Nutritional effects of oral zinc supplementation in cirrhosis

Citation
Gp. Bianchi et al., Nutritional effects of oral zinc supplementation in cirrhosis, NUTR RES, 20(8), 2000, pp. 1079-1089
Citations number
43
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
NUTRITION RESEARCH
ISSN journal
02715317 → ACNP
Volume
20
Issue
8
Year of publication
2000
Pages
1079 - 1089
Database
ISI
SICI code
0271-5317(200008)20:8<1079:NEOOZS>2.0.ZU;2-K
Abstract
Poor zinc status is common in cirrhosis. Experimental studies proved that z inc supplementation produces metabolic effects, and trends towards improved liver function and nutritional status have previously been reported. We me asured liver function by means of dynamic, quantitative tests and biochemic al indices of nutrition in response to zinc treatment in patients with cirr hosis. Fifteen patients with advanced cirrhosis were studied before and after long -term oral zinc-sulfate supplementation (200 mg t.i.d, for 2-3 months). Liv er function was measured by routine biochemistry, galactose elimination cap acity and antipyrine clearance; nutritional assessment included the measure ment of daily urinary creatinine excretion, and albumin, prealbumin, retino l-binding protein and insulinlike growth factor-1 (IGF-1) serum or plasma c oncentrations. In 10 patients data were correlated with the parameters of g lucose metabolism obtained during a frequently-sampled i.v, glucose toleran ce test. At baseline, serum zinc was low normal or reduced, and returned to normal r ange in all patients after supplementation. Liver function improved signifi cantly. All nutritional indices improved as well, but remained on average b elow normal. IGF-1 increased on average by 30%, but was in the normal range in only 2 cases. Changes in IGF-1 correlated with improved glucose toleran ce after i.v. glucose load, namely with the increased non-insulin-mediated glucose uptake. The study confirms that oral zinc produces metabolic effects in zinc-defici ent patients with cirrhosis. Improved liver function and nutritional status may increase glucose disposal via increased IGF-1, responsible for the non -insulin-dependent fraction of glucose disappearance. (C) 2000 Elsevier Sci ence Inc.