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1 ppear to be a direct effect of leptin on the pancreatic alpha cell.
2 a-aminobutyric acid A receptor activation in pancreatic alpha cells.
3 B and in relation to glucose fluctuations in pancreatic alpha cells.
4  insulin and is specifically produced by the pancreatic alpha cells.
5  in certain areas of the brain as well as in pancreatic alpha cells.
6  were also observed in a line of transformed pancreatic alpha cells.
7 lucagon release via blockade of NaChs in the pancreatic alpha-cells.
8 hypoglycemia and dramatic hyperplasia of the pancreatic alpha-cells.
9  of proglucagon to mature active glucagon in pancreatic alpha-cells.
10                       Glucagon released from pancreatic alpha cells and glucagon-like peptide 1 (GLP-
11 in inhibition of glucagon release from mouse pancreatic alpha cells and the somatostatin subtype-5 re
12 onflicting views of the relationship between pancreatic alpha-cells and beta-cells and seek to unders
13 he differential processing of proglucagon in pancreatic alpha-cells and intestinal L cells leads to p
14             In mice, some glucagon-producing pancreatic alpha-cells and somatostatin-producing delta-
15 asis, there are additional links between the pancreatic alpha-cells and the hepatocytes, often collec
16 poglycaemia stimulates glucagon release from pancreatic alpha-cells, and are involved in glucose upta
17 n NOD mice, inhibits glucagon secretion from pancreatic alpha-cells, and mimics other actions of the
18                                              Pancreatic alpha-cells are important in maintaining meta
19 brane in several tissues including heart and pancreatic alpha cells, but not in beta cells.
20                The recent demonstration that pancreatic alpha cells can be continuously regenerated a
21 ies descendants of renin-expressing cells as pancreatic alpha cells despite a lack of active renin ex
22                           Glucagon-producing pancreatic alpha cells develop normally in HNF-3alpha-/-
23  concluded that postprandial lipemia induces pancreatic alpha cell dysfunction characteristic of type
24 type 2 diabetes and, therefore, propose that pancreatic alpha cell dysfunction could be viewed, at le
25           Type 2 diabetes is associated with pancreatic alpha cell dysfunction, characterized by elev
26 ceride-rich lipoproteins (TGRLs) might cause pancreatic alpha cell dysfunction.
27   We investigated whether TGR5 activation in pancreatic alpha cells enhances hyperglycemia-induced PC
28 le to cell type-specific features, revealing pancreatic alpha cell enrichment as the most statistical
29                                              Pancreatic alpha-cells express voltage-gated Na(+) chann
30 ch as endothelial cells (telangiectasia) and pancreatic alpha-cells (fatty liver and diabetes), with
31 o acids, which triggers the proliferation of pancreatic alpha-cells, forming a liver-alpha-cell loop.
32 GLP-1, dual, and triple receptor agonists on pancreatic alpha-cell functions.
33                                              Pancreatic alpha-cell gp130 knockout (alphagp130KO) mice
34                                          The pancreatic alpha cells have emerged as the primary amino
35 cagon and glucagon-like peptide-1 levels and pancreatic alpha cell hyperplasia, probably secondary to
36 eceptor (GCGR) causes hyperaminoacidemia and pancreatic alpha-cell hyperplasia, but the GCGR downstre
37 y hyperglucagonemia, hyperaminoacidemia, and pancreatic alpha-cell hyperplasia.
38  these data indicate that XBP1 deficiency in pancreatic alpha-cells induces altered insulin signaling
39 ow that ranolazine, via blockade of NaChs in pancreatic alpha-cells, inhibits their electrical activi
40                  Proglucagon is expressed in pancreatic alpha cells, intestinal L cells, and some hyp
41               Secretion of glucagon from the pancreatic alpha-cells is conventionally seen as the fir
42                        Glucagon, secreted by pancreatic alpha cells, is essential for maintaining nor
43            Glucagon, a hormone released from pancreatic alpha-cells, is critical for maintaining eugl
44                             Infection of the pancreatic alpha cell line alpha-TC6 with 7B2-encoding a
45  of NIPAL1 in alpha-TC6 glucagonoma cells (a pancreatic alpha-cell line) were similar to the observat
46 gon were co-expressed in either pituitary or pancreatic alpha cell lines, proglucagon processing was
47 mechanisms responsible for the regulation of pancreatic alpha cell mass and function are not complete
48 agon, resulting in a significant decrease in pancreatic alpha-cell mass.
49 ucagon hypersecretion involving expansion of pancreatic alpha-cell mass.
50              However, glucagon secreted from pancreatic alpha-cells may accumulate at high concentrat
51 lood glucose, however nutrient regulation of pancreatic alpha-cells remains poorly understood.
52  (SGLT2) inhibitors in glucagon secretion by pancreatic alpha-cells reported controversial results.
53 ctive of this study was to determine whether pancreatic alpha-cells respond to pregnancy and their co
54                                              Pancreatic alpha-cells secrete glucagon, an insulin coun
55 ntify major homeodomain proteins involved in pancreatic alpha-cell-specific proglucagon expression, w
56              Hypersecretion of glucagon from pancreatic alpha-cells strongly contributes to diabetic
57 ogical conditions, glucagon is released from pancreatic alpha cells to elevate circulating glucose le
58       We show that glucagon, secreted by the pancreatic alpha cell, up-regulates the expression of it
59                Incubation of mouse and human pancreatic alpha cells with GIP induced their production