Epidermal growth factor induces glucose transport in primary cell cultures derived from human astrocytic glioma biopsies

Murphy, Seán; Welk, Greg; Kardos, S.

doi:10.1016/0304-3940(92)90932-w

Cited by 3 publications

(1 citation statement)

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“…EGF and insulin share many biological proper- ties. EGF has been shown to increase luminal glucose uptake in enterocytes both in vivo and in vitro [3,27] , as well as in cell cultures derived from human astrocytic glioma biopsies [28] . Furthermore, EGF stimulates glycogen synthesis [6,7] and inhibits gluconeogenesis in the proximal tubules in the rat [29] .…”

Section: Discussionmentioning

confidence: 99%

Does Epidermal Growth Factor Participate in the Regulation of Glucose, Insulin and Glucagon Levels?

Jansen

Lundquist²,

Salehi³

et al. 2006

Eur Surg Res

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Background/Aims: The presence of receptors for epidermal growth factor (EGF) on β cells in the rat pancreatic islets has been established, but the physiological role remains to be settled. The aim of the present study was to evaluate the effect of EGF on glucose homeostasis. Methods: Fasted rats were treated with intraperitoneal injections of 10, 40 or 80 µg/kg body weight, either with EGF or 1% bovine serum albumin (controls). In a second experiment, fasted rats received an intraperitoneal injection of 1 mg glucose/kg body weight, followed by an injection of EGF or bovine serum albumin. Blood was drawn before the injections and at different time points afterwards. The plasma concentrations of glucose, insulin and glucagon were measured. Results:A modest elevation of the concentrations of glucose and insulin in plasma during the study was found in fasted rats in experiment 1. The increase in insulin concentration was attenuated by EGF, but after glucose injection this effect was reversed. Plasma glucagon levels were dose-dependently elevated by EGF and increased instead of decreased after glucose injection. Conclusion: Our data suggest that EGF might play an important role in the regulation of glucagon secretion by preventing the lowering effect of glucose on plasma glucagon levels.

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