Direct Measurement of the Hepatointestinal Extraction of Zinc in Cirrhosis and Hepatitis

Keeling, P. W. N.; Ruse, W.; Bull, J.; Hannigan, B.; Thompson, R. P. H.

doi:10.1042/cs0610441

Cited by 26 publications

(22 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The placenta concentrates zinc, suggesting an active uptake on the ma ternal side of the fetal syncytium against a high maternal plasma to placenta gradient, and the high placental concentration may provide a downhill gradient from placenta to fetal plasma; however, little is known of the nature of zinc pools in tissues apart from their zinc-containing enzymes [ 1 ]. It is possi ble that zinc is adsorbed to binding proteins in the placenta which limit its access to the fetus and may perform a temporary storage and protective function such as exercised by the liver [ 13]. Placental uptake of zinc and its transfer to the fetus may also be influenced by protein binding in both maternal and fetal plasmas [6].…”

Section: Discussionmentioning

confidence: 99%

Placental Handling of Zinc in the Guinea Pig

et al. 1985

View full text Add to dashboard Cite

The distribution of zinc between the mother and the fetoplacental unit, and its placental transfer, were studied using stable and isotopic zinc in unanaesthetized pregnant guinea pigs and an in situ perfusion preparation. The concentration of stable zinc in fetal plasma and skeletal muscle was higher than that in the maternal tissues: 2.0 compared with 1.4 μg/ml and 84 with 49 ng/mg dry weight, respectively. The placenta and maternal and fetal liver had similar zinc concentrations: 90, 75 and 88 ng/mg dry weight, respectively. The ability of the placenta to concentrate ⁶⁵Zn, measured 1 h after a single intravenous injection into the unanaesthetized mother, was comparable with that of the maternal liver. Maternal-fetal mass transfer of zinc was directly related to maternal plasma zinc concentrations from 0.7 to 24.1 μg/ml (b = 2 ng·min^––¹·g^––1·μg^––1, r = 0.92). At physiological plasma levels, the calculated transfer would supply the fetus with 0.12 mg zinc/day, similar to the accretion rate over the last trimester. Placental transfer of zinc was not influenced by the concentration of zinc in the placental perfusate. Extraction of zinc from the perfusate was also slow, and partly by absorption. Matemofetal transfer of zinc was directly related to both uterine and umbilical blood flows. The high concentration of zinc in the syncytium, relative to both maternal and fetal plasma levels, suggests active uptake at the maternal surface, combined with a slow release into the fetus, down a concentration gradient.

show abstract

Section: Discussionmentioning

confidence: 99%

Placental Handling of Zinc in the Guinea Pig

et al. 1985

View full text Add to dashboard Cite

show abstract

“…Multiple mechanisms underlie zinc deficiency or altered zinc metabolism in patients with liver disease, including inadequate intake, changes in protein and amino acid metabolism, diminished hepatic extraction, portosystemic shunts, alcohol-induced impaired absorption, and the influence of cytokines, mainly IL-6, known to alter zinc metabolism [25,28,32,33]. Diuretics administered to treat ascites in decompensated liver cirrhosis may also contribute to zinc deficiency.…”

Section: Causes Of Zinc Deficiency In Liver Diseasementioning

confidence: 99%

Zinc in liver disease

Grüngreiff¹

2002

J Trace Elements Exper Med

View full text Add to dashboard Cite

The essentiality of zinc for humans was first documented by Prasad in the 1960s. During the past 35 years, zinc deficiency in humans a result of nutritional factors and several disease states has been recognized. Many of the clinical features of liver cirrhosis have been linked to zinc deficiency, including loss of body hair, testicular atrophy, poor appetite, immune dysfunction, altered taste and smell, reduced vitamin A and thyroid hormone metabolism, altered protein metabolism, delayed wound healing, and diminished drug elimination capacity. One of the most interesting and novel aspects concerning the presumable role of zinc deficiency in producing clinical features of liver cirrhosis is the possible relationship between zinc and hepatic encephalopathy (HE). Long-term zinc supplementation in patients with HE improves neurological symptoms and metabolic parameters. In Wilson's disease, an inherited defect of hepatic copper, zinc is used for maintenance as well as treating presymptomatic, pregnant, and pediatric patients. Zinc may be involved in the pathogenesis of chronic hepatitis C. This work is an attempt to review the information available in this field to understand the important role that zinc plays in the pathogenesis and therapy of several liver diseases. J. Trace Elem. Exp. Med. 15:67À78, 2002.

show abstract

“…In chronic liver disease/cirrhosis, the sinusoid complex structure and microvascular exchange are impaired, which markedly decreases the sinusoid bioavailable zinc delivered to the hepatocytes. 46,47 In individuals that have early malignant and premalignant conditions, the decrease in zinc availability will exacerbate the decrease in the cellular uptake and accumulation of zinc; thereby eliminating the cytotoxic/suppressive effects of zinc on the developing malignant cells. We believe this is a plausible expectation and explanation of the role of zinc in the association of chronic liver disease/cirrhosis and HCC.…”

Section: The Implication Of Zinc In the Predisposition Of Hcc Developmentioning

confidence: 99%