The goals and destinations of these tests, guided over the past 30 years, are a) how frequent alcohol consumption promotes folate deficiency and b) how folate deficiency contributes to the pathogenic production of alcoholic liver disease (ALD). The digestive assimilation of folic acid in hard-core drinkers was reduced, and, temporarily, alcohol care was taken in volunteers with low folate sludge. Weaned monkeys for two years developed low hepatic folate reserves, increased folic acid malabsorption, and prolonged urination of folic acid, known as decreased hepatic take-up. Micropygm contains alcohol for one y ALD-formed elements, concerning folate transporter motility and decreased digestion. Another review of ethanol in preserving micro pigs showed abnormal hepatic methionine and DNA nucleotide disorder and diffuse hepatocellular apoptosis. When alcohol conservation was associated with folate deficiency, the micro pig maintained standard histological components of the ALD at 14 weeks, with increased plasma homocysteine levels, decreased liver S-adenosylmethionine and glutathione, and increased DNA and lipid oxidation. Marker. In reduction, continued alcohol exposure weakens folate retention by suppressing the expression of reduced folate transporter and reducing hepatic intake of hepatic folate and kidney protection. At the same time, folate deficiency induces changes in hepatic methionine digestion due to alcoholism, while advanced oxidation further exacerbates the histopathology of liver injury and ALD.
Alcohol is a diet that provides 8 kcal / g and, as a reward, is the drug that almost 66% of Americans burn. Ongoing alcohol abuse affects 5% of the US population. These people burn more alcohol and are at risk for Alcoholic Liver Infection (ALD). Thoughts on the role of nutrition in the pathogenesis of ALD have ranged from the prevailing belief that alcohol is the sole pathogenic to the setting that alcohol is an essential component of the American eating routine. , Affects access to many supplements and hepatic digestion. For> 30 y, folate deficiency is a common medical sign of persistent alcohol abuse in this particular case. For example, low serum folate levels greater than 56 (80%) were found in 70 Boston heavy drinkers, and 33 (half) of 65 Seattle patients with ALD had a megaloblastic pallor.
Causes of folate deficiency in alcoholism
While dietary folate deficiency is common in neglected heavy drinkers, clinical trials and experiments with organic models demonstrate the significant effects of ongoing alcohol exposure on folate homeostasis in the body. Transiently, folate homeostasis involves a two-step cycle that initiates the hydrolysis of polyglutamyl dietary folate. The monoglutamil attachment is transported to the epithelial cells of the upper small gastrointestinal tract, ingested and digested, and enterohepatic. . Huh through the renal tube. Folate-clearing proteins dictate each of these cycles. Therefore, the digestion of dietary polyglutamyl folate requires brush line hydrolase, now known as glutamate carboxypeptidase (GCPII), and a reduced folate transporter (RFC) for transport in the brush line and basolateral films. Is required. Both folate-inhibitory protein (FBP) and RFC are involved in the restriction and transport of monoglutamyl folate, mainly 5-methyltetrahydrofolate (5-MTHF), in the liver plasma membrane and the renal tubule brush line films. Our research organization is engaged in research on these cycles and others affected by well-being and persistent alcohol abstinence.
Small digestive system
In preliminary clinical research from our research center using the Triple Lumen Tube Perfusion Strategy, [3 h] we found that the average gestational take-up of folic carcinogens was reduced to <20% in the form of alcohol addictions with late alcoholism and malnutrition. 35.% in contrast to alcohol withdrawal after two weeks and emergency clinic regimen. An upcoming review demonstrated that genital take-up at folate was observed in corrosive alcoholic volunteers [3h] for six weeks with a low-folate diet and alcohol mixture. In subsequent trials in the macaque monkey model, we observed folate deficiency. We lowered liver folate levels after consuming alcohol at half a kilocalories with the regular folate diet. We showed digestive malabsorption by 5-d waste discharge and reduced discharge in these monkeys. We then reduced the overall body maintenance of radioactive traces of the intragastric organization of folic acid in contrast to the [3 h] non-alcoholic benchmark group. These discoveries in wine led to the preservation of monkeys, as confirmed by others.
Liver intake and renal excretion
We focus on these components of folate homeostasis in similar macaque monkeys. After two years of postpartum care, further measurement of [3H] folic acid was inserted into each animal, and liver biopsies were obtained more than 4 d in a row from each pair. In preservative alcohol for monkeys, we tracked low hepatic folate and tritium fixation and amplified tritium discharge, which may have reduced, methylated, formulated, and polyglutamilated folate liver homogenate regular dimensions from each collection. These tests are recommended to reduce hepatic take-up and maintain excess folate in the alcoholic liver. However, intracellular folate digestion is not affected. After four years of follow-up care, similar monkeys [3H] received another tracer fraction of folic carcinogen. Radioactivity was measured in the stool every day in the discharge classification and below 25 d. Both urine and waste tritium discharge in alcohol are diffuse, prions are observed during the initial trimester. However, the long-term velocity of tritium discharge does not change, and terminal liver tritium and folate levels are essentially low. Determining low hepatic take-up or potential folic acid maintenance in wine, these studies have suggested that total folate reduction may partly be due to reduced renal round reabsorption. Others exhibited diffuse urinary folate discharge in patients with persistent alcoholism and the care of alcoholic rats.
In short, continuous alcohol exposure weakens folate intake by inhibiting the activation of reduced folate transporter and reducing hepatic intake of incoming folate and renal protection.