0.5 CORRELATION OF ALTERED AMINO ACID (AA) AND CATION TRANSPORT IN CHRONIC RENAL FAILURE (cRF) W.Druml,R.A.Kelly,R.C.May and W.E.Mitch. 1st Medical University Clinic,Vienna Austria and Harvard Medical School,Boston,USA

Recently,we have shown that CRF is associated with profound alterations of cellular ion transport in adipose tissue and skeletal muscle (Kidney int.31:383,1987). To test the pathophysiologic importance of these findings for AA metabolism in u+$mia we investigated the activity of the sodium pump (ouabain-sensitive I&-uptake) and a sodium dependent AA transport system (system A) in isolated adipocytes from CRF (SUN 125 4 13 mg/dl) and pair fed,sham-operated control rats (SO).AA transport was evaluated by the uptake of a specific non-metabolizable probe methyl- y&no-isobutyric acid (MeAIB) .

Rb-uptake was decreased by 45% from 9.2 + 1.57 in SO to 4.6 + 1.2 ?06cells/min in CRF (pC.o.ool).MeAIB uptake,evaluated in parallel in-

nmol

cubatiogs was decreased by 43 % from 72.06 + 2.2 in SO to 6.84 f 0.69 nmol/lo cells/min in CRF (p<o.ool). There was a direct relationship between the decrease in cation transport and AA up&ke (r = o.91,pco.ool) Uremic serum failed to decrease ouabain sensitive Rb uptake in normal adipocytes (6.29 + 0.18 with uremic vs. 5.76 + 0.24 nmol/lo cells/min with control serum) and uremic serum did not xnhibit MeAIB transport into normal adipocytes (16.31 + 0.43 in uremic vs. 18.78 2 0.94 nmol/lo

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cells/min in control serum). - Thus,altered ion transport directly correlates with impaired AA uptake in uremia and participates in the altered protein metabolism of the uremic syndrome.

0.6 1~SULI~ RESISTANCE IN CIRR~OTXC PATIENTS: EFFECTS OR GLUCOSE ARD LIPID META3O~ISM. M,Merli, F.Leonetti*, S.Busco*, A.Giaccari*, O.Riggio§, G.Tamburrano*, and L.Capocaccia. 2"Dept. of Gastroenterology and * 1" Dept. of Endocrinology, University "La Sapienza", Rome. $ Dept. of Internal Medicine University of L'Aquila, Italy.

Insulin action on carbohydrate metabolism is known to be reduced in cirrhotic patients; however, little is known about the effect of insulin on lipid metabolism in these patients. To investigate this aspect we studied the decrease in plasma FFA and Glycerol (Gly) during insulin infusion using a sequential euglycemic glucose clamp technique. For this purpose, 11 cirrhotic patients and 5 controls were infused with insulin at two rates:0.25 mlJ/kg+min from 0 to 100 min and 1 mU/Kg*min from 100 to 200 min. Glucose was infused at a variable rate to maintain euglycemic levels. Samples for plasma FFA and Gly were taken at 10 min intervals during the first 100 min of the study. The glucose metabolizing capacity (Ml was evaluated during the second step. In the cirrhotic patients, the M value was lower than in controls (3.98ti.47 vs 7.Ortp.93 ~/Kg/min respectively), confirming the well known insulin resistance on carbohydrate metabolism in liver cirrhosis. Basal plasma FFA and Gly were elevated in cirrhotic patients (FFA: 744 t195 vs 427+84 fimolil and Gly: 161+20 vs 139t20 pmol/l in cirrhotics and in controls respectivela. During insulin infusTon the decrease in FFA and Gly concentrations was less pronounced in cirrhotics than in controls (-50% vs -80% and -30% vs -45% at 100 min respectively) indicating a reduction in the ability of insulin to lower plasma FFA concentrations. Moreover, in these patients the percentual decrease of FFA was correlated with the M value (r=0.70; ~(0.01). In conclusion, our data suggest that insulin resistance in cirrhotic patients affects both FFA and glucose ~tabolism~

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