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Protein requirement and retention in malnourished patients with liver cirrhosis
days. Food was prepared in the metabolic ward and the nitrogen balance was calculated from (intake (I) - measured urinary nitrogen excretion (E) - 2.5 g N/d for faecal and skin losses). Protein turnover (15N-glycine), IGF-1, BP-3 (IGF-1 binding protein 3), insulin, glucagon, TQ, cortisol, a-aminonitrogen, branched chain amino acids, glutamine, arginine and ornithine were measured before and after hyperalimentation in the fed state. Results: Nitrogen balance increased 4-fold (p < 0.002). The protein synthesis (S) increased 1.27 + 0.07 fold (p < 0.05) while the degradation (D) was unchanged. The IGFl/BP-3 ratio increased 1.25 f 0.10 fold (p = 0.06) and insulin increased 1.31 + 0.08 fold (p = 0.07). The other effecters showed no change. ,+o=r!+s
P.121 Peripheral insulin resistance as main cause of impaired glucose tolerance in patients with liver cirrhosis E. Radoch. 0. Selberg, M. Schwarze, M. Manns and M.J. Miiller Medizinische Hochschule Hannover, Zentrum lnnere Medizin Abt. Gastroenterologie und Hepatologie, DD-3000 Hannover 67, Germany Purpose: Glucose intolerance is a characteristic feature of many patients with liver cirrhosis. About 40% of these patients are considered diabetic. Hepatic shunting of glucose and insulin have been proposed as the main causative factors. However, peripheral insulin resistance as measured by the glucose clamp technique is found regularly in liver cirrhosis. Methods: To investigate the significance of insulin resistance we performed a standard oral glucose tolerance test (OGTT; 1 g/kg body weight {bw}) and a euglycemic hyperinsulinemic (insulin infusion rate 1 .O mu/kg bw/min) clamp protocol with indirect calorimetry (Deltatrac Metabolic Monitor). Fat-free mass (FFM) and body cell mass (BCM) was determined by bioelectrical impedance analysis. A total of 13 patients with histologically proven liver cirrhosis (ci; age: 38.6 + 8.6 years {mean f SD}, sex: 8m/5f, aetiology: 4 ethanol induced, 2 posthepatitis, 2 obliterative cholangitis, 1 a,-antitrypsin deficiency, 4 cryptogenic; Child-Pugh classification: 5A/5B/3C, height: 172 + 14 cm, weight: 69 k 24 kg, FFM: 52.4 + 21 .O kg, BCM: 25.6 & 10.7 kg) were included in the study and compared with 10 healthy controls (co; age: 33.2 + 10.1 years, sex: 8m/2f, height 177 + 10 cm, weight: 73 + 14 kg, FFM: 52.6 & 12.0 kg, BCM: 20.9 + 4.8 kg). Results: 46% of patients had impaired glucose tolerance as indicated by plasma glucose concentrations > 180 mg/dl at 120 min of OGTT (263 f 90 mg/dl); the other 54% were considered normal (119 + 35 mg/dl). Clamp data were as follows: glucose disposal: ci 4.2 + 2.0 vs co 8.6 + 2.2 mg/kg bw/min, p < 0.05; glucose oxidation rate: ci 2.4 f 1.4 vs co 3.2 + 1.1 mg/kg bw/min, not significant; nonoxidative glucose metabolism: ci 1.8 & 1.6 vs co 5.6 + 2.5 mg/kg bw/min, p i 0.05. Whole body glucose disposal was different between patients with normal and impaired glucose tolerance (5.2 1 1.7 vs 2.4 + 0.7 mg/kg bw/min, p < 0.05). Moreover, whole body glucose disposal correlated with plasma insulin at 120 min of OGTT (r = 0.66, p c: 0.05). Conclusion: The degree of peripheral insulin resistance is a main determinant of glucose tolerance in patients with liver cirrhosis. However, insulin shunting and hyperinsulinemia may be an important cause of insulin resistance in liver cirrhosis.
El A mean f
0.95kO.07 1.76*016
g pr&in/(kg 1.90+0.29 1.92+0.37
d) 0.71+0.16 1.03+0.20
SEM. E = before hypedimentation,
2.12f0.26 2.67+0.34
A = after hyperalimentation
Conclusion: The increase in nitrogen balance was achieved exclusively by an increase in protein synthesis. We speculate that this increase in protein synthesis was due to the changes in insulin and the IGF-1 /BP-3 ratio rather than to changes in other regulators of protein synthesis.
P.123 Protein requirement malnourished patients with
and retention liver cirrhosis
in
K. Nielsen, J. Kondrup, L. Martinsen, H. Dossing and B. Stilling Division of Hepatology A-2 752, Rigshospitalet University Hospital, Copenhagen, Denmark
Aim: To examine whether malnourished patients with liver cirrhosis have a decreased utilization of protein. Methods: 15 malnourished patients with biopsy proven cirrhosis of the liver (2 Child grp. A, 10 Child grp. B and 3 Child grp. C) were investigated for a mean of 38 days. The intake of a normal hospital diet was gradually increased. Food was prepared in the metabolic ward. Nitrogen intake was calculated by means of food tables. Nitrogen excretion was calculated using 24 hours urinary urea nitrogen x 1.25 + 2.5 g nitrogen for faecal and skin losses (1). The correlation between protein intake and protein retention (g/(kg d)) was calculated by linear regression analysis from 4 days’ pools in each patient. The individual protein requirement for nitrogen balance was calculated as the intercept at zero retention and the protein retention g/g protein intake was calculated from the slope. Results: All patients achieved a positive energy and nitrogen balance. Protein intake increased from 0.9 f 0.1 to 1.8 & 0.1 g/(kg d), (mean + SEM, n = 15). The protein requirement for nitrogen balance was 0.8 f 0.1 g/(kg d). The incremental protein retention was 0.84 + 0.08 g/g and the mean R2 was 0.81 + 0.03. Protein retention as percent of intake was 29 * 4. Only one patient showed saturation of protein retention at the end of hyperalimentation at an intake of 3 g protein/
P.122 Nitrogen balance and whole body protein turnover during hyperalimentation of malnourished patients with liver cirrhosis K. Nielsen, J. Kondrup, B. Stilling, L. Martinsen. N. Skakkebtek’, A. Juul”, P. Elsner’” and E.S. Jensen*” Division of Hepatology, Department of Growth and Reproduction, Rigshospitalet University Hospital, Copenhagen, Denmark, **Dept. of Biochemistry A, PANUM Institute, Copenhagen, Denmark, *I EnvironmentalScienceand Technology Department, Rise National Laboratory, Roskilde, Denmark ??
??
(kg d).
Conclusion:
Protein retention is not saturated in malnourished patients with liver cirrhosis in the range up to about 2 g protein/(kg d). Protein requirement for nitrogen balance is similar to other studies (2) and higher than in malnourished patients without organ diseases (3). 1) Blackburn GL, et al. 1981. 2) Swart GR, et al. 1989. 3) Barac-Nieto M, et al. 1979.
Aim: To examine the nitrogen balance during hyper-alimentation of malnourished patients with alcoholic liver cirrhosis. Methods: Six moderately malnourished patients with cirrhosis were fed increasing amounts of food for a mean of 35 91
P.121 Peripheral insulin resistance as main cause of impaired glucose tolerance in patients with liver cirrhosis E. Radoch. 0. Selberg, M. Schwarze, M. Manns and M.J. Miiller Medizinische Hochschule Hannover, Zentrum lnnere Medizin Abt. Gastroenterologie und Hepatologie, DD-3000 Hannover 67, Germany Purpose: Glucose intolerance is a characteristic feature of many patients with liver cirrhosis. About 40% of these patients are considered diabetic. Hepatic shunting of glucose and insulin have been proposed as the main causative factors. However, peripheral insulin resistance as measured by the glucose clamp technique is found regularly in liver cirrhosis. Methods: To investigate the significance of insulin resistance we performed a standard oral glucose tolerance test (OGTT; 1 g/kg body weight {bw}) and a euglycemic hyperinsulinemic (insulin infusion rate 1 .O mu/kg bw/min) clamp protocol with indirect calorimetry (Deltatrac Metabolic Monitor). Fat-free mass (FFM) and body cell mass (BCM) was determined by bioelectrical impedance analysis. A total of 13 patients with histologically proven liver cirrhosis (ci; age: 38.6 + 8.6 years {mean f SD}, sex: 8m/5f, aetiology: 4 ethanol induced, 2 posthepatitis, 2 obliterative cholangitis, 1 a,-antitrypsin deficiency, 4 cryptogenic; Child-Pugh classification: 5A/5B/3C, height: 172 + 14 cm, weight: 69 k 24 kg, FFM: 52.4 + 21 .O kg, BCM: 25.6 & 10.7 kg) were included in the study and compared with 10 healthy controls (co; age: 33.2 + 10.1 years, sex: 8m/2f, height 177 + 10 cm, weight: 73 + 14 kg, FFM: 52.6 & 12.0 kg, BCM: 20.9 + 4.8 kg). Results: 46% of patients had impaired glucose tolerance as indicated by plasma glucose concentrations > 180 mg/dl at 120 min of OGTT (263 f 90 mg/dl); the other 54% were considered normal (119 + 35 mg/dl). Clamp data were as follows: glucose disposal: ci 4.2 + 2.0 vs co 8.6 + 2.2 mg/kg bw/min, p < 0.05; glucose oxidation rate: ci 2.4 f 1.4 vs co 3.2 + 1.1 mg/kg bw/min, not significant; nonoxidative glucose metabolism: ci 1.8 & 1.6 vs co 5.6 + 2.5 mg/kg bw/min, p i 0.05. Whole body glucose disposal was different between patients with normal and impaired glucose tolerance (5.2 1 1.7 vs 2.4 + 0.7 mg/kg bw/min, p < 0.05). Moreover, whole body glucose disposal correlated with plasma insulin at 120 min of OGTT (r = 0.66, p c: 0.05). Conclusion: The degree of peripheral insulin resistance is a main determinant of glucose tolerance in patients with liver cirrhosis. However, insulin shunting and hyperinsulinemia may be an important cause of insulin resistance in liver cirrhosis.
El A mean f
0.95kO.07 1.76*016
g pr&in/(kg 1.90+0.29 1.92+0.37
d) 0.71+0.16 1.03+0.20
SEM. E = before hypedimentation,
2.12f0.26 2.67+0.34
A = after hyperalimentation
Conclusion: The increase in nitrogen balance was achieved exclusively by an increase in protein synthesis. We speculate that this increase in protein synthesis was due to the changes in insulin and the IGF-1 /BP-3 ratio rather than to changes in other regulators of protein synthesis.
P.123 Protein requirement malnourished patients with
and retention liver cirrhosis
in
K. Nielsen, J. Kondrup, L. Martinsen, H. Dossing and B. Stilling Division of Hepatology A-2 752, Rigshospitalet University Hospital, Copenhagen, Denmark
Aim: To examine whether malnourished patients with liver cirrhosis have a decreased utilization of protein. Methods: 15 malnourished patients with biopsy proven cirrhosis of the liver (2 Child grp. A, 10 Child grp. B and 3 Child grp. C) were investigated for a mean of 38 days. The intake of a normal hospital diet was gradually increased. Food was prepared in the metabolic ward. Nitrogen intake was calculated by means of food tables. Nitrogen excretion was calculated using 24 hours urinary urea nitrogen x 1.25 + 2.5 g nitrogen for faecal and skin losses (1). The correlation between protein intake and protein retention (g/(kg d)) was calculated by linear regression analysis from 4 days’ pools in each patient. The individual protein requirement for nitrogen balance was calculated as the intercept at zero retention and the protein retention g/g protein intake was calculated from the slope. Results: All patients achieved a positive energy and nitrogen balance. Protein intake increased from 0.9 f 0.1 to 1.8 & 0.1 g/(kg d), (mean + SEM, n = 15). The protein requirement for nitrogen balance was 0.8 f 0.1 g/(kg d). The incremental protein retention was 0.84 + 0.08 g/g and the mean R2 was 0.81 + 0.03. Protein retention as percent of intake was 29 * 4. Only one patient showed saturation of protein retention at the end of hyperalimentation at an intake of 3 g protein/
P.122 Nitrogen balance and whole body protein turnover during hyperalimentation of malnourished patients with liver cirrhosis K. Nielsen, J. Kondrup, B. Stilling, L. Martinsen. N. Skakkebtek’, A. Juul”, P. Elsner’” and E.S. Jensen*” Division of Hepatology, Department of Growth and Reproduction, Rigshospitalet University Hospital, Copenhagen, Denmark, **Dept. of Biochemistry A, PANUM Institute, Copenhagen, Denmark, *I EnvironmentalScienceand Technology Department, Rise National Laboratory, Roskilde, Denmark ??
??
(kg d).
Conclusion:
Protein retention is not saturated in malnourished patients with liver cirrhosis in the range up to about 2 g protein/(kg d). Protein requirement for nitrogen balance is similar to other studies (2) and higher than in malnourished patients without organ diseases (3). 1) Blackburn GL, et al. 1981. 2) Swart GR, et al. 1989. 3) Barac-Nieto M, et al. 1979.
Aim: To examine the nitrogen balance during hyper-alimentation of malnourished patients with alcoholic liver cirrhosis. Methods: Six moderately malnourished patients with cirrhosis were fed increasing amounts of food for a mean of 35 91