Hypothalamic control of adrenaline secretion in response to insufficient glucose

Himsworth, R. L.

doi:10.1113/jphysiol.1970.sp009021

Cited by 88 publications

(28 citation statements)

References 8 publications

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“…In previous studies we performed hypoglycemic clamp studies in bilaterally VMH lesioned rats as well as in rats with lesions in different brain areas (6). A marked inhibition of both the glucagon and catecholamine response to hypoglycemia was evident only in the VMH-lesioned animals, consistent with earlier studies implicating the hypothalamus in the activation of hypoglycemic counterregulation (13)(14)(15).…”

Section: Discussionsupporting

confidence: 66%

Local ventromedial hypothalamus glucose perfusion blocks counterregulation during systemic hypoglycemia in awake rats.

Borg¹,

Sherwin²,

Borg³

et al. 1997

J. Clin. Invest.

338

267

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The ventromedial hypothalamic nucleus (VMH) is necessary for the integrated hormonal response to hypoglycemia. To determine the role of the VMH as a glucose sensor, we performed experiments designed to specifically prevent glucopenia in the VMH, while producing hypoglycemia elsewhere. We used awake chronically catheterized rats, in which local VMH glucose perfusion (100 mM or 15 mM of D-glucose) was combined with a sequential euglycemichypoglycemic clamp. In two control groups the VMH was perfused either with ( a) an iso-osmotic solution lacking glucose, or with ( b ) nonmetabolizable L-glucose (100 mM). During systemic hypoglycemia glucagon and catecholamine concentrations promptly increased in the control animals perfused with either 100 mM L-glucose or the iso-osmotic solution lacking glucose. In contrast, glucagon, epinephrine and norepinephrine release was inhibited in the animals in which the VMH was perfused with D-glucose; hormonal secretion was partially suppressed by the VMH perfusion with 15 mM D-glucose and suppressed by ‫ف‬ 85% when the VMH was perfused with 100 mM D-glucose, as compared with the control groups. We conclude that the VMH must sense hypoglycemia for full activation of catecholamine and glucagon secretion and that it is a key glucose sensor for hypoglycemic counterregulation. ( J. Clin. Invest. 1997. 99:361-365.)

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Section: Discussionsupporting

confidence: 66%

Local ventromedial hypothalamus glucose perfusion blocks counterregulation during systemic hypoglycemia in awake rats.

Borg¹,

Sherwin²,

Borg³

et al. 1997

J. Clin. Invest.

338

267

View full text Add to dashboard Cite

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“…Morgane described a similar result in rats with lesion of the far-lateral hypothalamic area, attributing this effect to impairment of metabolic functions independently from that of food intake. Interference with metabolic functions by the lateral hypothalamus was demonstrated by Himsworth (1970), who found that lesions in this area reduces release of catecholamines from adrenal medulla in cytoglucopoenic rats, and by Teixeira, Antunes-Rodrigues & Migliorini (1973), who showed a decrease in peripheral mobilization of fatty acids in the same condition.…”

Section: Discussionmentioning

confidence: 96%

Neural systems responsible for the gastric secretion provoked by 2‐deoxy‐D‐glucose cytoglucopoenia.

Kadekaro¹,

Timo-Iaria²,

Valle³

1975

The Journal of Physiology

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SUMMARY1. The central structures responsible for the gastrosecretory effect of cytoglucopoenia caused by 2-deoxy-D-glucose (2-DG) were investigated in 105 cats prepared with chronic gastric fistulae and subjected to various experimental procedures.2. Bilateral electrolytic lesion of the caudalmost two thirds of globus pallidus almost suppressed the secretary response and caused aphagia and adipsia.3. Secretion in response to 2-DG and feeding behaviour were entirely blocked after making a lesion in a large ventromedial area of the meso diencephalic transition comprising the ventral tegmental area of Tsai, the ventral tegmental decussation, the red nucleus, a ventral portion of the central grey matter, the interstitial nuclei of Darkschewitsch and of Cajal, the pre-rubral fields, the reticular part of substantia nigra, the internal portion of the cerebral peduncle and the ventral part of the mesencephalic rerticula formation.4. Microinjection of 2-DG in the medial forebrain bundle, at the level of the hypothalamus, caused intense gastric secretion, whereas the same procedure was totally ineffective when the caudalmost two thirds of the globus pallidus were stimulated.5. Increasing doses of 2-DG, systemically injected, restored the secretory response in volume and acid concentration and output after intercollicular transaction of the brain stem. After the transaction, secretion of pepsin was only slightly increased when large doses of 2-DG were administered, thus suggesting a differential control of water, acid and pepsin secretion in response to cytoglucopoenia.6. It is concluded that there are at least three reflex systems involved in gastric secretion due to cytoglucopoenia: (a) a reflex consisting of afferent MASSAKO KADEKARO AND OTHERS and efferent pathways in the medial forebrain bundle area; (b) a reflex whose afferent side is from the hypothalamus and efferent side is from the globus pallidus; (c) a reflex with the afferent side probably originating in the liver and the efferent side in the lower brain stem.7. The pathways involved in the first two arcs run along Nauta's limbic mid-brain circuit. The three systems are possibly related to control of secretion and feeding behaviour.

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“…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)(5)(6). It has been frequently suggested that ventromedial hypothalamus (VMH),' known as a regulator of food intake ("satiety center") (7,8), may also contain glucosensitive tissues that could mediate the responses to hypoglycemia (9,10).…”

Section: Introductionmentioning

confidence: 99%

Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia.

Borg

During²,

Sherwin³

et al. 1994

J. Clin. Invest.

245

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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Hypothalamic control of adrenaline secretion in response to insufficient glucose

Cited by 88 publications

References 8 publications

Local ventromedial hypothalamus glucose perfusion blocks counterregulation during systemic hypoglycemia in awake rats.

Local ventromedial hypothalamus glucose perfusion blocks counterregulation during systemic hypoglycemia in awake rats.

Neural systems responsible for the gastric secretion provoked by 2‐deoxy‐D‐glucose cytoglucopoenia.

Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia.

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