0.81 lzTXXXG DI?TEmIN INGcZBXESTASIS~~SE INFUSION. E.Cmlandand0. Mathisen, Wpaxtmnt of Surgery B, The Natior!al Ikxapital, university of Oslo, Norway.

Intiavemus infusion of hypertonic glucose elevates plasma mlality, plasma glucose ~nser&ation and plasma insulin level, tile hepatic bile formation is reduced (&o&stasis) (ESPEI'? 1981, 1982 and 1983). fnsulin ina~ses bile formation, *ream hypezosrmlalitycauses cM.estasis. Theaimof this studywas todetemine the role of plasm glucose wncentration and insulin in cholestasis pmvoked lq' glucose during constant plasma osnolality. acute experiments were perform& on 5 anaesthetized pigs (20-25 kg b.w.). Bile was smpled fran the camon bile duct. Bile mt used for investigation was reinfused into the distal ileum to ensure a patent enterohe~tic circulation. Lu.&ng control (100 %) bile flow averaged 0.420.05 ml/mi.n, secretion of bile acids, bicarbonate amI chloride was 16.1h2.7 ml/min, 18.1k4.0 ml/tin and 36.2f3.7 ml/min, r&qxxM.vely (=bile formation). 1sot0ni.c glucose infusion raised plasm glucose concentration fm 6.3*0.6 WI to 17.820.4 nM. Bile formation fell to 66f3 % of wntrol. ZxIministration of insulin (10 I.E./kg b.w.) reduced plasma gluwse wncentratior~ to 6.tiO.7 zM. Bile formation was thereby increased to 9of3 % of control. Bile acid secretionwasunaltered, IXrirqinSulin ~~ioni~~~cgluw~ra~ UL3*1.4 r&l.

lasmagluwse concentration to Bile formation was depressed to 7 3f 2

secretion increased by lo*2 % of wntrol. % of wntrol, but bicarbonate

Hcmver, duringhyperglucemia the increase in insulin administration to 60 I.E./kg b.w. raised overall bile formation to 9ti3 % of wntml. Plasnaosmlality rmainedunalteredduring the different experimental pxicds and averaged 289*3 mm/kg H20. Cmclusion: Hyperglucmia causes oholestasis despite no changes in plasm osmlality. Insulin increases bile formation by stimulating biliary bicarkmnate secretion both during no~lucmia and hyperglucxmia. Cholestasis associated with glucose infusion my therefore be curtailed by insulin administration.

0.82 OSCILLATIONS IN PLASMA GLUCOSE, INSULIN AND C-PEPTIDE IN MAN AFTER MEALS OR DURING CONTINUOUS ENTERAL NUTRITION. G. Brandenberger, C. Simon, M. Follenius. Laboratoire de Physiologie et de Psychologie Environnementales, CNRS-INRS, Strasbourg, France.

Rapid oscillations in plasma levels of glucose and insulin with a periodicity of Q-14 min have been identified in animals and in humans. The present experiments were designed to document the existence in man of additional rhythmic components of longer periodicity, which have been suggested by some recent experiments.

The profiles of plasma glucose (G), insulin (I) and C-Peptide (CP) were studied in 12 normal men either on continuous enteral nutrition or receiving a standard meal in the afternoon or in the evening.

During continuous enteral nutrition, blood was collected every 10 min over 24 h. Large oscillations occurred in plasma G, I &nd CP with a period of 53-113 min. Their mean amplitudes, expressed as percent of the 24-h mean were as high as 20% for G, 54% for I and 56% for CP. Postprandial profiles were studied from 1200 to 2000 h and from 1900 to 0800 h. Blood was collected every 4 min. Two to five synchronous oscillations, with a period of 51-112 min were detected. The oscillations in amplitude were highest after meals and were then damped, reverting to fasting levels after up to 340 min. Plasma GIP concen- trations increased concomitantly with the G, I and CP first peaks and remained high with no further low-frequency fluctuations.

These results indicate that in addition to the previously described 8-14 mirr oscillations, plasma G, I and CP oscillate after meals or during continuous enteral nutrition at a mean SO-min periodicity. These oscillations are not explained by GIP variations. They may reflect a pancreatic oscillatory mechanism or may be linked to cyclic variations in gastrointestinal motility.

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