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Biomedical subjects

N Haugaard

Publications and source records attributed to N Haugaard.

At least 55 records · Page 3Linked to original sources
PubMed1987

In vitro studies of glucose metabolism of the rabbit urinary bladder.

The urinary bladder, as do all smooth muscle organs, depends on the delivery of oxygen and metabolic substrates for proper functioning. Although glucose metabolism has been studied and evaluated for a variety of smooth muscle systems, little is known about carbohydrate metabolism of the urinary bladder. In the present investigation glucose metabolism and glycogen formation of the urinary bladder of the rabbit was studied in vitro. Isolated urinary bladder strips were prepared from bladder base and body and the following metabolic determinations were made: glucose utilization, glycogen formation, CO2, and lactic acid formation. In addition, the effect of insulin on glucose metabolism was investigated. Glucose utilization was similar in bladder base and body (6.57 +/- 0.67 mumols/gm./2 hours in combined tissues). Eighty-one percent of the glucose utilized was metabolized to lactate whereas 11% was oxidized to CO2 and 4.7% was incorporated into glycogen. Insulin caused a small but significant increase in glucose utilization by bladder strips.

Animals↗
PubMed1986

Metabolic effects of acarbose in normal and diabetic rats: long- and short-term administration.

The effects of acarbose administration to normal and streptozotocin-diabetic rats were studied in animals given the drug for 3 or 21 days. The acarbose was incorporated into control diets or diets fortified with sucrose and starch. After extirpating the hearts, they were perfused by the Langendorff procedure and ventricular rate and isometric force of contraction were recorded in the presence or absence of isoproterenol. Frozen samples of heart and liver were used for metabolic measurements. At a low dose of isoproterenol (0.01 microgram) the positive inotropic response was the same in control and diabetic animals. With a higher dose of the amine (0.1 microgram) the contractile response was increased further in hearts from normal animals but not enhanced in hearts from diabetic rats. Cardiac phosphorylase activation by isoproterenol was accentuated by diabetes only when the smaller dose of the amine was given. The markedly elevated heart glycogen content of diabetic rats was decreased in response to a high carbohydrate diet. Inclusion of acarbose in the diet prevented this diminution in cardiac glycogen. In normal and diabetic rats fed the high carbohydrate diet for 3 weeks, liver glycogen was elevated. The increase in hepatic glycogen was not observed when acarbose was present in the diet. A comparison of the results of the short- and long term-administration of acarbose show that the onset of action of the drug is prompt and that the effect of the treatment is undiminished over an extended period of time.

Acarbose↗
PubMed1984

Metabolic effects of acarbose administration in normal and diabetic rats.

The effect of acarbose on cardiac and hepatic metabolism was investigated in normal and diabetic rats. Groups of rats were fed one of the three following diets for 7 days: (1) ground Purina chow, (2) ground Purina chow fortified with raw corn starch and sucrose, and (3) the above high carbohydrate diet, with added acarbose (40 mg/100 g food). At the end of the dietary period the rats were decapitated, and a sample of liver tissue was removed and frozen in liquid nitrogen. The heart was extirpated for subsequent perfusion by the Langendorff technique. Increases in liver and heart glycogen produced by the high carbohydrate diet in the normal rats were prevented completely when acarbose was incorporated into the food. In diabetic animals, liver glycogen was uniformly lower than normal, irrespective of the diet or the presence of acarbose. With animals fed the control diet, cardiac glycogen was higher in diabetic than in normal rats. The high carbohydrate diet caused a lowering of heart glycogen in diabetic rats and this reduction in glycogen content was reversed by including acarbose in the diet. Effects of isoproterenol on myocardial phosphorylase a activity were determined in hearts from normal and diabetic rats given one of the three diets. The high carbohydrate diet decreased the enzymatic response to the catecholamine in hearts from both normal and diabetic animals, and this phenomenon was prevented by the presence of acarbose in the diet. In diabetic rats fed any of the three diets, the activation of cardiac phosphorylase by isoproterenol was greatly accentuated. Measurements of heart uridine kinase showed that the activity of this enzyme was lower than normal in hearts from diabetic rats given either the control or the high carbohydrate diet. The presence of acarbose in the latter diet resulted in a significant decrease in cardiac uridine kinase activity in hearts from normal rats. The results of this study demonstrate the effectiveness of acarbose in modulating tissue metabolism in normal and diabetic animals.

Acarbose↗
PubMed1984

Inhibition of growth and decreased survival of B104 rat neuroblastoma cells after exposure to hyperbaric oxygen.

The toxic effects of hyperbaric oxygen (HBO) on growth and survival of B104 rat neuroblastoma cells were investigated. Cells in log phase growth were incubated at 37 degrees C with 10 atm O2 for 1 to 4 h. After exposure to HBO, cells were monitored for their subsequent growth and survival. Two hours of exposure caused a slowing of growth, which returned to normal by the end of the 7th d of the postexposure period. Exposures to O2 of 3 h or longer caused a complete cessation of growth for 4 d after the exposure and very little or no recovery after this period. Increased hydrostatic pressure for 6 h using helium as the inert gas had no effect on growth. A colony formation assay was used to quantitate the degree of cell death induced by HBO. The resulting survival curve was of the exponential type with a broad shoulder between 0 to 2.5 h of exposure to 10 atm O2. The curve fell off sharply at 2.5 h with an exponential decrease in survival when the exposure to HBO was extended to 4 h. At 2 h about 50% of cells were killed, but at 4 h only 2% survived the treatment. These results show that the depression of the growth rate by HBO is related to the number of cells that are killed by the exposure. This system provides a model in which the molecular and cellular effects of HBO can be investigated.

Animals↗
PubMed1984

Effects of dichloroacetate on brain pyruvate dehydrogenase.

The action of dichloroacetate (DCA) on pyruvate dehydrogenase (PDH) activity of rat brain has been studied in vitro and in vivo. In a crude brain mitochondrial fraction, DCA inhibits PDH kinase and in rat brain slices this compound increases PDH activity and stimulates glucose oxidation. In the whole animal, intraperitoneal injection of DCA causes activation of brain PDH, indicating that this inhibitor crosses the blood-brain barrier. The same treatment with DCA also produced a large increase in heart PDH activity. Further studies of the effects of DCA on the CNS should lead to results of considerable importance.

Acetates↗
PubMed1981

The relationship between uracil nucleotide concentrations and glycogen synthesis in hepatocytes from fed and fasted rats.

The relationship between glycogen synthesis and uracil nucleotide content was studied in rat hepatocytes. When hepatocytes were incubated in the presence of uridine in the incubation medium there was an increase in the rate of incorporation of U-14C-glucose into glycogen. In hepatocytes incubated in the absence of uridine for 1 hr there were large decreases in the cellular contents of UDPG and UTP, while in the presence of 5 mM uridine the concentrations of these nucleotides increased 2 to 3 fold. In hepatocytes from fasted rats uracil nucleotide contents were lower than in hepatocytes from fed rats and the effect of uridine on glycogen synthesis was greater.

Animals↗
PubMed1980

Effects of thyroid hormone on UTP content and uridine kinase activity of rat heart and skeletal muscle.

In rats made hyperthyroid by daily intramuscular injections of 250 microgram thyroxine (T4)/100 g body wt for 5 days, uridine kinase activity of extracts of psoas and cardiac muscle was markedly increased Vmax of the enzyme was elevated with no change in the apparent Km for uridine. In animals treated as above, significant increases in UTP and total uracil nucleotide contents were observed in heart and skeletal muscle. Twelve hours after a single intraperitoneal injection of 30 microgram/100 g body wt of 3,5,3'-triiodothyronine (T3), cardiac uridine kinase was significantly increased. Brain uridine kinase was unaffected by thyroid hormone treatment. In thyroidectomized rats, uridine kinase activity was lower than normal. The effect of thyroidectomy on uridine kinase activity was overcome by daily subcutaneous injections of 3 microgram T4/100 g body wt for 7 days. The rise in cardiac uridine kinase activity produced by T3 could be prevented by prior administration of actinomycin D.

Animals↗
PubMed1977

Inhibitory effect of high oxygen pressure on potassium- induced activation of pyruvate dehydrogenase and glucose metabolism in rat brain slices.

The effects of high oxygen pressure on pyruvate dehydrogenase (pyruvate: lipoate oxidoreductase (decarboxylating and acceptor-acylating), EC 1.2.4.1) activity, tissue concentration of ATP, and CO2 production from glucose were studied in rat brain cortical slices. The increase in pyruvate dehydrogenase activity and the lowering of cellular ATP, occurring during potassium-induced depolarization at 1 atm of oxygen, were reversed by increasing the oxygen pressure to 5 atm. When brain slices were incubated at 1 atm oxygen with [U-14C]glucose, a high potassium medium approximately doubled the production of 14CO2. Oxygen at 5 atm abolished this potassium-dependent increase in 14CO2 production with no significant effect on glucose oxidation in normal Krebs-Ringer phosphate medium. Adding 4 atm helium to 1 atm oxygen did not interfere with the ability of potassium ions to activate pyruvate dehydrogenase, lower ATP, or increase glucose oxidation. The results show that toxic effects of hyperbaric oxygen, not manifest in "resting" tissue, may be revealed during stress such as potassium depolarization. The site of the toxic effects of oxygen is probably the cell membrane where excess oxygen appears to interfere with the action of the sodium pump, calcium transport or other processes stimulated by increased concentrations of extracellular potassium.

Adenosine Triphosphate↗
PubMed1977

Effect of uridine on cellular UTP and glycogen synthesis in skeletal muscle: stimulation of UTP formation by insulin.

The relation between cellular uracil nucleotides and ability to synthesize glycogen was studied in rat diaphragm incubated in vitro. In the absence of exogenous uridine the tissue content of UTP and rate of glycogen synthesis decreased with time. Uridine added to the medium increased cellular UTP and UDPG and stimulated glycogen synthesis. Insulin significantly increased the synthesis of UTP from extracellular uridine. This action of insulin appeared to be due to a stimulation of phosphorylation of the nucleoside and not to an effect on transport at the concentrations of uridine studied. However, an effect of insulin on transport of uridine at low concentrations cannot be excluded.

Animals↗
PubMed1977

Alteration by halothane of glucose and glycogen metabolism in rat skeletal muscle.

Exposure of resting rat diaphragm for one hour in vitro to halothane (1-1.5, 2-2.5 and 4-4.5 per cent in oxygen) produced significant alterations of intracellular glucose disposition. Glycolysis (as measured by lactate production) increased, while glycogen formation was inhibited in a dose-related fashion. Net glucose uptake was unaffected by the anesthetic except during exposure to 4-4.5 per cent halothane, when 14 per cent depression of uptake was found. Total glycogen content decreased, due mainly to the inhibition of glycogen synthesis and to some extent to a stimulation of glycogenolysis. The anesthetic did not interfere with the effect of insulin on glucose uptake or the intracellular disposition of glucose. Creatine phosphate concentrations decreased following exposure of diaphragm to 1-1.5, 2-2.5 and 4-4.5 per cent halothane, while the adenosine triphosphate concentration declined after exposure to 4-4.5 per cent only. Although the mechanism(s) whereby halothane alters glucose and glycogen metabolism are unknown, it is possible that the anesthetic acts primarily by affecting membranes containing enzymes involved in the metabolism of glycogen.

Adenosine Triphosphate↗