Effect of intact parathyroid hormone on hepatic glucose release in the dog

K. A. Hruska, J. Blondin, R. Bass, J. Santiago, L. Thomas, P. Altsheler, K. Martin, S. Klahr

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Abstract

The liver has been shown to remove parathyroid hormone (PTH) from its arterial circulation by a mechanism that is selective for the intact form of the peptide (PTH 1-84). The present studies demonstrate that PTH has biologic effects on the liver in vivo. Bovine PTH 1-84 stimulated hepatic glucose release in dogs with indwelling hepatic vein catheters from basal values of 31 ± 8 to 68 ± 9 mg/min per kg after bolus injections of PTH. The effect on hepatic glucose release was apparent by 5 min and persisted for the 80 min of observation. The NH2-terminal PTH fragment (syn b-PTH 1-34) had no effect. Bovine PTH 1-84 administered in doses designed to produce circulating levels of immunoreactive PTH similar to the endogenous levels observed in uremic dogs also increased the incorporation of 14C from infused [14C]alanine into glucose, and increased estimated hepatic uptake of both chemical and [14C]alanine, while increasing hepatic glucose release. Thus, administration of 'physiologic levels' of b-PTH 1-84 stimulated hepatic glucose release in part through increased gluconeogenesis in vivo, whereas syn b-PTH 1-34 had no demonstrable effect. Circulating levels of insulin rose after PTH administration, an increase which presumably represents a secondary response to the rise in glucose release. These results suggest that the liver is a target organ of PTH, and that PTH might potentially after carbohydrate metabolism during hypersecretion. They also suggest that hepatic uptake of PTH may be related in part to production of a specific biologic effect rather than just simple peptide degradation.

Original languageEnglish
Pages (from-to)1016-1023
Number of pages8
JournalJournal of Clinical Investigation
Volume64
Issue number4
DOIs
StatePublished - 1979

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