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Extrapancreatic Glucagon and Its Regulation

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Glucagon II

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 66 / 2))

Abstract

The A-cell of the islets of Langerhans of the pancreas has long been considered to be the only site of origin of glucagon. This dogma was challenged, in the mid-1970s, when three groups, working independently, almost simultaneously reported that the plasma of totally depancreatized dogs contained normal, or even increased, quantities of a material immunometrically indistinguishable from pancreatic glucagon by radioimmunoassays regarded as highly specific for this hormone (Vranic et al. 1974; Matsuyama and Foà 1974; Mashiter et al. 1975). These observations prompted a series of experiments which soon firmly established that the fundus of the dog stomach possesses A-cells identical to the pancreatic A-cells and that it contains and releases a material identical, by all criteria, to pancreatic glucagon. In fact, the presence of glucagon (then called the “hyperglycemic glycogenolytic factor”) in the canine stomach had been mentionned 35 years ago by Sutherland and Deduve (1948) who had written:

One might therefore conclude that the α-cells [of the islets of Langerhans] are the site of formation of the glycogenolytic factor. However, the presence of an apparently identical factor in the upper two-thirds of the gastric mucosa of the dog raises the question of specificity, unless it were shown that the stomach mucosa contains cell types related to the α-cells of the pancreas.

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Lefebvre, P.J., Luyckx, A.S. (1983). Extrapancreatic Glucagon and Its Regulation. In: Lefebvre, P.J. (eds) Glucagon II. Handbook of Experimental Pharmacology, vol 66 / 2. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69019-8_11

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  • DOI: https://doi.org/10.1007/978-3-642-69019-8_11

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