1982
DOI: 10.1113/jphysiol.1982.sp014415
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Glucose‐sensitive afferent nerve fibres in the hepatic branch of the vagus nerve in the guinea‐pig.

Abstract: SUMMARY1. Afferent discharges were recorded from nerve filaments dissected from the hepatic branch of the vagus nerve in the guinea-pig in situ.2. A significant decrease in the discharge rate was observed following the administration of D-glucose into the portal vein but not after the administration of D-mannose, D-fructose, D-galactose, L-glucose, D-xylose or D-arabinose.3. The mean discharge rate ofthese fibres was inversely related to the concentration of glucose in the portal blood.4. These results suggest… Show more

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Cited by 233 publications
(115 citation statements)
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“…This results in an increased glucose-stimulated insulin secretion in the intact mouse [107], suggesting that sensory nerves through their inhibitory neuropeptide CGRP exert a tonic inhibition of insulin secretion. The result in vivo of potentiated glucose-stimulated insulin secretion in mice treated with capsaicin could also indicate that the sensory nerves are involved in a neural reflex activated by glucose, perhaps through activation of glucose sensors in the portal area [108]. Such a reflex could involve efferent adrenergic nerves, judging from studies showing that a-adrenoceptor blockade is unable to increase circulating insulin after capsaicin treatment in mice [107].…”
Section: Sensory Nervesmentioning
confidence: 99%
“…This results in an increased glucose-stimulated insulin secretion in the intact mouse [107], suggesting that sensory nerves through their inhibitory neuropeptide CGRP exert a tonic inhibition of insulin secretion. The result in vivo of potentiated glucose-stimulated insulin secretion in mice treated with capsaicin could also indicate that the sensory nerves are involved in a neural reflex activated by glucose, perhaps through activation of glucose sensors in the portal area [108]. Such a reflex could involve efferent adrenergic nerves, judging from studies showing that a-adrenoceptor blockade is unable to increase circulating insulin after capsaicin treatment in mice [107].…”
Section: Sensory Nervesmentioning
confidence: 99%
“…However, the methodology used to manipulate vagal afferents is rudimentary at best, as they do not allow selective ablation or stimulation of functionally specific neurons. For example, given that ghrelin (Date et al, 2002) and hyperglycemia (Niijima, 1982) can suppress, while gastric distension and CCK (Schwartz et al, 1993) can increase firing activity of specific populations of vagal afferents, simply cutting or stimulating both populations should theoretically lead to cancellation of their central effects. By learning more about the functional specificity of vagal afferents and the availability of more selective tools to manipulate them, they are still a worthwhile target for prevention or treatment of obesity.…”
Section: Evidence For Vagal Afferents In Short-but Not Long-term Contmentioning
confidence: 99%
“…Whatever the nature of the signal, the hypothalamus is likely to be involved in its integration. Afferent signals from the liver are conducted to the hypothalamus by the vagus nerve, with the afferent firing rate in the hepatic branch of the vagus being inversely proportional to the glucose concentration in the portal vein (Niijima, 1982). Stimulation of ventromedial hypothalamic signalling, in turn, has been shown to enhance muscle glucose uptake, an effect that can be prevented with sympathetic blockade (Minokoshi et al 1994).…”
Section: Portally Delivered Glucose: the 'Portal Signal'mentioning
confidence: 99%