Effects of Vagal Stimulation on Glucagon and Insulin Secretion

Kaneto, Akio; Miki, Eishi; Kosáka, Kinori

doi:10.1210/endo-95-4-1005

Cited by 105 publications

(35 citation statements)

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“…Electrical stimulation of pancreatic sympathetic nerve (46), local infusion of the classical sympathetic neurotransmitter norepinephrine (47), or a pancreatic sympathetic neuropeptide, such as galanin (48), all increase glucagon secretion. Similarly, electrical stimulation of parasympathetic nerves (49,50), local infusion of the classical parasympathetic neurotransmitter acetylcholine (51), or a pancreatic parasympathetic neuropeptide, such as vasoactive intestinal peptide (52,53), also stimulates glucagon release from the ␣-cell. During the noninsulin-induced hypoglycemia generated in the present study, epinephrine could not have contributed to the stimulation of glucagon secretion, because its concentration in plasma did not change.…”

Section: Discussionmentioning

confidence: 99%

α- and β-Cell Responses to Small Changes in Plasma Glucose in the Conscious Dog

et al. 2001

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The responses of the pancreatic ␣-and ␤-cells to small changes in glucose were examined in overnight-fasted conscious dogs. Each study consisted of an equilibration (-140 to -40 min), a control (-40 to 0 min), and a test period (0 to 180 min), during which BAY R3401 (10 mg/kg), a glycogen phosphorylase inhibitor, was administered orally, either alone to create mild hypoglycemia or with peripheral glucose infusion to maintain euglycemia or create mild hyperglycemia. Drug administration in the hypoglycemic group decreased net hepatic glucose output (NHGO) from 8.9 ± 1.7 (basal) to 6.0 ± 1.7 and 5.8 ± 1.0 µmol · kg -1 · min -1 by 30 and 90 min. As a result, the arterial plasma glucose level decreased from 5.8 ± 0.2 (basal) to 5.2 ± 0.3 and 4.4 ± 0.3 mmol/l by 30 and 90 min, respectively (P < 0.01). Arterial plasma insulin levels and the hepatic portalarterial difference in plasma insulin decreased (P < 0.01) from 78 ± 18 and 90 ± 24 to 24 ± 6 and 12 ± 12 pmol/l over the first 30 min of the test period and decreased to 18 ± 6 and 0 pmol/l by 90 min, respectively. The arterial glucagon levels and the hepatic portal-arterial difference in plasma glucagon increased from 43 ± 5 and 4 ± 2 to 51 ± 5 and 10 ± 5 ng/l by 30 min (P < 0.05) and to 79 ± 16 and 31 ± 15 ng/l by 90 min (P < 0.05), respectively. In euglycemic dogs, the arterial plasma glucose level remained at 5.9 ± 0.1 mmol/l, and the NHGO decreased from 10 ± 0.6 to -3.3 ± 0.6 µmol · kg -1 · min -1 (180 min). The insulin and glucagon levels and the hepatic portal-arterial differences remained constant. In hyperglycemic dogs, the arterial plasma glucose level increased from 5.9 ± 0.2 to 6.2 ± 0.2 mmol/l by 30 min, and the NHGO decreased from 10 ± 1.7 to 0 µmol · kg -1 · min -1 by 30 min. The arterial plasma insulin levels and the hepatic portal-arterial difference in plasma insulin increased from 60 ± 18 and 78 ± 24 to 126 ± 30 and 192 ± 42 pmol/l by 30 min, after which they averaged 138 ± 24 and 282 ± 30 pmol/l, respectively. The arterial plasma glucagon levels and the hepatic portal-arterial difference in plasma glucagon decreased slightly from 41 ± 7 and 4 ± 3 to 34 ± 7 and 3 ± 2 ng/l during the test period. These data show that the ␣-and ␤-cells of the pancreas respond as a coupled unit to very small decreases in the plasma glucose level. Diabetes 50:367-375, 2001 G lucagon secretion increases in response to a decrease in the plasma glucose concentration and decreases in response to a rise in the plasma glucose level. Furthermore, insulin has been postulated to exert a paracrine influence on glucagon secretion when its release is modified in response to changes in the plasma glucose concentration. To date, studies have not provided a complete understanding of the relationship between a decrement in the plasma glucose level and glucagon or insulin secretion, because the insulin level itself has been elevated to decrease the glucose level, and insulin per se can affect not only its own secretion (1), but also the release of other counterregulatory hormones, inclu...

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Section: Discussionmentioning

confidence: 99%

α- and β-Cell Responses to Small Changes in Plasma Glucose in the Conscious Dog

et al. 2001

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“…Thus, the receptor-mediated control of glucagon secretion is likely to be very complex. aAdrenoceptor, fl2-adrenoceptor, muscarinic cholinoceptor and somatostatin receptors may all be present on A cells to control glucagon release (Kaneto et al, 1974;Itoh & Gerich, 1982;Schuit & Pipeleers, 1986;Schuit et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Selective stimulation of glucagon secretion by β₂‐adrenoceptors in isolated islets of Langerhans of the rat

Lacey

Berrow

Scarpello

et al. 1991

British J Pharmacology

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1 In rat isolated islets of Langerhans the selective fl2-adrenoceptor agonist, clenbuterol (1 to 20#M), significantly increased the level of adenosine 3': 5'-cyclic monophosphate (cyclic AMP) within 2 min of incubation. 2 The cyclic AMP response to clenbuterol was inhibited in the presence of the selective f2 adrenoceptor antagonist, ICI 118551 (0.1 or 10pM) but remained unchanged when the fl1-antagonist, atenolol (0.1 pM) was administered.3 Despite causing an elevation in cyclic AMP, clenbuterol (up to 20#M) failed to influence insulin secretion at any glucose concentration tested, even in the presence of a phosphodiesterase inhibitor. 4 By contrast, clenbuterol elicited a dose-dependent rise in the rate of glucagon secretion; the maximal agonist-induced increase in secretion was two fold, a response equivalent to that observed with 20 mM L-arginine.5 ICI 118551 significantly inhibited the rise in glucagon secretion induced by clenbuterol (up to 20pM). 6 The results indicate that the rat islet A cell population is equipped with functional If2-adrenoceptors which influence glucagon secretion via the second messenger cyclic AMP, but that the B cells are deficient in functional fl-receptors.

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“…The fact that glucose is the primary energy source for the central nervous system (CNS) demands that blood glucose levels be tightly regulated within a narrow range and, thus, a complex system of central and peripheral mechanisms is involved in the regulation of glucose homeostasis (23). Peripherally, circulating glucose levels directly control the secretion of insulin and glucagon, while the CNS is involved in central control of insulin and glucagon secretion through the autonomic nervous system (ANS) (7,22,23,39). Therefore, the ANS, which undergoes substantial postnatal development that coincides with the HC dietary intervention (41), may play an important role in the programming of hyperinsulinemia in HC rats.…”

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confidence: 99%

Role of the autonomic nervous system in the development of hyperinsulinemia by high-carbohydrate formula feeding to neonatal rats

Mitrani¹,

Srinivasan²,

Dodds³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Mitrani P, Srinivasan M, Dodds C, Patel MS. Role of the autonomic nervous system in the development of hyperinsulinemia by high-carbohydrate formula feeding to neonatal rats. Am J Physiol Endocrinol Metab 292: E1069 -E1078, 2007. First published December 12, 2006 doi:10.1152/ajpendo.00477.2006.-An early dietary intervention in the form of a high-carbohydrate (HC) milk formula in neonatal rat pups results in immediate onset of hyperinsulinemia. While increased insulin secretion in HC rats has been shown to be related to hypersensitivity to glucose, the immediate onset of hyperinsulinemia and its persistence throughout the suckling period suggest involvement of multiple systems that enhance insulin secretion in response to increased demand. Evidence presented here in 12-day-old HC rats indicates that altered activity of the autonomic nervous system contributes to enhanced insulin secretory responses to glucose stimulation through increased parasympathetic and decreased sympathetic signaling. Both in vivo and in vitro studies have shown that HC rats secrete significantly higher levels of insulin in response to glucose in the presence of acetylcholine, a cholinergic agonist, while sensitivity to inhibition of insulin secretion by oxymetazoline, an ␣ 2a-adrenergic receptor (␣2aAR) agonist, was reduced. In addition, HC rats showed increased sensitivity to blockade of cholinergicinduced insulin secretion by the muscarinic type 3 receptor (M3R) antagonist 4-diphenylacetoxy-N-methylpiperidine methobromide, as well as increased potentiation of glucose-stimulated insulin secretion by treatment with yohimbine. Increases in islets levels of M3R, phospholipase C-␤1, and protein kinase C␣ mRNAs, as well as decreased ␣ 2aAR mRNA, in 12-day-old HC rats provide a mechanistic connection to the changes in insulin secretion seen in HC rats. In conclusion, altered autonomic regulation of insulin secretion, due to the HC nutritional intervention, contributes to the development of hyperinsulinemia in 12-day-old HC rats.high-carbohydrate milk formula; parasympathetic nervous system; sympathetic nervous system RECENT EVIDENCE SUGGESTS that changes in the quality of nutrition during critical periods of early development (fetal and neonatal) may play a decisive role in the metabolic programming of early adaptive responses into adulthood which result in metabolic disease (6). Metabolic programming is the phenomenon in which a stimulus or insult that occurs during a critical period of organogenesis in early life results in permanent alterations in the structure and function of affected organs and increased susceptibility to adult onset of diseases (6). The late fetal and early postnatal periods of rat development constitute a period during which the ontogeny of the endocrine pancreas is vulnerable to nutritional perturbations that result in permanent structural and functional adaptations (9).Studies from our laboratory found that an early high-carbohydrate (HC) dietary intervention during the immediate postnatal period (days 4-24) in rats r...

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Effects of Vagal Stimulation on Glucagon and Insulin Secretion

Cited by 105 publications

References 0 publications

α- and β-Cell Responses to Small Changes in Plasma Glucose in the Conscious Dog

α- and β-Cell Responses to Small Changes in Plasma Glucose in the Conscious Dog

Selective stimulation of glucagon secretion by β₂‐adrenoceptors in isolated islets of Langerhans of the rat

Role of the autonomic nervous system in the development of hyperinsulinemia by high-carbohydrate formula feeding to neonatal rats

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Effects of Vagal Stimulation on Glucagon and Insulin Secretion

Cited by 105 publications

References 0 publications

α- and β-Cell Responses to Small Changes in Plasma Glucose in the Conscious Dog

α- and β-Cell Responses to Small Changes in Plasma Glucose in the Conscious Dog

Selective stimulation of glucagon secretion by β2‐adrenoceptors in isolated islets of Langerhans of the rat

Role of the autonomic nervous system in the development of hyperinsulinemia by high-carbohydrate formula feeding to neonatal rats

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Selective stimulation of glucagon secretion by β₂‐adrenoceptors in isolated islets of Langerhans of the rat