Adrenaline release during insulin hypoglycaemia in the rabbit

Armin, J.; Grant, R. T.

doi:10.1113/jphysiol.1959.sp006337

Cited by 25 publications

(17 citation statements)

References 22 publications

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“…Moreover, epinephrine secretion is increased further when the blood glucose level declines under the influence of insulin, even before the normal fasting level of glucose is restored (31,40). In contrast in the normal animal, there is a definite level of blood glucose, well below fasting glucose concentration, at which epinephrine release abruptly begins (41 ). Thus, neuroaxis transection itself produces an abnormal condition, promoting nonspecific release of epinephnne.…”

Section: Resultsmentioning

confidence: 97%

Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia.

Borg

During²,

Sherwin³

et al. 1994

J. Clin. Invest.

247

182

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The central nervous system has been implicated in the activation of counterregulatory hormone release during hypoglycemia. However, the precise loci involved are not established. To determine the role of the ventromedial hypothalamic nuclei (VMH) in the hormonal response to hypoglycemia, we performed hypoglycemic clamp studies in conscious SpragueDawley rats with bilateral VMH lesions produced by local ibotenic acid injection 2 wk earlier. Rats with lesions in the lateral hypothalamic area, frontal lobe, sham operated (stereotaxic needle placement into hypothalamus without injection), and naive animals served as control groups. The clamp study had two phases. For the first hour plasma glucose was fixed by a variable glucose infusion at euglycemia ( 5.9 mM). Thereafter, for an additional 90 min, glucose was either allowed to fall to (a) mild hypoglycemia ( -3.0 mM) or (b) more severe hypoglycemia ( -2.5 mM). Glucagon and catecholamine responses of lateral hypothalamic area-, frontal lobe-lesioned, sham operated, and naive animals were virtually identical at each hypoglycemic plateau. In contrast, glucagon, epinephrine, and norepinephrine responses in the VMH-lesioned rats were markedly inhibited; hormones were diminished by 50-60% during mild and by 75-80% during severe hypoglycemia as compared with the other groups. We conclude that the VMH plays a crucial role in triggering the release of glucagon and catecholamines during hypoglycemia. (J. Clin. Invest. 1994. 93:1677-1682.) Key words: ventromedial hypothalamus * hypoglycemia * glucagon -epinephrine * counterregulation Introduction The role of the central nervous system (CNS) in the regulation of counterregulatory responses to hypoglycemia remains controversial. Although several lines ofevidence strongly implicate the CNS in hypoglycemia detection and counterregulation ( 1-3), the precise brain regions involved are not known. While various nuclei have been implicated, current data suggest that counterregulatory responses during hypoglycemia are activated, at least in part, via the hypothalamus (4-6). It has

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Section: Resultsmentioning

confidence: 97%

Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia.

Borg

During²,

Sherwin³

et al. 1994

J. Clin. Invest.

247

182

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“…The sensitivity of the sympathectomized ears of different sheep to adrenaline infusion was more varied than the responses obtained from the denervated heart (compare Fig. la and b), but was of similar sensitivity to the denervated (sympathectomized and sometimes also motor-and sensory-denervated) 202 B. P. SETCHELL AND G. M. H. WAITES ears of rabbits (Armin & Grant, 1959;Fig. la).…”

Section: Resultsmentioning

confidence: 99%

“…In (a) the range and mean fall of denervated ear temperature of rabbits is also given (from Fig. 5, Armin & Grant, 1959) as vertical lines with points. temperature tests of sensitivity to adrenaline done on the same animal at different times gave similar results if the environmental temperature was the same on each occasion; and similarly the results of the heart-rate test were not affected by removal of one adrenal gland and denervation of the other.…”

Section: Resultsmentioning

confidence: 99%

Adrenaline release during insulin hypoglycaemia in the sheep

Setchell¹,

Waites²

1962

The Journal of Physiology

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“…It has subsequently been shown that the secretion from the adrenal medulla evoked by hypoglyeaemia is adrenaline and that the R. L. HIMS WORTH output of noradrenaline is little affected (Hokfelt, 1951;Euler & Luft, 1952). This selective release of adrenaline would appear to be an emergency response to hypoglycaemia and not an element in the normal homeostasis of the blood glucose, for it ceases when the blood glucose concentration rises above the level at which it is initiated and before the blood glucose returns to normal (Armin & Grant, 1959).…”

Section: Introductionmentioning

confidence: 99%

Compensatory reactions to a lack of metabolizable glucose

Himsworth¹

1968

The Journal of Physiology

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SUMMARY1. Following the injection of adrenaline into rats pre-treated with thyroxine, there is a pronounced and prolonged increase in their oxygen consumption. On this basis a method is described for following increases in the rate of secretion of adrenaline in response to physiological stimuli in rats.2. Using this method the onset and the cessation of the increased rate of secretion of adrenaline during insulin induced hypoglycaemia has been found to correspond to a blood glucose concentration of approximately 40 mg/100 ml.3. 3-Methylglucose (3-0-methyl-D-glucopyranose) is shown to cause a marked and sustained increase in the blood glucose concentration.4. This action of 3-methylglucose can be accounted for by an increase in the rate of secretion of adrenaline, as it is accompanied by a rise in oxygen consumption in thyroid treated rats and is prevented by interruption of the central nervous connexions of the adrenal medulla.5. These findings can be explained by 3-methylglucose's acting upon the receptor which reacts to insulin hypoglyeaemia by bringing about the secretion of adrenaline. It is shown that the effective stimulus to this receptor is not a low blood glucose concentration. The stimulus is possibly a depressed rate of utilization of glucose by the receptor tissue.

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Adrenaline release during insulin hypoglycaemia in the rabbit

Cited by 25 publications

References 22 publications

Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia.

Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia.

Adrenaline release during insulin hypoglycaemia in the sheep

Compensatory reactions to a lack of metabolizable glucose

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