomized fish and optic nerve sectioned fish were exposed to the photoregimes to assess the potential role of the pineal organ and retinal pathways in mediating photoperiod effects. Neither photoperiod manipulation nor exposure to constant darkness affected liver glycogen levels in experiments conducted during October and January. Photoperiod alteration and exposure to constant darkness resulted in changes of liver glycogen and plasma glucose levels during May, suggesting that response to photoperiod varies with season. Likewise, optic nerve sectioning altered liver glycogen levels during May, but not during October or January, indicating that retinal pathways may be involved in mediating photoperiod effects. During both October and May pinealectomy resulted in a lowering of liver glycogen levels independent of photoregime ; the extent to which hepatic glycogen levels were decreased by pinealectomy was affected by lighting conditions. Plasma glucose levels were elevated in pinealectomized fish regardless of photoregime during May ; the degree of this increase varied with lighting conditions. Our data suggest that the pineal organ does not mediate photoperiod effects on plasma glucose and hepatic glycogen levels, but that there is a functional relationship between this organ and carbohydrate metabolism.

Animals↗
PubMed1977

[Purification and kinetic properties of glycogen phosphorylase A from rabbit liver].

The purification of phosphorylated form of rabbit liver glycogen phosphorylase (phosphorylase A) using the chromathography on a omega-amino-hexyl-Sepharose column has been carried out. The yield is about 90%, the specific activity is equal to 90 mkmol Pi/min. mg. The enzyme samples appeared essentially homogeneous when analyzed by polyacrylamide gel electrophoresis. The Km value of glucose-1-phosphate in the presence of AMP is 4--6 mM, which is higher than that found previously. When the glucose-1-phosphate concentration was varied, deviations from Michaelis-Menten kinetics were observed in the presence of glucose or ATP (Hill slopes of 1.6), but these deviations were virtually abolished by the presence of AMP. With glucose-1-phosphate as the substrate the Ki value of glucose is 57 mM in the absence of AMP and 150 mM in the presence of this effector. The Ki value of ATP is less dependent on the presence of AMP. The synergism in combined action of glucose and ATP has been revealed.

Adenosine Monophosphate↗