Uso Potencial de AGCC

La mayoría de las fórmulas entera les poseen polisacáridos digeribles pero escasa o ninguna cantidad de fibra. Se ha demostrado que las dietas enterales libres de fibra inducen a la atrofia del colon y del intestino delgado distal (79, 83) Y la nutrición parenteral total (NPT) induce a la atrofia en todo el tracto intestinal.

En pacientes con tracto gastrointestinal funcionante y quienes reciben una fórmula definida como dieta, la adición de fibra altamente fermentable, como por ejemplo pectina, previene la atrofia del colon y del intestino delgado distal o hace reversible la atrofia asociada a la dieta sin fibra (68, 80, 82). La diarrea ocurre en un 60% de los pacientes que reciben régimen enteral con fibra (88, 89). Se ha demostrado que al agregar pectina a los regímenes enterales libres de ella se previenen las deposiciones líquidas resultantes de la exclusiva ingestión de fibra por sujetos normales; mejora la función colónica medida por pH y electrolitos (Na y K) (90).

El proceso de fermentación de la fibra en el colon y la liberación de AGCC y su absorción, representan un potencial significativo de una fuente calórica alternativa que puede representar un 30% omás del aporte calórico (32, 91). En pacientes con intestino disminuido en su capacidad de absorción pero con un colon normal, sometidos a dietas enterales, el seguimiento calórico puede lograrse administrando fibra.

Enfermedad Intestinal

El reposo intestinal absoluto o relativo como modalidad terapéutica, indicado en pacientes con enfermedad Intestinal o en posoperatorio o en casos de resecciones intestinales, priva a la mucosa intestinal de sus sustratos preferidos y condiciona la atrofia intestinal. En varios modelos animales la adición de pectina a dietas entera les libres de fibra, ha facilitado la cicatrización y la resistencia a la tensión de anastomosis colónica (92), efectos favorables en colitis inducidas químicamente (93) y en readaptación intestinal luego de resecciones masivas (94) y síndromes de intestino corto (95).

Otra ventaja adicional es el mantenimiento de la microflora normal (96) la cual protege de colonización por bacterias patógenas (97) y la tras locación bacteriana desde el tracto gastrointestinal (98)

La provisión de nutrientes enterales no siempre es posible, aunque los nutrientes intraluminales sean más tróficos para la mucosa intestinal (84, 89, 101). El suministro de lossustratos oxidativos preferidos por la mucosa intestinal (AGCC, cuerpos cetónicos o glutamina) en soluciones deNPT, ha demostrado que puede inhibir la atrofia de la mucosa intestinal asociada a la administración de la NPT en animales.

En perspectiva, los AGCC, y sus precursores (fibra fermentable o almidones resistentes) y sus metabolitos (cuerposcetónicos), pueden ser utilizados en casi todas las situaciones en las cuales han sido propuestos los ácidos grasos de cadena media (104). Una ventaja potencial de usar AGCC y cuerpos cetónicos, es que éstos son solubles en agua y pueden administrarse como ácidos libres o como sales en los límites fisiológicos de carga de ácidos y sales.

Cuerpos Cetónicos

Igual que los AGCM, los AGCC y los cuerpos cetónicos pueden suministrarse a animales como monoglicéridos solubles en agua (105); administrados en esta forma, no han ocasionado efectos adversos (monoacetato y monobutirin), aportando hasta el 70% de las calorías no proteicas (78, 106, 108); también pueden darse como triglicéridos. Unicamente el triacetín (glicerol triacetato) es un triglicérido soluble en agua (109); su infusión intravenosa no ha tenido efectos adversos aparentes sobre el metabolismo del Ca o del fosfato ni toxicidad demostrable (110, 111).

En síntesis, la extensa revisión bibliográfica del tema, en la cual debemos destacar las publicaciones de Rombeau (112), Settle (113) y Campos (114), nos abre un nuevo panorama en las posibles indicaciones de los AGCC en situaciones clínicas, como complemento o alternartiva de apoyo nutricional.

Posteriores estudios clínicos evaluarán el tiempo recomendado de administración, su uso en NPT y en circunstancias clínicas complejas tales como insuficiencia hepática, renal, cardíaca, respiratoria, diabetes y sepsis.

Lea También: Ácidos Grasos Omega-6 pueden ser Buenos

Abstract – Uso Potencial de AGCC 

Long chain fatty acids are isotonic, providing high calorie content (9 kcal/gram). They prevent essential fatty acid deficiency and may be administered peripheraliy together with aminoacids and glucose. Among their unfavorable metabolic effects it should be pointed out that they needcarnitine for their oxidation and that they metabolize slowly in stress situationso AIso, blockade of the reticuloendothelial system has been reported in in vitro models and doses in excess of 3 g have been associated with liver steatosis and reduced capacity of lung diffusion in healthy men. 

Medium chain fatty acids do not require carnitine for their oxidation and they penetra te promptly in the mitochondria, but they do not prevent essential fatty acid deficiency. 

Short chain fatty acids are metabolized in the cecum with production of acetic acid, propionic acid and butyric acido The latter is the main substrate of the colonocyte. In addition, short chain fatty acids stimulate sodium and water absorption by the colon, exert a trophic action in the bowel and promote healing. They are water-soluble and they may be administered as free acids or as salts. Additionally, they could be given as complementary calorie input. Further studies are needed to demonstrate their potential clinical uses.

Referencias

1. Ooodgame J T, Lowey S F, Brennan M F: Essenlial fally acid deficiency syndrome in 10lal parenleral nulrilion: Time course of developmenl and suggeslions for Iherapy. Surgery 1978; 84: 271-7

2. Barr L H, DUDO O D, Brennan M F: Essenlial fally and deficiency during tolal parenleral nulrition. Ann Surg 1981; 193: 304-11

3. Meguid M M, Akahoshi M, Jeffers S, Hayashi R, Hammond W: Amelioralion of melabolic complicalions of convenlional TPN: A prospeclive randomized sludy. Arch Surg 1984; 119: 1294-8

4. Meguid M M, Akahoshi M, Debonis D, Hayashi R J, Hammond W O: Use of 20% fal emulsion in lolal parenleral nulrilion. Cril Care Med 1986; 14: 29- 31

5. Tessari P, Nissen S L, Miles J M, Haymond M W: Inverse relalionship of leucine flux and oxidalion lo free fally acid availabilily in vivo. J Clin Invesl 1986; 77: 575-81

6. Skele B, Askanazi J, Rolhkoof M M, Ooldslein S, Rosembun S H: The beneficial effecls of ral on venlilalion and pulmonary funclion. Nulrilion 1987; 3: 149-54

7. Slafford W W, Day O E: Regression of alherosclerosis effecled by inlravenous phospholipid. Arlery 1975; 1: 106-14

8. Fujiwara T, Kauarasaki H, Fonkalsrud E W: Reduclion of poslinfusion venous endolhelial injury wilh Inlralipid. Surg Oynecol Obslel 1984; 158: 57-65

9. Kurzer M, Tice D, Meguid M M el al:Nalural Killer cell aclivily in rals infused wilh inlralipid. J Clin Invesl 1988 (in press).

10. Heird W I.., Orundy S M, Hubbard VS: Slruclured lipids and Iheir use in c1inical nulrilion. Am J Clin Nulr 1986; 43: 3320-4

11. Balch A L, Babayan V K: Mediumcahin Iriglycerides: An updale. Am J Clin Nulr 1982; 36: 950-62

12. Nordenslrom J, Carpenlier y A, Askanazi J el al: Free fally acid movilizalion and oxidalion during 10lal parenleral nulrilion and Irauma and infeclion. Ann Surg 1983; 198: 725-35

13. Wolfe B M, Ney D M: Lipid Melabolism in parenleral nulrilion. In: Clinical NUlrilion, Rombeau J L. Caldwell M D, eds, W. B. Saunders, Philadelphia, Vol 11 1986, pp 72-99

14. Salvian A J, Allardyce D B: Impaired bilirubin secrelion during 10lal parenleral nulrilion. J Surg Res 1980; 28: 547-55

15. Allardyce D B: Choleslasis caused by lipid emulsions. Surg Gynecol Obslel 1982; 154: 641-7

16. Fisher O W, Wilson S R, Hunler K W el al: Diminished bacterial defense wilh inlralipid. Lancel 1980; 2: 819-20

17. Jarslrand C, Berghem I.., Lahnborg O: Human granulacyte and relicoloendOlhelial syslem funclion during in- Iralipid infusion. JPEN 1978; 2: 663-70

18. Nordenslron J, Jarslrand C, Wiemik A: Decreased chemolalic and random migralion of leucocyles during inlralipid infusion. Am J Clin Nulr 1979; 32: 2416-22

19. Meguid M M, Kuzer M, Hayashi R J, Akahoski M P: Shorl-Ierm effecls. JPEN 1988 (in press)

20. Johnson R C, C.aller R: Melabolism of medium chain Iriglyceride lipid emulsion. Nulr Inl 1986; 2: 150-8

21. McGarry J D, Fosler D W: Regulalion of hepalic fally acid oxidalion and kelone body produclion. Annu Rev Biochem 1980; 49: 395-420

22. Gordon E E, Duga J: Experimenlal hyperosmolar diabelic syndrome, kelogenic response lo medium chain Iriglycerides. Diabeles 1975; 24: 301-6

23. Rodríguez N, Schwenk W F, Beaufrere B, Miles J M, Haymond M W: Trioclanoin infusion increases in vivo leucine exidalion: A lesson in isolope modeling. Am J Physiol 1986; 251: E343-8

24. Miles J M, Callalini M, Wold L, Ocrich J E, Haymond M W: Toxicily of inlravenous medium-chain Iriglyceride emulsion in dogs. Clin Res 1983; 31: 243A

25. Ashbrook J D, Speclor A A, Fletcher J E: Medium-chain fally acid binding lo human plasma albumin. J Biol Chem1972; 247: 7043-50

26. Coller R, Taylor O A, Johnson R, Rowe W B: A melabolic comparison of a pure long-chain Iriglyceride lipid emulsion (LCT) an various medium-chain Iriglyceride (MCT)-LCT combinalion emulsions in dogs. Am J Clin Nulr 1987; 45: 927-39

27. Crowe P J, Dennison A R, Royle O T: A new inlravenous emulsion conlaining medium-chair Iriglycerides: Sludies of ils melabolic effecls in Ihe perioperalive period compared wilh a convenlional long-chain Iriglyceride emulsion. JPEN 1985; 9: 720- 4

28. Goulel D, Narcy P, Hanafy H, Oorski M Ricour C: Inlravenous fal emulsion and reliculoendolhelial syslem: Medium-(MCI) vs. Long-chain Iriglycerides (LCI) (abslr). Clin Nulr 1987; 6 (suppl): 41

29. Jauch K W, Hailer S, Wolfram O: Differenl fal emulsion in posloperalive TPN (abslr). Clin Nulr 1987; 6 (suppl): 44

30. Adolph M, Eckarl J, Melges C, Neeser O, Wolfram O: Oxidalion of medium chain Iriglycerides in 10lal parenleral nulrilion of polylraumalized palienls (abslr). Clin Nulr 1987; 6 (suppl): 42

31. Babayan V K: Medium chain lenghl fally acid eslers and Iheir medical and nulrilional applicalions. Oil Chem Soc 1981 58: 49A- 51A

32. Wrong O M: The large inlesline: Its role in Mammalian Nulrili~n and Homeoslasis. New York, 1981 John Wiley & Sons

33. Cummings J H, Branch W J: Fermenlalion and Ihe produclion of shorl chain fally acids in Ihe human large inslesline. In: Dielary Fiber. Basic and Clinical Aspecls. O.B. Vahouny. D. Krilchenevsky (eds), New York, Plcnum Press 1986 pp. 131-52

34. Englysl H N. Cummings J H: Digeslion of Polysaccharides of polaloin Ihe small inlesline of mano Am Clin Nulr 1987; 45: 423-31

35. Bond J H, Currier B E, BUlchwaid H el al: Colonic Conservalion of malabsorbed carbohydrale. Oaslroenlerology 1980; 78: 444-7

36. Ravich W J, Bayl T M, Thomas M: Fruclose: Incomplele inleslinal absorlion in Humans. Gaslroenlerology 1983; 84: 26-9

37. Miller T L, Wolin M J: Fermenlalions by Saccharolylic inleslinal bacleria. Am Clin Nulr 1979; 32: 164-72

38. Nyman M, Asp N G: Fermenlalion of dielary fiber componenls in ral inleslinallracl. Br J Nulr 1982; 47: 357-66

39. McNeil N 1, Cummings J H, James W P T: Shorl-chain fally acid absorlion by Ihe human inlesline. Oul 1978; 19: 819- 22

40. Hoverslad T, Bohner T, Fausa O: Absorlion of shorl-chain fally acid by human color measured by Ihe CO brealh lesl. Scand J Oaslroenlerol 1982; 17: 373-8

41. Ruppin H, Bar-Meir S, Soeregel K H el al: Absorlion of shorl-chain fally acid by Ihe colon. Oaslroenlerology 1980; 78: 1500-7

42. Hoverslad T: Sludies of short-chain fally acids absortion in mano Scand J Gastroenterol 1986; 21: 257-60

43. Cummings J H: Colonic Absortion. The importance of short- chain fally acids in mano Scand J Gastroenterol 1984; 20: 88-99

44. Hilditch T P, Williams P N, eds: The chemical constitution of the natural fats. 4th ed., New York, Wiley, 1964

45. Roediger W E W: Role of Anaerobic Bacteria in the metabolic welfare of the colonic mucosa in mano Gut 1980; 21: 793-8

46. Roediger W E W: Utilization of nutrients by isolated epithelial cells of the rat colon, Gastroenterology 1982; 83: 424-9

47. Remesy C, Demigne C: Partition ando absortion of volatile fally aeids in the alimentary canal of the ra!. Ann Reeh Vet 1976; 7: 39-55

48. Henning S J, Hird F J R: Ketogenesis from butyrate and acetate by the ceeum and colon of rabbits. Biochem J 1982; 130: 785-90

49. Ardawi M S M, Newsholme E A: Fuel utilization in colonocytes of the rato Biochem J 1985; 231: 713-9

50. Marty J F, Vemay M Y, Abravanel G M: Acetate absortion and metabolism in the rabbit hindgu!. Gut 1985; 26: 562-9

51. Dankert J, Zijlstra J B, Wolthers B G: Volatile fally acids in human peripheral and portal blood. Quantitative delerminalion by vaeuum distilation and gas chromalography. Clin Cbim Acta 1981; 110: 301-7

52. Buckley B M, Williamson D H: Origins of blood acetale in the ra!. Biochem J 1977; 166: 539-47

53. Hermann D B J, Herz R, Frolich J:Role of gastrointestinal traet and liver in acetate metabolism in rat and man. Eur J Clin Invest 1985; 15: 221-6

54. Lazarus D D, Zimmaro D M, RolandelIi R R et al: Non-gut origin of plasma acetate in humans and rats (abstr) 1988; 2: A444

55. Desmoulin F, Canioni P, Cozzone P J: Glutamate-glutamine metabolism in the perfused rat liver: C. NMR study using (2. C) enriched acetale. FEBS lellers 1985; 185: 29-32

56. Cross T A, Pahl C, Oberhansli R et al: Ketogenesis in the living rat followed by C. NMR Sleloscopy. Biochem 1984; 23: 6398-402

57. Windmueller H G, Spacth A E: Idcntification of ketone bodies and glutamine as the major respiratory fuels in vivo for post absorptive rat small intestine. J Biol Chem 1978; 253: 69-76

58. Hanson P J, Parsons D S: Faclors affeeting the ulilizalion of ketone bodies and other substrates by rat jejunun: Effeets if fasting and of diabetes. J Physiol 1978; 278: 55-67

59. Souba W W. Scoll T E. Wilmore D W: Intestinal Comsumolion of intravenous- Iy administered fuels. JPEN 1985; 9:18- 22.

60. Roedigfer W E W, Moore A: Effeet of short-chain fally acids on sodium absortion in isolated human colon perfused through the vascular bed. Dig Dis Sci 1981; 26: 100-6.

61. Sakata T, Engerhardt W V: Stimulatory effeet of short-chain fally acids. on the epithelial cell proliferation in rat large intestine. Comp Biochem Physiol 1983; 74A:459-62.

62. Sakata T: Stimulatory effeet of shortchain fally acids on epilhelial cell proliferation in the ral inlesline. Apossible explanation for Ihe lrophic effeels of fermentable fiber, gat microbes and luminallrophic effeels. Br J Nutr 1987; 58:95-103.

63. Kripke S A, Fox A D, Berman J M el al: Stimulalion of inlestinal mucosal growlh wilh inlracolonic infusion of short-chain fally aeids. JPEN 1989 (in press).

64. Rolandelli R, Koruda M J, Sellle R G el al: Effeels of intraluminal infusion of short-chain fally acids on the healing of colonic anastomosis in the ra!. Surgery 1986; lOO: 198-203.

65. Harig J M, Soergel K H: Treatment of diversion colitis with short-chain fally acids (SCFA) irrigation (abstr). Gastroenterology 1987; 92: 1425

66. Fleming S E, Marlhisen D, Kuhniein H: Colonic function and fermenlation in men consuming high fiber diets. J Nulr 1983; 112: 2535-44

67. Cummings J H, Southgate D A T, Brach W et al: 111C digestion of peetin in the human gUI and its effeet on calcium absorption and large bowel funclion. Br J Nutr 1979; 41: 477-85

68. Jacobs L R, Lupton J R: Effeets of dielary fiber on rat large bowel mucosal growth and cell proliferation. Am J Physiol 1984; 246: 6378•85

69. Sakata T, Yajima T: Influence of shortchain fally acids on the epithelial cell division of digestive trac!. Q J Exp Physiol 1984; 69: 639-48

70. Tullon P J M, Barkla D H: Further studies on Ihe effeet of adenosine cyclic monophosphate derivatives on cell proliferalion in jejunal crypts of ra!. Clin Exp Pharmacol Physiol 1982; 9: 671-4

71. Koruda M, Rolandelli R, Sellle R et al: The effecls of shorl-chain fally acids (SCFA) on the small bowel mucosa (abstr) JPEN 1987; 11: (suppl): 8

72. Bates M W, Krebs H A, Williamson D H: Yurnover rates of ketone bodies in normal, starved and alloxan diabetic rats. Biochem J 1968110: 655-61

73. McGarry J D, Guest M J, Foster D W: Ketone body metabolism in the ketosis of starvation and alloxan diabetes. J Biol Chem 1970; 245: 4382•90

74. Bates M W: Kinetics of ketone body metabolism in fasted and diabetic rats. Am J PhysioI1971; 221: 984•91

75. Scheld H P, Wilson H D: Effeets of diabetes on intestinal growth in the ra!. J Exp ZooI1971; 176: 487-96

76. J Miller D L, Hanson W, Scheld H P et al: Proliferation rate and transit time of mucosal cells in small intestine of the diabetic ral. Gastroenterology 1977; 73: 1326-32

77. Sheld H P, Wilson H D. Ramaswamy K et al: Gastrin and growth of the alimenlary tract in the streptozotocindiabetic rato Am J Phisiol 1982; 242: G460-3

78. Kroke S A, Fox A D, Berman J M el al: Inhibition of TPN associated intestinal mucosal atrophy with monoacetoacetin. J Surg Res 1988; 44: 436•44

79. Jane P, Carpentier Y, Willems G: Colonic mucosal atrophy induced by a liquid elemental diel in rats. Am J Dig Dis 1977; 22: 808-12

80. Ryan G P, Dudrick S J, C.opeland E M el al: Effeet of varius diets on colonic growth in rats. Gastroenlerology 1979; 77: 658-63

81. Morin O L, Ling V, Bourassa D: Small intestinal and colonic changes induced by a chemically defined diet. Dig Dis Sci 1980; 25: 123-8

82. Ecknauer R, Sicar B, Johnson L R: Effeet of dietary bulk on small intestinal morphology and cell renewal in the rat. Gaslroenterology 1981; 81: 781-6

83. Sicar B, Johnson Lr. Lichtenberger L M: Effeet of synthetic diets on gastrointeslinal mucosal DNA synthesis in rats. Am J Phisiol 1983; 244: G327-35

84. Levine G M, Deren J J, Steiger E et al: Role of oral intake in maintenance of gUI mass and disaccharide activity. Gastroenterology 1974; 67: 975-82

85. Johnson R, Copeland E M, Dudrick S J et al: Slructural and normal alterations in the gastrointe>tinal tract of parenterally fed rats. Gastroenterology 1975; 68: 1177-83

86. Hughes C A, Dowling R H: Speed of onset of adaptive mucosal hypoplasia and hypofunction in the intestine oC parentcrally fed rats. Clin Sci 1980; 59: 317-27

87. Goldstein R M, Hebiguchi T, Luk G D et al: Tbe effeets of total parenteral nutrition on gastrointestinal growth and development. J Pediatr Surg 1985; 20: 785-91

88. Kelly T W, Hillman K M: Study ofdiarrhea io critically-i11 patients. Crit Care Med 1983; 11: 7-9

89. Flyn K T, Norton C C, Fisher R L: Enteral tube feeding: iodications, practices and outcomes. lmage J Nurs Scholarship 1987; 19: 16-19

90. Zimmaro D M. Rolaodelli R H, Koruda M J et al: lsotonic tube feeding formula induces liquid stool io normal subjeet: Reversal by peetin. JPEN 1989; (in press)

91. Milton K. McBee R H: Rates of fermentative digestion io the howler monkey.. alouatta palliate primates: ceboidea. (‘.omp Biochem Physiol 1983; 74A: 29-31

92. Rolandelly R H, Koruda M J, Settle R G et al: Tbe effeets of enteral feedings supplemented with peetin on the healing of colonic anastomoses in the rat. Surgery 1986; 99: 703-7

93. Rolandelli R H, Saul S H, Settle R G et al: A comparison of parenteral nutrition and enteral nutrition with peetin in experimental colitis in the rat. Am J Clin Nutr 1986; 47: 715-21

94. Koruda M J, Rolandelli R H, Srellle R G et al: Tbe effeet of a peetin-supplemented elemental diet on intestinal adaptation lo massive small bowel reseetion. JPEN 1986; 10: 343-50

95. Kripke S, Fox A D, DePaula J et al: Peetin-supplemented elemental diet (PED) improves outcomes in shortbowel syndrome (SBS) (abstr). Arn J Clin Nutr 1988; 47: 759 Clin Res 1988; 36: 763A

96. Crowther J S, Drasar B S, Goddard P et al: Tbe effeet of a chemically defined diet on the faeeal flora steroid concentration. Gut 1973; 14: 790-3

97. Fleming S E, Arce D S: Volatile fally acids: Tbeir production, absortion, utilization and roles in human health. Clio Gastroenterol 1986; 15: 787: 814

98. Berg R D, Dwens W E: Inhibition of translocation of viable Escherichia colli from the gastrointestinal tract of mice by bacterial antagonismo Infeet lmmun 1979; 25: 820-7

99. Speetor M H, Taylor J, Young E A et al: Stimulation of mucosal growth by gastric and ileal infusion of single amino acids in parenterally nourished rats. Digestion 1981; 21: 33-40

100. Weser E, Vandeventer A, Tawil T: Stimulation of small bowel mucosal growth by midgut infusion of different sugars in rats maintained by parenteral nutrition. J Pediatr Gastroenterol Nutr 1982;1:411-6

101. Weser E, Babbitt J, Hoban M et al: Intestinal adaptation: Different growth responses to disaccharides compared with monosaccharides in rat small bowel. Gastroenterology 1986; 91: 1521-7

102. Koruda M J. Rolandelly R H, Settle R G et al: Tbe effeet of parenteral nutrition supplemented with short-chain fatty acids on adaptation to massive small bowel reseetion. Gastroenterology 1988; 95: 715-20

103. Hwang T L, O’Owver S T, Smith R J et al: Reservation of small bowel mucosa using glutamine-enriched parenteral nutrition. Surgical Forum 1986; 37: 56- 8

104. Bach A C, Babavan V K: Mediumchain triglycerides: An Update. Am Clin Nutr 1982; 39: 950-62

105. Birkhahn R H, Border J R: Altemate of supplemental energy sources. JPEN 1981; 5: 24-31

106. Birkhahn R H. McMenarny R H, Border J R: Intravenous feeding of the rat with short-chain fatty acid esters. I. Glycerol monobutyrate. Arn J Clin Nutr 1977; 30: 2078-82

107. Birkhahn R H, Border J R: Intravenous feeding of the rat with short-chain fatty acid esters. n. Monoacetoacetin. Arn J Clin Nutr 1978; 31: 436-44

108. Kirvela O K, Takala J A: (‘.omparison of monogryceryl acetoacetate and glucose as parenteral energy substrate after experimental trauma. Eur Surg Res 1986; 18: 80-5

109. Windholz M (ed). Tbe Merck lndex Merck and (‘.(l, New Yersey, 1983

110. Bailey J, Rodríguez N, Marsh H et al: Metabolic effeets of an intravenous short-chain triglyceride infusion in dogs (abstr). JPEN 1987; 11 (suppl. 1): 6

111. Bailey J, Marsh H, Heath H et al: Effeets of intraavenous short-chain triglycerides on mineral metabolism and energy expenditure in dogs (abstr). JPEN 1988; 12 (suppl. 1): 14 112. Rombeau J: Colonic infusion of shortchain fatty acids JPEN 1988; 12 (6) (suppl)

113. Sellle G: Short-chain fatty acids and their potential role in nutritional support. JPEN 1988; 12 (6)

114. Campos A C: Short-chain fatty acids: Present prospeet, future altemative. JPEN 1988; 12 (6)

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