Disease relevance of Glucagon-Secreting Cells

• Although pancreatic alpha-cells were functional in Kir6.2-/-, the mice exhibited a severe defect in glucagon secretion in response to systemic hypoglycemia [1].
• In an attempt to study pancreatic A cell function at an early stage of pancreatic diabetes secondary to chronic pancreatitis, both intravenous glucose (0.5 g/kg) and insulin (0.5 U/kg) tolerance tests were performed on seven dogs with pancreatolithiasis and seven normal control dogs [2].
• Our results also suggest that the pancreatic A-cell response to blood glucose decrement is totally suppressed in patients with pheochromocytoma by the chronically high levels of circulating catecholamines [3].
• To further assess pancreatic alpha-cell function in hyperthyroidism, plasma glucose, glucagon, and insulin resonses to a protein meal were determined in normal subjects and hyperthyroid patients [4].
• Surprisingly, available data in the literature appear to document a frequent breakdown of this well-established interdependence between plasma glucose and pancreatic alpha cells, as reflected by a sustained elevation of plasma glucagon levels in several physiologic and pathologic states with concurrent euglycemia or hyperglycemia [5].

High impact information on Glucagon-Secreting Cells

• To determine the character of the glucagon secretion and its modification by streptozotocin, were studied the plasma of a patient with recurrent pancreatic alpha-cell carcinoma [6].
• Glicentin-like material has been demonstrated in the pancreatic A cell, wherein it is located in the periphery of the secretory granules, whereas glucagon is located in the centre of the granules [7].
• Intra-islet insulin permits glucose to directly suppress pancreatic A cell function [8].
• These data indicate that glucokinase may serve as a metabolic glucose sensor in pancreatic alpha-cells and, hence, mediate a mechanism for direct regulation of glucagon release by extracellular glucose [9].
• Essential interaction of Egr-1 at an islet-specific response element for basal and gastrin-dependent glucagon gene transactivation in pancreatic alpha-cells [10].

Chemical compound and disease context of Glucagon-Secreting Cells

• In contrast, pancreatic alpha-cell functioning (glucagon response to arginine) was preserved in both pancreatitis groups [11].

Biological context of Glucagon-Secreting Cells

• Glucagon gene regulatory region directs oncoprotein expression to neurons and pancreatic alpha cells [12].
• In the present study, we investigated whether L-glutamate is secreted through exocytosis by alphaTC6 cells (clonal mouse pancreatic alpha-cells) [13].
• Dysregulation of Bridge-1 signaling increases pancreatic apoptosis with a reduction in the number of insulin-expressing pancreatic beta-cells and an expansion of the complement of glucagon-expressing pancreatic alpha-cells in pancreatic islets [14].
• Proglucagon was processed as in the fetal islet to products representative of both pancreatic alpha-cell and intestinal L-cell phenotypes, with glucagon and Glp-1 (7-36)amide as the major extractable products [15].
• Because individual amino acids (AA) stimulate glucagon release from pancreatic alpha-cells, the purpose of this study was to determine if individual AA could influence glucagon gene expression [16].

Anatomical context of Glucagon-Secreting Cells

• Proglucagon is processed differentially in the pancreatic alpha cells and the intestinal L cells to yield either glucagon or glucagon-like peptide 1, respectively, structurally related hormones with opposing metabolic actions [17].
• Two high affinity sulfonylurea receptors were identified in clonal pancreatic alpha cells (alpha TC-6): a 140-kDa species observed previously in clonal pancreatic beta cells (HIT) and a second 150-kDa protein [18].
• This poor nutrient-induced insulin release from purified B cells is attributed to their low cAMP levels and is markedly increased after addition of (Bu)2cAMP, of glucagon, or of pancreatic A cells [19].
• Gt2 alpha mRNA was also shown to be present in a clonal mouse pancreatic alpha-cell line (alpha TC1-6) as well as in adrenal gland, pituitary, and a clonal mouse anterior pituitary cell line (AtT20) [20].
• The GLP-1 receptor is expressed in a variety of other tissues important for carbohydrate metabolism, including pancreatic alpha-cells, hypothalamus and brainstem, and proximal intestinal tract [21].

Associations of Glucagon-Secreting Cells with chemical compounds

• These results indicate that the pancreatic alpha cell of the diabetic Chinese hamster responds excessively to arginine, as is seen in the human diabetic [22].
• We tested for the presence of sulfonylurea receptors in pancreatic alpha cells [18].
• We have investigated the short-term effects of the saturated free fatty acid (FFA) palmitate on pancreatic alpha-cells [23].
• Currents mediated by functional kainate receptors were also observed in a line of transformed pancreatic alpha cells [24].
• We therefore concluded that gliclazide inhibits glucagon release by a direct action on the pancreatic A cell [25].

Gene context of Glucagon-Secreting Cells

• Glucagon, the counter-regulatory hormone to insulin, is secreted from pancreatic alpha cells in response to low blood glucose [26].
• When expressed in alphaTC1-6 (transformed pancreatic alpha-cells) or in rat primary pancreatic alpha-cells in culture, PC3 converted MPGF to tGLP-1 [27].
• Foxa2 is required for the differentiation of pancreatic alpha-cells [28].
• sox4b is a key player of pancreatic alpha cell differentiation in zebrafish [29].
• Stanniocalcin 2: characterization of the protein and its localization to human pancreatic alpha cells [30].

Analytical, diagnostic and therapeutic context of Glucagon-Secreting Cells

• A pancreatic alpha-cell tumor can be identified and stained by immunocytochemistry with glucagon antibodies [31].
• The effects of the two prandial glucose regulators, repaglinide and nateglinide, on ATP-sensitive K(+) (K(ATP)) channel activity, membrane potential and exocytosis in single rat pancreatic A-cells were investigated using the patch-clamp technique [32].
• Using immunoelectron microscopy, clusterin-positive cells showed the typical ultrastructural features of pancreatic alpha cells [33].

References