Modulation of insulin and glucagon secretion from the perfused rat pancreas by the neurohypophysial hormones and by desamino-D-arginine vasopressin (DDAVP)

Dunning, Beth E.; Moltz, J. H.; Fawcett, C. P.

doi:10.1016/0196-9781(84)90109-8

Cited by 89 publications

(69 citation statements)

References 10 publications

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“…The V1 A vasopressin receptor has been studied in most detail and found to couple to G q and to activate PLC. Vasopressin is known to stimulate the secretion of both insulin and glucagon (Dunning et al 1984). Recent studies have ex-plored the receptor subtype responsible for these islet actions.…”

Section: Vasopressin Receptorsmentioning

confidence: 99%

G-protein-coupled receptors and islet function—Implications for treatment of type 2 diabetes

Winzell

Åhrén

2007

Pharmacology & Therapeutics

161

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Islet function is regulated by a number of different signals. A main signal is generated by glucose, which stimulates insulin secretion and inhibits glucagon secretion. The glucose effects are modulated by many factors, including hormones, neurotransmitters and nutrients. Several of these factors signal through guanine nucleotide-binding protein (G-protein) coupled receptors (GPCRs). Examples of islet GPCRs are GPR40 and GPR119, which are GPCRs with fatty acids as ligands, the receptors for the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), the receptors for the islet hormones glucagon and somatostatin, the receptors for the classical neurotransmittors

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Section: Vasopressin Receptorsmentioning

confidence: 99%

G-protein-coupled receptors and islet function—Implications for treatment of type 2 diabetes

Winzell

Åhrén

2007

Pharmacology & Therapeutics

161

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“…These findings suggested that a-cells are more sensitive to AVP than p-cells in hormone release. Our findings are consistent with those obtained from the perfused rat pancreas 10 and isolated rat islets 18 and different from those obtained from the mouse islets. 20 In addition, these findings indicated that AVP may physiologically increase glucagon release, since AVP increased glucagon release at physiological concentrations of AVP plasma level (<30 pmol/L) 39 , while it failed to increase insulin release at these concentrations.…”

Section: Effects Of a Vp On Somatostatin Releasesupporting

confidence: 82%

“…These findings suggest that a-cells are more sensitive to AVP than p-cells in hormone release. These findings are consistent with those obtained from the perfused rat pancreas (Dunning et al, 1984a) and isolated rat islets (Dunning et al, 1984b) and are different from those obtained 125 from the mouse islets . In addition, our findings support the notion that AVP has a direct stimulatory effect on glucagon release in a-cells.…”

Section: Glucose-dependency Of Avpsupporting

confidence: 81%

“…This implies that AVP is not a primary insulin secretagogue, but is an enhancer of glucose-induced insulin secretion. In the perfused rat pancreas, AVP (185 pmol/L) in 5.5 mmol/L glucose caused a small insulin release (Dunning et al, 1984b). In contrary, AVP inhibited glucose-induced insulin release in rat islets (Khalaf and Taylor, 1988) and in hamster beta cell line (HIT) .…”

Section: Effect Of Glucose On a Vp-induced Insulin And Glucagon Releasementioning

confidence: 99%

“…In the perfused rat pancreas, AVP in 5.5 mmol/L glucose caused a small insulin release. 10 In contrast, AVP inhibited glucose-induced insulin release in rat islets 21 and in clonal /3-cells HIT-T15. 22 AVP (1-100 nmol/1) failed to stimulate somatostatin release in the absence of extracellular glucose, however, AVP increased somatostatin release in the presence of glucose mmol/L).…”

mentioning

confidence: 99%

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Arginine vasopressin-induced glucagon release: interaction with glucose and cyclic AMP-dependent protein kinase

Abu-Basha

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This manuscript has been reproduced from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be from any type of computer printer.The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction.In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion.Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand comer and continuing from left to right in equal sections with small overlaps.

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Autonomic Regulation of Hepatic Glucose Production

Bisschop

Fliers

Kalsbeek

2014

Comprehensive Physiology

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Glucose produced by the liver is a major energy source for the brain. Considering its critical dependence on glucose, it seems only natural that the brain is capable of monitoring and controlling glucose homeostasis. In addition to neuroendocrine pathways, the brain uses the autonomic nervous system to communicate with peripheral organs. Within the brain, the hypothalamus is the key region to integrate signals on energy status, including signals from lipid, glucose, and hormone sensing cells, with afferent neural signals from the internal and external milieu. In turn, the hypothalamus regulates metabolism in peripheral organs, including the liver, not only via the anterior pituitary gland but also via multiple neuropeptidergic pathways in the hypothalamus that have been identified as regulators of hepatic glucose metabolism. These pathways comprise preautonomic neurons projecting to nuclei in the brain stem and spinal cord, which relay signals from the hypothalamus to the liver via the autonomic nervous system. The neuroendocrine and neuronal outputs of the hypothalamus are not separate entities. They appear to act as a single integrated regulatory system, far more subtle, and complex than when each is viewed in isolation. Consequently, hypothalamic regulation should be viewed as a summation of both neuroendocrine and neural influences. As a result, our endocrine-based understanding of diseases such as diabetes and obesity should be expanded by integration of neural inputs into our concept of the pathophysiological process.

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Modulation of insulin and glucagon secretion from the perfused rat pancreas by the neurohypophysial hormones and by desamino-D-arginine vasopressin (DDAVP)

Cited by 89 publications

References 10 publications

G-protein-coupled receptors and islet function—Implications for treatment of type 2 diabetes

G-protein-coupled receptors and islet function—Implications for treatment of type 2 diabetes

Arginine vasopressin-induced glucagon release: interaction with glucose and cyclic AMP-dependent protein kinase

Autonomic Regulation of Hepatic Glucose Production

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