Nonalcoholic fatty liver disease (NAFLD) is a medical and chronic liver condition associated with fat accumulated over time, without the presence of excessive alcohol use.
NAFLD can be classified into non-inflammatory fatty liver (NAFL) and inflammatory nonalcoholic steatohepatitis (NASH).
Untreated Nonalcoholic fatty liver disease (NAFLD) has been found to induce cirrhosis, a major cause of liver cancer.
According to world statistics, nonalcoholic fatty liver disease (NAFLD) is normally known as a disease of the Western world. However, today, due to the economic prosperity of Southeast Asia over the past few decades,, the disease also was found in a large number of populations in the cities, causing concerns of many scientists in the region.
The prevalence rate of non-alcoholic fatty liver disease (NAFLD) among the more affluent regions of China, is approximately 15%. The number may decrease substantially if the poor rural populations where obesity is non-existence are also taken into account.
In the US, over 100 million people have non-alcoholic fatty liver disease and the condition is more doubled over the past 20 years. Today, the disease also is also prevalent in liver disease in children.
Most people at the early stage of NAFLD are asymptomatic. However, as the disease progresses into the later stage, most patients experience symptoms of right upper abdominal discomfort, fatigue, and/or malaise, and jaundice(20) with yellowing of the skin and eyes.
The exact causes of NAFLD are not identified. Some researchers suggested that certain risk factors such as long-term use of certain medications, genetic preposition, insulin resistance, high cholesterol and triglycerides, polycystic ovary syndrome, metabolic syndrome, obesity, and type 2 diabetes are associated with the onset of the disease.
Some researchers suggested that an unhealthy diet such as the promotion of a high-fat diet in the Western world over the last few decades may also have a strong implication on NAFLD.
Dr. Jensen VS, the lead scientist in the study of high-fat diet-induced non-alcoholic fatty liver disease, wrote, "In humans and animal models, excessive intake of dietary fat, fructose, and cholesterol have been linked to the development of non-alcoholic fatty liver disease (NAFLD)".
And, " Only HFr-fed rats developed dyslipidemia as characterized by higher levels of plasma triglycerides compared to all other groups (p < 0.0001). Hepatic dysfunction and inflammation were confirmed in HFD-fed rats by elevated levels of hepatic MCP-1 (p < 0.0001), TNF-alpha (p < 0.001), and plasma β-hydroxybutyrate (p < 0.0001), and in NASH-fed rats by elevated levels of hepatic MCP-1 (p < 0.01), increased hepatic macrophage infiltration (p < 0.001), and higher plasma levels of alanine aminotransferase (p < 0.0001) aspartate aminotransferase (p < 0.05), haptoglobin (p < 0.001) and TIMP-1 (p < 0.01) compared to Control".
Lycopene is a phytochemical in the class of carotenoids, a natural pigment with no vitamin A activity found abundantly in tomatoes and other red fruits and vegetables, such as red carrots, watermelons, and papayas,
Tomatoes provide about 80% of the lycopene in the world's diet. In plants, lycopene protects the host against excessive photodamage and performs various functions in photosynthesis.
In finding a potential compound for the prevention of alcoholic fatty liver disease, researchers evaluated the effect of lycopene (LYC) on chronic or excessive alcohol intake-related liver injury.
Lycopene inhibited the expression of cytochrome P450 2E1 (CYP2E1) enzyme associated with chronic and excessive alcoholic drinking.
Where cytochrome P450 2E1(CYP2E1) not only represents the major enzymes in the CNS that catalyze ethanol oxidation but also plays a vital role in alcohol, drug, toxin, lipid, and carcinogen metabolism associated with reactive oxygen species-induced oxidative stress that promotes hepatocyte injury and death.
In other words, excessive alcohol drinking induced the production of free radicals that lead to liver damage in the initiation of inflammation, fibrosis, and lipid peroxidation.
More precisely, lycopene prevented liver injury in the induction of alcoholic fatty liver disease by targeting the expression of CYP2E1 induction.
Taken together, lycopene found in tomatoes may be considered supplements for the prevention and treatment of alcoholic fatty liver disease, pending the confirmation of the larger sample size and multicenter human study.
Intake of lycopene in the form of supplements should be taken with extreme care to prevent overdose acute liver toxicity.
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the Karate GB Daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as the international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) Lycopene Improves Diet-Mediated Recuperation in Rat Model of Nonalcoholic Fatty Liver Disease by Piña-Zentella RM1, Rosado JL1, Gallegos-Corona MA2, Madrigal-Pérez LA3, García OP1, Ramos-Gomez M. (PubMed).
(2) Tomato lycopene prevention of alcoholic fatty liver disease and hepatocellular carcinoma development by Stice CP1, Xia H1, Wang XD. (PubMed)
(3) The Herbal Medicines Which Treat Non-Alcoholic Fatty Liver Disease (NAFLD) Naturally, According to Studies by Kely J. Norton
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