EFFECT OF SYNTHETIC HUMAN 1,39-CORTICOTROPHIN ON BLOOD GLUCOSE LEVEL IN MICE

1970 ◽  
Vol 65 (3) ◽  
pp. 481-489
Author(s):  
F. A. László ◽  
I. Szijj ◽  
F. Durszt ◽  
K. Kovács
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
The Other ◽  
Glucose Content ◽  
High Blood Glucose ◽  
Adrenocortical Activity ◽  
Initial Blood

ABSTRACT The hypoglycaemic action of synthetic human 1,39-corticotrophin was determined in mice and its effectiveness compared with highly purified porcine corticotrophin. Synthetic human 1,39-corticotrophin (0.01 mg = 1.0 IU) and porcine corticotrophin (1.0 IU) induced a transient hypoglycaemia. After the administration of the porcine corticotrophin the decrease in the blood glucose concentration was somewhat more marked and prolonged. Adrenocortical activity was not necessary for the development of hypoglycaemia. In adrenalectomized mice, dexamethasone substitution by increasing the initial blood glucose content, made the effect more pronounced. Pretreatment with corticotrophin reduced the extent of the alloxan-induced transitory hyperglycaemia. On the other hand, it did not influence the high blood glucose values in manifest alloxan diabetic animals. It is possible that corticotrophin induces hypoglycaemia through insulin release. This is an extra-adrenal effect of corticotrophin as it is also observed in adrenalectomized mice.

scholarly journals Blood glucose level in rats with different behavioral activity in the dynamics of repeated stress exposures

2019 ◽  
Vol 27 (1) ◽  
pp. 10-19
Author(s):  
Anastasiya Yu. Abramova ◽  
Elena V. Koplik ◽  
Irina V. Alekseyeva ◽  
Sergey S. Pertsov
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Stress Factors ◽  
Behavioral Activity ◽  
Glucose Content ◽  
Control Measurement ◽  
Repeated Stress

Aim. To study the effect of repeated stress on blood glucose level in rats with various behavioral characteristics and with different resistance to the development of adverse consequences of negative emotiogenic exposures. Materials and Methods. The animals were initially subjected to open field test to calculate the index of activity. Daily 4-h immobilization of rats in individual plastic cages for 8 days was used as a model of stress. Blood glucose concentration was measured with a glucometer (control measurement and on the 1st, 3rd and 8th days of repeated stress). Results. The basal level of glucose in behaviorally active (stress-resistant) rats was lower than in passive (stress-predisposed) specimens. Repeated exposure of rats to stress resulted in development of hyperglycemia. However, the dynamics of blood glucose concentration was different in specimens with different parameters of behavior. The increase in glucose concentration in active animals was most pronounced after a single exposure. By the 3rd and 8th days of stress exposures, glucose level in these rats progressively decreased (as compared to the 1st day), but remained above the basal level. Passive specimens were characterized by the increase in blood glucose concentration after a single and, particularly, after three-time restraint stress. Glucose content in these animals slightly decreased by the 8th day (as compared to the previous periods), but was above the basal level. Conclusion. The dynamics of abnormalities in carbohydrate metabolism (in particular, changes in blood glucose level) during chronic emotiogenic exposures differed in specimens with different resistance to stress factors. These data illustrate the importance of an indivi-dual approach to studying the pathophysiological mechanisms of progression and development of stress-induced disorders.

scholarly journals Glucose Tolerance and Insulin Release in Malnourished Rats

1976 ◽  
Vol 50 (3) ◽  
pp. 153-163 ◽  
Author(s):  
C. Weinkove ◽  
E. A. Weinkove ◽  
B. L. Pimstone
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Protein Energy Malnutrition ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Protein Energy

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a ‘functional immaturity’ of the pancreas.

THE EFFECTS OF HORMONES ON THE CARBOHYDRATE METABOLISM OF THE LAMPREY LAMPETRA FLUVIATILIS

1965 ◽  
Vol 31 (2) ◽  
pp. 127-137 ◽  
Author(s):  
P. J. BENTLEY ◽  
B. K. FOLLETT
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Carbohydrate Metabolism ◽  
Glucose Concentration ◽  
Skeletal Muscles ◽  
Blood Glucose Concentration ◽  
Liver Glycogen ◽  
Arginine Vasotocin ◽  
Glycogen Concentration ◽  
Muscle Glycogen Concentration

SUMMARY River lampreys regulated their blood glucose concentration when injected with glucose. Mammalian insulin decreased the blood glucose concentration in the lamprey while adrenaline, cortisol and arginine vasotocin increased it. Glucagon had no effect initially but after a delay of 4 hr. decreased the blood glucose level. Insulin and cortisol increased the liver glycogen concentration. Adrenaline decreased the muscle glycogen concentration; vasotocin increased it. Treatment with alloxan increased the blood glucose concentration. Fat and glycogen in the lamprey are stored mainly in the skeletal muscles and their histochemical distribution in muscle is described. The results are discussed in relation to the metabolism of the migrating lamprey and the evolution of the control of carbohydrate metabolism in vertebrates.

ON THE ACTION OF TOLBUTAMIDE IN NORMAL MAN

1973 ◽  
Vol 72 (3) ◽  
pp. 506-518 ◽  
Author(s):  
A. Widström ◽  
E. Cerasi
Keyword(s):  
Blood Glucose ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Insulin Response ◽  
Blocking Agent ◽  
Significant Inhibition ◽  
Normal Man ◽  
Adrenergic Blocking ◽  
Plasma Insulin Response

ABSTRACT The plasma insulin response to intravenously administered tolbutamide was measured in healthy subjects under experimentally induced variations in the blood glucose concentration. Decreasing blood glucose concentration down to 51 and 25% of the basal level by the iv administration of 0.05 and 0.10 IU of insulin/kg body weight, respectively, resulted in significant inhibition of the insulin response to tolbutamide. The degree of inhibition was correlated to the extent of the hypoglycaemia. This inhibition seems to be only partially mediated by catecholamines, since blocking the α-adrenergic receptors with phentolamine could not restore the action of tolbutamide. Furthermore, whereas the prevention of the hypoglycaemia that normally follows tolbutamide administration resulted in an enhancement of the insulin response to the drug, phentolamine had no such effect. These results indicate that the decrease in blood glucose concentration as such, rather than activation of the adrenergic mechanisms, is responsible for the inhibition of tolbutamide-induced insulin release. Hence, the blood glucose level at the time of tolbutamide administration seems to determine the insulin response to the drug. The administration of the β-adrenergic blocking agent propranolol, in doses known to suppress glucose-induced insulin release in man, had no effect on the insulin response to tolbutamide. Our studies thus do not confirm the reports of other investigators that sulphonylureas may act on the islet cell as β-adrenergic agonists.

scholarly journals Glucocorticoid-Induced Preterm Birth and Neonatal Hyperglycemia Alter Ovine β-Cell Development

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3763-3776 ◽  
Author(s):  
Amita Bansal ◽  
Frank H. Bloomfield ◽  
Kristin L. Connor ◽  
Mike Dragunow ◽  
Eric B. Thorstensen ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Preterm Birth ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Cell Mass ◽  
Β Cell ◽  
High Blood Glucose ◽  
Increased Risk

Adults born preterm are at increased risk of impaired glucose tolerance and diabetes. Late gestation fetuses exposed to high blood glucose concentration also are at increased risk of impaired glucose tolerance as adults. Preterm babies commonly become hyperglycemic and are thus exposed to high blood glucose concentration at an equivalent stage of pancreatic maturation. It is not known whether preterm birth itself, or complications of prematurity, such as hyperglycemia, alter later pancreatic function. To distinguish these, we made singleton preterm lambs hyperglycemic (HYPER) for 12 days after birth with a dextrose infusion and compared them with vehicle-treated preterm and term controls and with HYPER lambs made normoglycemic with an insulin infusion. Preterm birth reduced β-cell mass, apparent by 4 weeks after term and persisting to adulthood (12 mo), and was associated with reduced insulin secretion at 4 months (juvenile) and reduced insulin mRNA expression in adulthood. Hyperglycemia in preterm lambs further down-regulated key pancreatic gene expression in adulthood. These findings indicate that reduced β-cell mass after preterm birth may be an important factor in increased risk of diabetes after preterm birth and may be exacerbated by postnatal hyperglycemia.

Intraportal glucose infusion and pancreatic islet blood flow in anesthetized rats

2000 ◽  
Vol 279 (4) ◽  
pp. R1224-R1229 ◽  
Author(s):  
Per-Ola Carlsson ◽  
Masanori Iwase ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Blood Glucose ◽  
Portal Vein ◽  
Insulin Release ◽  
Pancreatic Islet ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Islet Blood Flow ◽  
Blood Flow Increase ◽  
Selective Increase

The aim of the study was to evaluate whether a selective increase in portal vein blood glucose concentration can affect pancreatic islet blood flow. Anesthetized rats were infused (0.1 ml/min for 3 min) directly into the portal vein with saline, glucose, or 3- O-methylglucose. The infused dose of glucose (1 mg · kg body wt−1 · min−1) was chosen so that the systemic blood glucose concentration was unaffected. Intraportal infusion of d-glucose increased insulin release and islet blood flow; the osmotic control substance 3- O-methylglucose had no such effect. A bilateral vagotomy performed 20 min before the infusions potentiated the islet blood flow response and also induced an increase in whole pancreatic blood flow, whereas the insulin response was abolished. Administration of atropine to vagotomized animals did not change the blood flow responses to intraportal glucose infusions. When the vagotomy was combined with a denervation of the hepatic artery, there was no stimulation of islet blood flow or insulin release after intraportal glucose infusion. We conclude that a selective increase in portal vein blood glucose concentration may participate in the islet blood flow increase in response to hyperglycemia. This effect is probably mediated via periarterial nerves and not through the vagus nerve. Furthermore, this blood flow increase can be dissociated from changes in insulin release.

CASE STUDY OF HIGH BLOOD GLUCOSE CONCENTRATION EFFECTS OF 850 MHZ ELECTROMAGNETIC FIELDS USING GTEM CELL

2012 ◽  
Vol 40 ◽  
pp. 55-77 ◽  
Author(s):  
Nattaphong Boriraksantikul ◽  
Kiran D. Bhattacharyya ◽  
Paul J. D. Whiteside ◽  
Christine O'Brien ◽  
Phumin Kirawanich ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Electromagnetic Fields ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Concentration Effects ◽  
High Blood Glucose ◽  
Gtem Cell

The Initial Blood Glucose Concentration in Patients with Isolated Traumatic Brain Injury

2006 ◽  
Vol 18 (4) ◽  
pp. 304-305
Author(s):  
B Wolcke ◽  
U Abu-Tair ◽  
S Schaefer ◽  
W Rommel ◽  
C Lott ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Glucose ◽  
Brain Injury ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Initial Blood

THE CRITICALLY ILL CHILD: SALICYLATE INTOXICATION

PEDIATRICS ◽  
1969 ◽  
Vol 44 (3) ◽  
pp. 440-444
Author(s):  
William E. Segar
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Carbohydrate Metabolism ◽  
Glucose Level ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Co2 Concentration ◽  
Pharmacologic Agent ◽  
Peripheral Tissues ◽  
Salicylate Intoxication

Salicylate is a potent pharmacologic agent, and the rational therapy of salicylate intoxication must be based on an understanding of its pharmacologic actions and consequent pathophysiologic effects.l Because it acts to uncouple oxidative phosphorylation in a manner analogous to that of 2,4-dinitrophenol, salicylate is, first of all, a general metabolic stimulant.2 Oxygen consumption, carbon dioxide formation, and heat production are increased by its action; consequently, oxygen requirement, blood CO2 concentration, and the need to eliminate heat are also increased. Respiration, heart rate, and cardiac output must increase to satisfy the demands imposed by the acceleration of metabolic processes. Second, saiicylate interferes in a complex manner with the normal metabolism of carbohydrate.3 Many factors seem to be involved, some tending to decrease and others to increase the blood glucose concentralion, and, clinically, either hyperglycemia or hypoglycemia may be observed. Hyperglycemia may be partially explained by the release of epinephrmne due to activation of hypothalamic sympathetic centers. However, large doses of salicyiate also decrease aerobic metabolism and increase glucose-6-phosphatase activity, effects which tend to increase the blood glucose level. Hypoglycemia, on the other hand, may be caused by an increased utilization of glucose by peripheral tissues or by interference with gluconeogenesis by salicylates. Recent studies suggest that brain glucose concentration may be decreased despite minimal alterations in blood glucose level.4 As a result of these salicylate-mnduced alterations in carbohydrate metabolism, organic acids, particularly lactic, pyruvic, and acetoacetic, accumuiate.5 Infants appear to be particularly susceptible to the toxic effects of salicylate on carbohydrate metabolism and are more likely to have disturbances in blood glucose concentration and metabolic acidosis than are older children.

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