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Göteborgs universitets publikationer

Glucagon secretion from pancreatic alpha-cells

Författare och institution:
L. Briant (-); Albert Salehi (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi); E. Vergari (-); Q. Zhang (-); Patrik Rorsman (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi)
Publicerad i:
Upsala Journal of Medical Sciences, 121 ( 2 ) s. 113-119
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Type 2 diabetes involves a menage a trois of impaired glucose regulation of pancreatic hormone release: in addition to impaired glucose-induced insulin secretion, the release of the hyperglycaemic hormone glucagon becomes dysregulated; these last-mentioned defects exacerbate the metabolic consequences of hypoinsulinaemia and are compounded further by hypersecretion of somatostatin (which inhibits both insulin and glucagon secretion). Glucagon secretion has been proposed to be regulated by either intrinsic or paracrine mechanisms, but their relative significance and the conditions under which they operate are debated. Importantly, the paracrine and intrinsic modes of regulation are not mutually exclusive; they could operate in parallel to control glucagon secretion. Here we have applied mathematical modelling of alpha-cell electrical activity as a novel means of dissecting the processes that underlie metabolic regulation of glucagon secretion. Our analyses indicate that basal hypersecretion of somatostatin and/or increased activity of somatostatin receptors may explain the loss of adequate counter regulation under hypoglycaemic conditions, as well as the physiologically inappropriate stimulation of glucagon secretion during hyperglycaemia seen in diabetic patients. We therefore advocate studying the interaction of the paracrine and intrinsic mechanisms; unifying these processes may give a more complete picture of the regulation of glucagon secretion from alpha-cells than studying the individual parts.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Klinisk medicin
diabetes, electrophysiology, experimental diabetes, glucagon, intrinsic mechanisms, pancreatic alpha-, antagonism improves glucagon, k-atp channels, beta-cell, somatostatin, receptor, dependent exocytosis, glucose suppression, electrical-activity, potassium channels, diabetic-rats, release, General & Internal Medicine
Postens nummer:
Posten skapad:
2016-06-28 11:15

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