all kinds of important things happen in a healthy liver, including d3 hydroxylation to 25(OH)d3, and conversion of ammonia (from amino acid breakdown) to uric acid (which requires adequate zinc).
here's a bunch of stuff. with tie in for LC. i think i also posted some relevant trace element links to venous insufficiency on the ccvi thread.
Quote:
To investigate the effect of trace element concentrations in liver disorders, we conducted tests comparing the concentrations of trace elements among patients at various stages of chronic liver disease, and found a significant correlation between trace element metabolism and disease presence and progression. There is also a correlation between serum trace element concentrations and metalloprotein concentrations in the body, imbalances in which play a role in chronic liver disease. Excess or deficiency can be rectified for improvement of chronic liver disease. Because trace element concentrations are markers of oxidative stress levels in the liver, analysis of the concentrations can also be used for diagnosis of liver disease as well as indicating the effectiveness of antioxidant therapy.
Quote:
The association between liver cirrhosis and variations of glucose tolerance has been extensively documented and discussed. Zinc is an essential trace element necessary for normal protein metabolism, for the function of more than 200 zinc metalloenzymes, and for a host of physiologic functions. A poor zinc status is common in both liver cirrhosis and diabetes mellitus. Many of the clinical features of liver cirrhosis and diabetes mellitus have been linked to zinc deficiency. Zinc supplementation improved in patients with liver cirrhosis and hepatic encephalopathy with and without diabetes mellitus neurological symptoms and signs of malnutrition. Furthermore, zinc supplementation increased glucose disposal.
Summarising these facts, we hypothesise that zinc deficiency is a link between liver cirrhosis and the “liver” diabetes mellitus.
Quote:
Organisms that cannot easily and quickly remove ammonia usually have to convert it to some other substance, like urea or uric acid, which are much less toxic. Insufficiency of the urea cycle occurs in some genetic disorders (inborn errors of metabolism), and in liver failure. The result of liver failure is accumulation of nitrogenous waste, mainly ammonia, which leads to hepatic encephalopathy.
Quote:
In North America, suboptimal zinc status is more common than once realized. ...marginal zinc deficiency increased the susceptibility to LPS-induced liver injury in rats. These results indicate that patients with sepsis who have suboptimal zinc nutrition status may be at higher risk of developing greater liver damage.
Quote:
The total soluble ammonia level in a healthy adult with 5 L of circulating blood is only 150 mcg, in contrast to approximately 1000 mg of urea nitrogen present. Because urea is the end product of ammonia metabolism, the disparity in blood quantities of the substrate and product illustrates the following 2 principles:
* The CNS is protected from the toxic effects of free ammonia.
* The metabolic conversion system that leads to production of urea is highly efficient.
Quote:
The serum zinc levels were inversely correlated with blood ammonia in the fasting state.
Quote:
Zinc deficiency is common in patients with end-stage liver disease but its prevalence and resolution in liver transplant recipients has not been reported. We hypothesized that with normalization of liver function after transplant, zinc levels should rapidly return to normal, obviating the need for oral supplementation... Thirty-two of the 34 patients (94%) had a zinc level in the subnormal range. There were no differences in zinc levels between patients with alcoholic and non-alcoholic liver failure, males versus females, UNOS status (low = status 1 and 2, high = 3 and 4), pre-transplant use of TIPS nor correlation between age and zinc level. All 22 patients who had a post-transplant zinc level demonstrated an increase from 40.1±9.7 μg/dl to 68.5±14.1 μg/dl (p≤0.0001, paired t-test). Our findings indicate that zinc deficiency, generally profound, should be assumed to be present in every patient with end-stage liver disease awaiting transplant... Following transplantation, zinc levels rapidly recover, obviating the need for checking levels and oral supplementation.
Login
Register
FAQ
Search
