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Glycerol Clearance in Alcoholic Liver Disease

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Glycerol Clearance in Alcoholic Liver Disease Gut: first published as 10.1136/gut.23.4.257 on 1 April 1982. Downloaded from Gut, 1982, 23, 257-264 Glycerol clearance in alcoholic liver disease D G JOHNSTON,* K G M M ALBERTI, R WRIGHT, AND P G BLAIN From the Departments ofMedicine, Clinical Biochemistry and Metabolic Medicine and Clinical Pharmacology, Royal Victoria Infirmary, Newcastle upon Tyne, and the Department ofMedicine, Southampton General Hospital, Southampton, SUMMARY Glycerol clearance was studied by a primed dose-constant infusion technique in 14 patients with alcoholic liver disease and six normal control subjects. Fasting blood glycerol concentrations were raised in the alcoholic subjects (0.09±0.01 vs 0.06±0-01 ,umol/l, P<0.05) and glycerol clearance was impaired (24.5 ± 1.9 vs 37.5 ± 3.2 ml/kg/min, P<0.005). Endogenous produc- tion rate of glycerol and distribution space at steady state were similar in alcoholic and control subjects. The metabolic clearance rate of glycerol correlated negatively with basal glycerol concen- trations. Thus tissue uptake of glycerol is impaired in liver disease. As glycerol is metabolised primarily in the liver by conversion to glucose, these data suggest a defect of gluconeogenesis in alcoholic liver disease. The liver is the principal organ of glucose production Clearance of an intravenous glycerol load may thus in the fasting statel 2 with small contributions from provide an index of liver dysfunction and an estimate the kidney and small intestine. Hypoglycaemia may of gluconeogenic capacity in cirrhotic man. We have complicate acute severe liver disease or end-stage investigated glycerol clearance in patients with alco- chronic liver damage,3 but in most patients with chro- holic liver disease by a primed dose-constant infusion http://gut.bmj.com/ nic liver disease fasting blood glucose concentrations technique to steady state, with analysis of decay of are either normal or mildly raised.4 5 Nonetheless, blood glycerol levels on cessation of the infusion. defects in glycogen storage and glycogen degradation are apparent from catheterisation experiments6 or Methods analysis of the glycaemic response to glucagon in some7 8-although not all9 '0-studies. Little is PATIENTS known about gluconeogenesis in chronic liver disease Fourteen patients with alcoholic liver disease (11 on September 25, 2021 by guest. Protected copyright. but catheterisation studies suggest a compensatory male, three female, age 36-70 years) were compared increase in cirrhotics." This may also be inferred with six normal controls (five males, one female, age from radioactive tracer experiments showing normal 22-64 years). Eight patients had hepatic cirrhosis rates of total glucose production after an overnight and six alcoholic hepatitis or fatty liver on biopsy fast,'2 although other investigators have shown a (Table 1). The duration of heavy intake of alcohol small decrease in glucose production.13 admitted by the patients ranged from five to 30 years. Glycerol is highly gluconeogenic in man and ani- Patient number 2 had mild chronic hepatic encepha- mals and is preferentially metabolised to glucose in lopathy but no other patient was clinically in liver favour of other gluconeogenic precursors.'1'6 In failure at the time of study. Patients were on a variety fasting, 40-100% of circulating glycerol is converted of medications (Table 1) but no drugs were taken on to glucose,'5 17 conversion increasing as blood con- the day of study. Four patients had spontaneous centrations rise.18 The liver is responsible for 70- portal-systemic shunting as shown by oesophageal 90% of glycerol uptake'9 20 with the remainder meta- varices on barium swallow or endoscopy, and four bolised by the kidneys,2' 22 small intestine, and other patients had clinically evident ascites. No patient had tissues.23 Renal uptake of glycerol is not increased in evidence of renal impairment. Control subjects were cirrhotic man.6 normal laboratory personnel or their acquaintances and none was on any drug therapy, or suffering from Address for correspondence: Dr D G Johnston, Department of Medicine, Royal Victoria Infirmary, Newcastle upon Tyne, NEI any known disorder. Informed consent was obtained 4LP. from all subjects for the study, which was approved Received for publication 30 July 1981 by the Southampton Hospitals Ethical Committee. 257 Gut: first published as 10.1136/gut.23.4.257 on 1 April 1982. Downloaded from 258 Johnston, Alberti, Wright, and Blain E E E Z QmSo oo Co _-~~~~o~~ o O O 0. g W I Z I ' r: XI I II 0 N - 00ClUm q0 0000t tO0 0 0 Om 00 0% D CIA ( t)%* ._ t-O>qt-*(1 C- V, C ,, 0oN- b m'I 00 http://gut.bmj.com/ 1 + 111 + 1 +1 I cn on September 25, 2021 by guest. Protected copyright. I 1+ + + *3 c0 0 C) 0Cu 0% r 0% ) Cm V) - 0% N Ia 0c ra0Cl - 00Cl0 0 - Cx Cl '0 C) .Cu C) '0 Su > > P.vC P.C Z DCu a) oo0 C) C0U . C a) Cu Cu O .0 > )0 J. O C0 > H"I 0 0 0 0 a)0 z Gut: first published as 10.1136/gut.23.4.257 on 1 April 1982. Downloaded from Glycerol and liver disease 259 Studies were performed on recumbent subjects ponential function of the form, Ae-klt+Be-k2t after an overnight (10-12 hours) fast. Subjects had where A, B, kl, k2 are constants. Curve fitting was abstained from alcohol for at least 48 hours and had a performed by computer to the points of the blood daily carbohydrate intake in excess of 250 g for this glycerol decay curve, after the basal glycerol concen- period. Teflon intravenous cannulae (Venflon, Vig- tration had been subtracted, by minimising the sum gio, Helsingborg) were sited in an antecubital vein on of squares of deviations. The area under the curve each side and patency was maintained by flushing (area, mmol/lxmin) was calculated using the polyex- with 0*154 mol/l saline after every sample. Thirty and ponential equation. The excess amount of glycerol 40 minutes after cannulation basal samples were (Qg, mmol/kg) in the body at steady state was calcu- taken. After an initial loading dose (100 ,umol/kg lated as the product of the metabolic clearance rate body weight diluted with water to isotonicity and and the area under the decay curve. administered over two minutes), a continuous in- Qg (mmol/kg)=MCR (1/kg/min)x travenous infusion of glycerol, 19 ,umol/kg/min area (mmol/l x min) (Boots, Nottingham, 1-1 molI1), was begun through the contralateral cannula and continued for 40 min- The apparent volume of distribution of glycerol at utes with a Harvard continuous infusion pump. steady state (V, 1/kg) was calculated as the amount of Blood samples were taken two minutes after the glycerol present divided by the increase in blood loading dose and at 10, 7.5, 5, and 2.5 minutes before glycerol above basal at steady state (modified from the continuous infusion ended. Additional blood Riegelman et al.26). samples were taken 0, 2.5, 5, 7.5, 10, 12.5, 15, 20, 30, V(/kg)=Qg (mmol/kg) 45, and 60 minutes after the infusion ended. All urine Gss (mmol/1)- produced over the experimental period was collected MCR (1/kg/min) x area (mmol/l x min) after the last blood sample, its volume measured and Gss a 20 ml aliquot taken for glycerol analysis. (mmol/l) Venous blood (1.5 ml) was mixed immediately The endogenous production rate of glycerol (PR, with 5 ml of 5% (V/V) ice-cold perchloric acid. Blood ,umol/kg/min) was calculated as the product of the glycerol, glucose, lactate, pyruvate, and alanine were basal glycerol concentration (Gb, mmol/l) and the measured by an automated fluorimetric enzymatic metabolic clearance rate. http://gut.bmj.com/ method (Lloyd et al., 1978 ?4)Urine glycerol was esti- PR (,umol/kg/min)=Gb (mmol/l)x mated by a spectrophotometric enzymatic method.25 MCR (1/kg/min)x 1000 Plasnia aspartate aminotransferase, lactate dehyd- rogenase, bilirubin, and albumin were measured by It is assumed in these calculations that the endogen- standard Autoanalyser techniques (Technicon). ous production rate of glycerol remains constant Results are expressed as mean±SEM. Statistical throughout the experimental period. analysis was performed using Student's paired and on September 25, 2021 by guest. Protected copyright. unpaired t tests where appropriate. Correlations Results were sought by Spearman's ranking method. The distribution of certain data was skewed (plasma Basal blood metabolite concentrations are shown in aspartate aminotransferase and bilirubin) and statis- Table 2. Fasting blood glucose concentrations were tical analysis was performed on log-transformed similar in patients and controls. Blood lactate con- data. centrations were increased by 27% (P<0.02) in the patient group, but the blood lactate:pyruvate ratio MATHEMATICAL ANALYSIS was similar in patients and controls. Blood alanine A steady state for blood glycerol was accepted if a levels did not differ in the two groups. Fasting blood change of <5% in blood glycerol concentrations glycerol concentration was raised in the alcoholic occurred over the last 10 minutes of the intravenous patients (0.09±0.01 vs 0.06±0 01 mmol/l, P<0.05). infusion. The metabolic clearance rate (MCR, I/kg/ Data obtained during glycerol infusion are shown min) was calculated as the infusion rate (mmol/kg/ in Table 3. At 2.5 minutes after administration of the min) divided by the increase in blood glycerol at loading dose, blood glycerol concentrations ranged steady state above the basal glycerol concentration from 0-35 to 1.22 mmolIl. In the patient group, (Gss, mmol/l).
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