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Renal Metabolism of Gut Glucagon-Like Immunoreactivity^*

A. ROVIRA, J. M. LÓPEZ-NOVOA, M. ZUBIAUR, R. MATESANZ, M. GHIGLIONE, J. M. PASCUAL and I. VALVERDE

Fundacion Jimenez Diaz, Universidad Autoonoma de Madrid, Madrid, Spain

Address correspondence and request for reprints to: Isabel Valverde, M.D., Fundacion Jimenez Diaz, Avenida Reyes Catolicos, 2, Madrid 3, Spain.

Abstract

To examine the role of the kidney in the catabolism of gut glucagon-like immunoreactivity (GLI), we compared the plasma GLI responses of normal and nephrectomized dogs given intraduodenal glucose loads and studied the clearance of gut GLI by the isolated perfused rat kidney. Both basal and postload plasma samples were analyzed with a glucagon C-terminal specific antibody and a GLI-reacting N-terminal antibody. The GLI response was taken to be the difference between the increments seen with these two antibodies after glucose loading. Although glucose-induced GLI increments could not be detected in untreated plasma from nephrectomized dogs, chromatographed plasma revealed a significant rise in GLI-fraction II (7000–12000 daltons) in both nephrectomized and normal dogs (732 ± 200 and 586 ± 111 pg/ml, respectively). We also found that crystalline glucagon was cleared by the isolated closedcircuit perfused rat kidney, but gut-GLI either as crude extract or as peak I (7000–12000 dalt ns) was not. Our data suggest that the kidney may not play an important role in gut-GLI catabolism.

Footnotes

^* Part of these results were presented at the 16th Annual Meeting of the European Association for the Study of Diabetes, Athens, September 24-27, 1980.

Research Fellow of the Fundacion Conchita Rabago de Jimenez Diaz.

Research Fellow of the Caja de Ahorros y Monte de Piedad de Madrid.

Received August 4, 1981.