A central nervous system component of epinephrine hyperglycemia

Rosenberg, F. J.; DiStefano, Victor

doi:10.1152/ajplegacy.1962.203.5.782

Cited by 26 publications

(7 citation statements)

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“…There is evidence that the splanchnic nerves exert direct neural control over liver phosphorylase [1,15,16], as discussed later. Rosenberg and DiStefano [17] and Ezdinli et al [18] have also shown that the hyperglycaemia induced by systemic administration of epinephrine is inhibited by section of the medulla or the spinal cord. However, the influence of glycogenolytic hormones, particularly pancreatic hormones, on phosphorylase activation after hypothalamic stimulation has to be taken into account.…”

Section: Hypothalamo-hepatic Axis In the Control Of Carbohydrate Metamentioning

confidence: 96%

Central nervous system regulation of liver and adipose tissue metabolism

Shimazu

1981

Diabetologia

253

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Hypothalamic and autonomic nervous regulation of carbohydrate and amino acid metabolism in the liver and of lipid metabolism in adipose tissues is described. The direct neural mechanism underlying this regulation has been evaluated. Electrical stimulation of the ventromedial hypothalamic nucleus (VMH)-splanchnic nerve system causes glycogenolysis in the liver by rapid activation of glycogen phosphorylase, whereas electrical stimulation of the lateral hypothalamic nucleus (LH)-vagus nerve system promotes glycogenesis in the liver by activation of glycogen synthetase, through direct neural and neural-hormonal mechanisms. Studies on chemical coding of the hypothalamic neurones have revealed that norepinephrine-sensitive neurones in the VMH and acetylcholine-sensitive neurones in the LH are specifically involved in the regulation of liver phosphorylase and glycogen synthetase, respectively. Acetylcholine-sensitive neurones of the LH were also found to be concerned in regulation of hepatic tyrosine and aminotransferase activity, through intermediation of the cholinergic system in the LH-vagal pathway. Finally, it has been shown that the VMH acts as a regulatory centre for lipolysis in adipose tissues by modulating activation of the sympathetic nervous system. In addition, stimulation of the VMH enhanced lipogenesis in brown adipose tissue preferentially, probably through a mechanism mediated by sympathetic innervation of this tissue. The latter finding suggests that both the breakdown and resynthesis of triglycerides in brown adipose tissue, but not in white adipose tissue, are accelerated by stimulation of the VMH.

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Section: Hypothalamo-hepatic Axis In the Control Of Carbohydrate Metamentioning

confidence: 96%

Central nervous system regulation of liver and adipose tissue metabolism

Shimazu

1981

Diabetologia

253

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“…The complex mechanism of E hyperglycemia [14] also includes a neurogenic component. It has been postulated that the hyperglycemic center in the floor of the fourth ventricle contains E sensitive receptors [17] and the efferent pathway of this reflex descends in the thoraco-cervical sympathetic tract to the thy roid gland [6]. We assume that bretylium prevented the hyperglycemic re sponse by blocking the efferent (adrenergic) pathway.…”

Section: Effect Of Hemorrhage On Bretylium-medicated Sheepmentioning

confidence: 85%

Course of Hemorrhagic Shock After Blockade of Norepinephrine Release

Halmagyi¹,

Neering²,

Varga³

1970

Eur Surg Res

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“…Since it had been suggested that epinephrine may stimulate glucagon secretion [10,26,32], it became necessary to observe the effects of epi nephrine in glucagon-free animals. Partial evisceration was chosen as a simple and efficient way to remove the source of glucagon.…”

Section: Effect Of Epinephrine On Acpc Uptake In Fasted Eviscerated mentioning

confidence: 99%

“…Sergeyeva [32] showed that there is a change in the population of a-and /9-cells in the pancreatic islets of cats after inject ing epinephrine. R osenberg and Di Stefano [26] identified a CNS com ponent to epinephrine-induced hyperglycemia and suggested that a neural pathway from the fourth ventricle of the brain to the pancreas is involved in epinephrine-induced hyperglycemia and further suggested that epi nephrine stimulates the CNS in the medullary region thereby causing an impulse to be initiated which travels to the pancreas where the a-cells are stimulated to release glucagon. In 1966 Ezdinli and Sokal [10] studied the comparative effects of epinephrine and glucagon on liver glycogen metabolism in dogs and concluded that the injection of epinephrine caused an increase in glucagon secretion.…”

Section: Hypothesis No 3: Adrenal-pancreas Involvement -Glucagon Secmentioning

confidence: 99%

Action of Epinephrine on Amino Acid Uptake into Rat Diaphragm in vitro and in vivo

Sanders¹,

Jacob²

1972

Pharmacology

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The injection of epinephrine (1 mg/kg) into rats caused a significant increase in the distribution ratio (DR) of previously injected 1-aminocyclopentanecarboxylic acid (ACPC) and α-aminoisobutyric acid (AIB) within 2 h. At the same time epinephrine depressed the concentration of AIB in serum. Epinephrine did not alter ACPC concentration or distribution ratio in the diaphragm of partially eviscerated rats with intact livers and kidney. Additional amino acid transport studies were conducted in vitro using ‘intact’ diaphragm preparations from rats and Krebs-Ringer bicarbonate buffer, pH 7.4, at 37°C. AIB uptake into the intact isolated diaphragm was linear during the first 90 min of incubation. Epinephrine (EPI), 183 µM, caused a 20- to 30-percent decrease in the rate of AIB uptake during this time. EPI concentrations of 1.83 to 91.3 µM had no significant affect on AIB transport during a 60-min incubation period. EPI, 183–787 µM diminished uptake 30%. EPI, 183 µM, had a similar effect on AIB transport into diaphragms from adrenalectomized rats. Varying glucose concentrations from 2.2 to 17.8 mM did not significantly alter the inhibitory response elicited by epinephrine. However, the response to epinephrine was abolished by either 0.0 or 36.5 mM glucose. Isoproterenol, 161–403 µM did not significantly alter AIB transport in this system. On the other hand norepinephrine, 119 to 239 µM. caused a 20-percent increase of AIB uptake by the isolated diaphragm. Additionally, glucagon (11.5 µM) caused a 150-percent increase in AIB uptake into diaphragm muscle in vitro. Injecting 1 mg of EPI/kg 60 min before the preparation of the diaphragm caused a 25-percent increase in AIB uptake. AIB concentrations in the buffer medium were not significantly altered by hormone treatments in any of these studies. These results suggest that the increase in AIB uptake caused by injecting EPI may be an indirect action of the catecholamine and that the direct effect of EPI on AIB transport into diaphragm is inhibitory. The results further suggest that the indirect EPI effect in vivo might be caused by glucagon.

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A central nervous system component of epinephrine hyperglycemia

Cited by 26 publications

References 0 publications

Central nervous system regulation of liver and adipose tissue metabolism

Central nervous system regulation of liver and adipose tissue metabolism

Course of Hemorrhagic Shock After Blockade of Norepinephrine Release

Action of Epinephrine on Amino Acid Uptake into Rat Diaphragm <i>in vitro </i>and <i>in viv</i><i>o</i>

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