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Nutritional state and abnormal metabolism of nutrients

  • A. J. McCullough
Part of the Intensivmedizinisches Seminar book series (INTENSIVM.SEM., volume 8)

Abstract

As a primarily metabolic organ, the liver orchestrates a mosaic of physiologic and biochemical processes, one of which is the regulation of protein-energy metabolism. Consequently, it is not surprising that abnormal protein calorie malnutrition (PCM) is a common complication of advanced liver disease. Furthermore, increasing information suggests that PCM may itself accelerate deteriorating liver function and adversely affect clinical outcome. Nutritional therapy has been proposed as a means to correct PCM and thereby improve clinical outcomes. The rationale for aggressive nutritional therapy in patients with advanced liver disease is based on promising but nascent clinical trials and the following nutritional axioms relevant to liver disease:
  • Malnutrition is common but underdiagnosed.

  • Alterations in energy metabolism and nutritional status are similar to those observed in starvation.

  • Hepatic encephalopathy, sepsis, and muscle wasting occur pari passu with a negative nitrogen state.

  • Correction of malnutrition may improve the clinical outcome of these patients.

  • The occasional need for protein and sodium restriction in these patients conflicts directly with nutritional requirements.

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References

  1. 1.
    McCullough AJ, Tavill AS (1991) Disordered energy and protein metabolism in liver disease. Sem Liv Dis 11: 265–277CrossRefGoogle Scholar
  2. 2.
    McCullough AJ, Mullen KD, Smanik EJ, Tabbaa M, Szauter K (1989) Nutritional therapy in liver disease. Gastro Clin North Am 18: 619–643. These reviews provide a comprehensive discussion of abnormal nutrient metabolism and nutritional therapy in liver disease. They also provide extensive lists of references in these areas.Google Scholar
  3. 3.
    Mendenhall CL, Anderson S, Weesner RE, Goldberg SJ, Crolic KA (1984) Protein-calorie malnutrition associated with alcoholic hepatitis. Am J Med 76: 211–222. This prospective multi-center VA Hospital study documents the ubiquitous nature of protein calorie malnutrition in hospitalized patients with alcoholic hepatitis. It emphasizes the need to use a composite of different techniques for assessing the nutritional status, especially in the present of liver disease.PubMedCrossRefGoogle Scholar
  4. 4.
    Soberon S, Pauley MP, Duplantier R, Fan A, Halsted CH (1987) Metabolic effects of enteral formula feeding in alcoholic hepatitis. Hepatology 7: 1204–1209. In this well controlled study of 21 patients with alcoholic hepatitis, patients who spontaneously ingested less than 75% of the dietary needs, had improved nitrogen balance and intestinal function when supplemented with an enteral formula. There was also a 100% prevalence of malnutrition in these patients.PubMedCrossRefGoogle Scholar
  5. 5.
    DiCecco SR, Wieners EJ, Wiesner RH, Southorn PA, Plevak DJ, Krom RAF (1989) Assessment of nutritional status of patients with end-stage liver disease undergoing liver transplantation. Mayo Clin Proc 64: 95–102. This study demonstrates the high prevalence of malnutrition in non-alcoholic liver disease patients awaiting hepatic transplantation. Nutritional assessment yielded different profiles, which varied according to the type of liver disease.Google Scholar
  6. 6.
    McMahon MM, Bistrian BR (1990) The physiology of nutritional assessment and therapy in protein-calorie malnutrition. Disease of the Month July: 375–417Google Scholar
  7. 7.
    Hill GL (1992) Body composition research: implications for the practice of clinical nutrition. JPEN 16: 197–218. These reviews provides in depth, well referenced discussions of the physiology and factors influencing nutritional assessment. They also discuss the clinical differences between the hypo-albuminemic and marasmic forms of protein calorie malnutrition.CrossRefGoogle Scholar
  8. 8.
    McCullough AJ, Mullen KD, Kaihan SC (1991) Measurements of total body and extracellular water in cirrhotic patients with and without ascites. Hepatology 14: 1102–1111PubMedCrossRefGoogle Scholar
  9. 9.
    Roginsky MS, Zanzi I, Cohn SH (1976) Skeletal and lean body mass in alcoholics with and without cirrhosis. Calcif Tiss Res 21 L [Suppl]: 386–391 These two studies using different methodologies (intracellular water and total body potassium) demonstrate that the body cell mass is decreased in cirrhosis, even without obvious clinical wasting.CrossRefGoogle Scholar
  10. 10.
    Heysmfield SB, Waki M, Reinus J (1990) Are patients with chronic liver disease hypermetabolic? Hepatology 11: 502–505. This is an excellent editorial which reviews those factors that influence the measurement of energy expenditure in cirrhosis and suggests what type of studies need to be done in the future.CrossRefGoogle Scholar
  11. 11.
    Müller MJ, Fenk A, Lautz HU, Selberty O, Canzler H, Balks HJ, Mühlen AVZ, Schmidt E, Schmidt FW (1991) Energy expenditure and substrate metabolism in ethanol-induced cirrhosis. Am J Physiol 260: E338 - E344PubMedGoogle Scholar
  12. 12.
    Müller MJ, Lautz HU, Plogmann B, Burger M, Korber J, Schmidt FW (1992) Energy expenditure and substrate oxidation in patients with cirrhosis: the impact of cause, clinical staging and nutritional state. Hepatology 15: 782–794 These two articles represent continuous work from the same group of investigators which demonstrate increased postprandial and fasting energy expenditure in cirrhosis based on lean body mass. However, there is a heterogeneity in energy expenditure among different patients with liver disease.PubMedCrossRefGoogle Scholar
  13. 13.
    Dolz C, Raurich JM, Ibane J, Obrador A, Marse P, Gaya J (1991) Ascites increases the resting energy expenditure in liver cirrhosis. Gastroenterology 100: 738–744 This study demonstrated in 10 patients with cirrhosis that energy expenditure (based on indirect calorimetry) decreased by 10% a short time after an average of 11 liters of ascitic fluid was removed.PubMedGoogle Scholar
  14. 14.
    Swart GR, Zillinkens MC, VanVuvre JK, van den Berg JW (1989) Effect of a late evening meal on nitrogen balance in patients with cirrhosis of the liver. Br Med J 299: 1202–1203. This study demonstrated that an evening meal improved nitrogen balance in cirrhosis as compared to the same amount of calories given without the evening meal.CrossRefGoogle Scholar
  15. 15.
    Petrides AS, DeFronzo RA (1989) Glucose metabolism in cirrhosis: a review with some perspectives for the future. Diabetes Metabolism Rev 5: 691–709. This is an excellent review of the known and proposed mechanisms involved in the carbohydrate intolerance and insulin resistance associated with cirrhosis.Google Scholar
  16. 16.
    Petrides AS, Groop LC, Riely CA, DeFronzo RA (1991) Effect of physiologic hyperinsulinemia on glucose and lipid metabolism in cirrhosis. J Clin Invest 88: 561–570. Using an insulin clamp at three different insulin levels, this study demonstrated decreased glucose utilization, which was due to a diminished non-oxidative glucose disposal (muscle glycogen synthesis) in cirrhotics. Glucose oxidation was increased.Google Scholar
  17. 17.
    Kruszynska Y, Williams N, Perry M, Home P (1988) The relationship between insulin sensitivity and skeletal muscle enzyme activities in hepatic cirrhosis. Hepatology 8: 1615–1619PubMedCrossRefGoogle Scholar
  18. 18.
    Krakenbuhl S, Weber FL, Brass EP (1991) Decreased hepatic glycogen content and accelerated response to starvation in rats with carbon tetrachloride-induced cirrhosis. Hepatology 14: 1189–1195. These two studies provide evidence that decreased glycogen synthesis in muscle may be the cause of glucose intolerance in cirrhosis.Google Scholar
  19. 19.
    Merli M, Leonetti F, Riggio O, Giaccari A, Romiti A, Sbraccia P, Tamburrano G (1990) Resistance to insulin suppression of plasma free fatty acids in liver cirrhosis. J Endocrinol Invest 13: 787–795. Using a euglycemic insulin clamp, cirrhotics were shown to have diminished suppression of plasma levels of free fatty acids in response to insulin.PubMedGoogle Scholar
  20. 20.
    Johnson SB, Gordon E, McClain C, Low Graeme, Holman RT (1985) Abnormal polyunsaturated fatty acid patterns of serum lipids in alcoholism and cirrhosis: arachidonic acid deficiency in cirrhosis. Proc Natl Acad Sci USA 82: 1815–1818PubMedCrossRefGoogle Scholar
  21. 21.
    Cabre E, Periago JL, Lacruz AA, Huix FG, Gonzalez J, Comas ME, Banares FF, Planas R, Gil A, Medina FS, Gassull MA. Plasma fatty acid profiles in advanced cirrhosis: unsaturation deficit of lipid fractions. These two studies characterize the abnormal fatty acid and lipid profiles in serum and emphasize the potential functional significance of polyunsaturated fatty acid deficiency.Google Scholar
  22. 22.
    Romijn JA, Endert E, Sauerwein HP (1991) Glucose and fat metabolism during short-term starvation in cirrhosis. Gastroenterology 100: 731–737PubMedGoogle Scholar
  23. 23.
    Owen OE, Trapp VE, Reichard GA, Mozzoli A, Moctezuma J, Paul P, Skutches CL, Boden G (1986) Nature and quantity of fuels consumed in patients with alcoholic cirrhosis. These 2 studies investigated patterns of fuel consumption in cirrhosis and found increases in both fatty acid oxidation and turnover (using [1-14C] palmitate).Google Scholar
  24. 24.
    Avgerinos A, Kourti A, Chu P, Harry DS, Raptis S, Mclntyre N (1988) Plasma lipid and lipoprotein response to carbohydrate feeding in cirrhotic patients. J Hepatol 6: 315–324. This study suggests that lipid synthesis may be decreased in cirrhosis and that this is another mechanism of insufficient storage of energy in cirrhosis.PubMedCrossRefGoogle Scholar
  25. 25.
    Mullen KD, Denne SC, McCullough AJ, Bruno D, Tavill AS, Kalhan SC (1986) Leucine metabolism is stable cirrhosis. Hepatology 6: 622–630. This study in stable cirrhotics was the first well-controlled work (using [1–13C] leucine) to show that protein turnover was normal despite decreased plasma leucine levels.PubMedCrossRefGoogle Scholar
  26. 26.
    Morrison WL, Bouchier IAD, Gibson JNA, Rennie MJ (1990) Skeletal muscle and whole body protein turnover in cirrhosis. Clin Sci 78: 613–619. This is the only in vivo study using [l-13C] leucine to show decreased protein synthesis in cirrhosis.PubMedGoogle Scholar
  27. 27.
    Petrides AS, Luzi L, Reuben A, Riely C, Defronzo RA (1991) Effect of insulin and plasma amino acid concentration on leucine metabolism in cirrhosis. Hepatology 14: 432–441PubMedCrossRefGoogle Scholar
  28. 28.
    McCullough AJ, Mullen KD, Tavill AS, Kalhan SC (1992) In vivo differences between the turnover rates of leucine and leucine’s keto-acid in stable cirrhosis. Gastroenterology 103. These two studies analyzed KIC as well as leucine enrichment during [1–13C] or [1–14C] labelled leucine infusion in cirrhosis. One showed increased while the other showed a normal rate of protein breakdown.Google Scholar
  29. 29.
    McCullough AJ, Mullen KD, Kalhan SC (1992) Body cell mass and leucine metabolism in cirrhosis. Gastroenterology 102: 1325–133. This study demonstrates the importance of considering body composition in metabolic studies, since protein breakdown during a [l-14C] leucine infusion was normal based on body weight and fat free body mass, but was increased based on body cell mass.PubMedGoogle Scholar
  30. 30.
    Badalamenti S, Gines P, Arroyo V, Llach J, Piera C, Rimola A, Jimenez W, Gaya J, Casamitjana R, Rivera F, Rodes J (1990) Effects of intravenous amino acid infusion and dietary proteins on kidney function in cirrhosis. Hepatology 11:379–386. This study demonstrates that a moderately high protein diet or intravenous amino acid administration increases renal plasma flow and glomerular filtration rate in cirrhosis.PubMedCrossRefGoogle Scholar
  31. 31.
    Okuno M, Nagayama M, Takai T, Rai A, Nakao S, Kamino K, Umeyama K (1985) Postoperative total parenteral nutrition in patients with liver disease. J Surg Res 39: 93–102. In this study of post-op cirrhotic patients, fructose (as an alternative fuel to glucose) plus glucose produced improved nitrogen balance as compared to glucose alone.PubMedCrossRefGoogle Scholar
  32. 32.
    Walker C, Peterson W, Unger R (1974) Blood ammonia levels in advanced cirrhosis during therapeutic elevation of the Insulin: glucagon ratio. N Engl J Med 291: 168–171. This important and largely overlooked article demonstrates that hourly supplements of oral glucose improved both nitrogen and carbohydrate metabolism in cirrhosis.PubMedCrossRefGoogle Scholar
  33. 33.
    Jenkins DJA, Thorne MJ, Taylor RH, Bloom SR, Sarson DL, Jenkins AL, Anderson GH, Blendis L (1987) Effect of modifying the rate of a food on the blood glucose, amino acid, and endocrine responses in patients with cirrhosis. Am J Gastroenterol 82: 223–230. By using food with a low glycemic index, cirrhotics had improved carbohydrate tolerance.PubMedGoogle Scholar
  34. 34.
    Diehl AM (1991) Nutrition, hormones, metabolism, and liver regeneration. Sem Liver Dis 11: 315–320. This is an excellent review of the current state of knowledge regarding the importance of nutrition hepatic regeneration.CrossRefGoogle Scholar
  35. 35.
    Benga G, Hodarnau A, Tilinca R, Borza V, Ferdinand W (1991) Amino acid composition of human liver mitochondrial membranes in normal and pathological conditions. Biosci Rep 11: 95–100. This study found the amino acid composition to be markedly abnormal in the mitochondrial membranes of cirrhotic patients. The potential clinical and functional consequences of these abnormalities are discussed.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag/Wien 1995

Authors and Affiliations

  • A. J. McCullough
    • 1
  1. 1.Department of Gastroenterology, Metro Health Medical CenterCase Western Reserve UniversityClevelandUSA

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