scholarly journals THE EFFECT OF HYPERGLYCEMIA ON HYPOTHALAMIC GOLD UPTAKE AND HYPERPHAGIA IN GOLDTHIOGLUCOSE-TREATED MICE

1965 ◽  
Vol 121 (3) ◽  
pp. 403-413 ◽  
Author(s):  
P. Michael Edelman ◽  
Irving L. Schwartz ◽  
Eugene P. Cronkite ◽  
George Brecher ◽  
Linda Livingston

The accumulation of gold in the hypothalamus and the development of hyperphagia and obesity were studied in mice given a single intravenous injection of goldthioglucose at various levels of blood glucose concentration. It was found that the glucose concentration prevailing at the time of goldthioglucose injection was correlated directly with the level of free and bound goldthioglucose in the blood 3 minutes later, with the hypothalamic uptake of gold, with the extent of the hypothalamic lesion, and with the severity of the subsequent hyperphagia and obesity. Hyperglycemia was associated with an increased gold deposition throughout the brain. A gold content of 88 ± 12 µg/mg wet tissue in the hypothalamus of fasted animals was associated with clearcut lesions in all animals studied, whereas a similar gold content in the control brain lobes of hyperglycemic animals was not associated with lesions in any animal. This finding indicates that some regions in the brain (e.g. the ventral hypothalamus) are more susceptible than others to damage by goldthioglucose.

1964 ◽  
Vol 206 (1) ◽  
pp. 133-135 ◽  
Author(s):  
I. Arthur Mirsky ◽  
Robert Jinks ◽  
Gladys Perisutti

The intravenous injection of anti-insulin serum produces an immediate increase in the blood glucose concentration of both normal and presumably "depancreatized" ducks. Whereas the blood glucose of the normal ducks returns to the preinjection concentration within 3.5 hr, the hyperglycemia of the depancreatized ducks persists for more than 5 hr. The response is attributed to an acute insulin insufficiency induced by insulin antibodies. Accordingly, insulin is as essential to the regulation of the blood glucose of the duck as it is to that of mammals. The data from depancreatized ducks suggest the presence of a remnant of splenic lobe of the pancreas or some extrapancreatic source of insulin.


2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
M. Higazy ◽  
Sudhanshu Aggarwal ◽  
Taher A. Nofal

In this paper, authors present a new method “Sawi decomposition method” for determining the primitive of Volterra integral equation (V.I.E.) with application. Sawi decomposition method is the combination of Sawi transformation and decomposition method. Some numerical problems have been considered and solved sequentially for explaining the complete methodology. For the practical application of the Sawi decomposition method, an advance problem of medical science for determining the blood glucose concentration during an intravenous injection has been considered and solved sequentially applying this method. Results of numerical problems depict that the Sawi decomposition method is a very effective decomposition method for determining the primitives of V.I.E.


1963 ◽  
Vol 204 (6) ◽  
pp. 1127-1132 ◽  
Author(s):  
Kazuki Sakata ◽  
Shigeo Hayano ◽  
Henry A. Sloviter

In the unanesthetized rabbit, systemic blood glucose concentration was measured periodically during the course of a slow, continuous infusion of glucose solution via the internal carotid artery. Under conditions otherwise identical, the same experiment was performed in the same rabbit, but the infusion was intravenous. In 7 of 14 such pairs of experiments, the curve of glucose concentration versus time was significantly lower for the intracarotid experiment and in the other seven cases there was no significant difference between the two curves. These results suggest that the brain responds to the increased concentration of glucose of its environment and by some mechanism acts to return it toward normal. Experiments were done in the same way with 2-deoxy-d-glucose, a substance which produces a cellular glucopenia. Of seven pairs of experiments, the systemic blood glucose curve was markedly higher in intracarotid infusion in three cases, moderately higher in two cases, and not significantly different in two cases from the curve for the intravenous infusion. These results suggest that the brain responds to decreased availability of glucose and acts, by way of the sympathetic nervous system, to raise the blood glucose concentration.


2014 ◽  
Vol 307 (4) ◽  
pp. H587-H597 ◽  
Author(s):  
Mark W. Sims ◽  
James Winter ◽  
Sean Brennan ◽  
Robert I. Norman ◽  
G. André Ng ◽  
...  

While it is well established that mortality risk after myocardial infarction (MI) increases in proportion to blood glucose concentration at the time of admission, it is unclear whether there is a direct, causal relationship. We investigated potential mechanisms by which increased blood glucose may exert cardiotoxicity. Using a Wistar rat or guinea-pig isolated cardiomyocyte model, we investigated the effects on cardiomyocyte function and electrical stability of alterations in extracellular glucose concentration. Contractile function studies using electric field stimulation (EFS), patch-clamp recording, and Ca2+ imaging were used to determine the effects of increased extracellular glucose concentration on cardiomyocyte function. Increasing glucose from 5 to 20 mM caused prolongation of the action potential and increased both basal Ca2+ and variability of the Ca2+ transient amplitude. Elevated extracellular glucose concentration also attenuated the protection afforded by ischemic preconditioning (IPC), as assessed using a simulated ischemia and reperfusion model. Inhibition of PKCα and β, using Gö6976 or specific inhibitor peptides, attenuated the detrimental effects of glucose and restored the cardioprotected phenotype to IPC cells. Increased glucose concentration did not attenuate the cardioprotective role of PKCε, but rather activation of PKCα and β masked its beneficial effect. Elevated extracellular glucose concentration exerts acute cardiotoxicity mediated via PKCα and β. Inhibition of these PKC isoenzymes abolishes the cardiotoxic effects and restores IPC-mediated cardioprotection. These data support a direct link between hyperglycemia and adverse outcome after MI. Cardiac-specific PKCα and β inhibition may be of clinical benefit in this setting.


2014 ◽  
Vol 19 (3) ◽  
pp. 527-533 ◽  
Author(s):  
Miho Senda ◽  
Susumu Ogawa ◽  
Kazuhiro Nako ◽  
Masashi Okamura ◽  
Takuya Sakamoto ◽  
...  

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