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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 hypoglycemia and dramatic hyperplasia of the pancreatic alpha-cells.
8 of proglucagon to mature active glucagon in pancreatic alpha-cells.
9 lucagon release via blockade of NaChs in the pancreatic alpha-cells.
11 in inhibition of glucagon release from mouse pancreatic alpha cells and the somatostatin subtype-5 re
12 he differential processing of proglucagon in pancreatic alpha-cells and intestinal L cells leads to p
13 poglycaemia stimulates glucagon release from pancreatic alpha-cells, and are involved in glucose upta
16 ies descendants of renin-expressing cells as pancreatic alpha cells despite a lack of active renin ex
18 concluded that postprandial lipemia induces pancreatic alpha cell dysfunction characteristic of type
19 type 2 diabetes and, therefore, propose that pancreatic alpha cell dysfunction could be viewed, at le
22 We investigated whether TGR5 activation in pancreatic alpha cells enhances hyperglycemia-induced PC
25 cagon and glucagon-like peptide-1 levels and pancreatic alpha cell hyperplasia, probably secondary to
26 these data indicate that XBP1 deficiency in pancreatic alpha-cells induces altered insulin signaling
27 ow that ranolazine, via blockade of NaChs in pancreatic alpha-cells, inhibits their electrical activi
30 gon were co-expressed in either pituitary or pancreatic alpha cell lines, proglucagon processing was
31 mechanisms responsible for the regulation of pancreatic alpha cell mass and function are not complete
34 ntify major homeodomain proteins involved in pancreatic alpha-cell-specific proglucagon expression, w
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