Hepatic steatosis or fatty liver (FL)is a distinct hepatic condition and one of the most common causes of chronic liver disease globally. Hepatic steatosis is divided into two parts: alcoholic liver disease and non-alcoholic fatty liver disease (NAFLD). In alcoholic liver disease, there is a build-up of scar tissue in the liver. NAFLD is more worse than simple fatty liver disease. It causes inflammation in the liver and it can damage to the liver cells. Worldwide, NAFLD has a reported prevalence of 35 percent. Prevalence of the disease is estimated to be 32% in the general Indian population, with a higher incidence rate amongst obese and diabetic patients. Another interesting trend noted is the increasing prevalence of NAFLD among pediatric age groups. Autopsy-based data showed that NAFLD prevalence among children aged 2–19 years to be 9.6% after adjustment for age, sex, race and ethnicity, and up to 38% in obese children.
Sources of fatty acids stored in liver
NAFLD is considered as a metabolic disorder that results from complex interaction between genetic, hormonal and nutritional factors. Recent evidence suggests that several genetic risk factors predispose to the development and progression of NAFLD. Obesity and its complications, especially type 2 diabetes and hypertriglyceridemia, are likely to be the main responsible of the current epidemic of FL, while alcohol intake plays an important role. In a nested case-control study of the Dionysos Project, study revealed that body mass index (BMI) was a stronger risk factor for FL than alcohol intake in the general population. Interestingly, this finding was confirmed by a recent study performed in China. Non-alcoholic fatty liver disease and non-alcoholic Steato-hepatitis (NASH) are both happened due to High levels of fats, particularly triglycerides, in the blood. Moreover Consumption of alcohol & excess calories in the diet (the excess caloric intake overwhelms the liver's ability to metabolize fat in a normal fashion, which results in fat accumulation in the liver).
Common findings in fatty liver disease
NASH represents the most severe histologic form of NAFLD, which is defined by fat accumulation in the liver exceeding 10% of its weight. Insulin resistance is related to obesity and is central to the pathogenesis of NAFLD. In addition, oxidative stress and cytokines are important contributing factors, together resulting in steatosis and progressive liver damage in genetically susceptible individuals. The disease can remain asymptomatic for years, or can progress to fibrosis, cirrhosis and hepatocellular carcinoma.
The mechanisms underlying alcohol & non-alcoholic induced hepatotoxicity are complex and multifactorial.
In fatty liver, there is increase in the activity of fatty acid synthase, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase), and sterol regulatory element-binding proteins (SREBPs) through the AMP-activated protein kinase (AMPK) pathway and downregulated the expression of carnitine palmitoyltransferase 1 (CPT1) and peroxisome proliferator-activated receptor alpha.
Adipose tissue lipolysis continues, even with hyperinsulinemia, because of the Insulin resistance that results in increased plasma Free fatty acid (FFA) concentration. Liver takes up the FFA in circulation, that is not oxidised gets stored in the liver in various forms or exported as very low-density lipoproteins.
In nutrition, high dietary intake of fructose and cholesterol are the risk factors that can predispose to non-obese NAFLD. The reduction in serum adiponectin concentrations were reported in Caucasians with lean NAFLD compared to controls in a recent report. Potential roles of various lysophosphatidylcholines, phosphatidylcholines, lysine, tyrosine and valine were revealed in these cases using metabolomics studies.
Protecting the liver is one of the best ways to prevent fatty liver and its complications. It can start by taking several steps in the direction of inhibiting the factors responsible for the liver damage such as Avoiding Alcohol can go a long way in protecting the liver as it is a hepatotoxic. Weight gain plays a damaging role in fatty liver, exercise can help in fat reduction of the patient. The case of high cholesterol, medicines to reduce high triglyceride can also be administered.
Makoi (Solanum nigrum) reduced blood triglyceride, sugar, and cholesterol levels, as well as fat accumulation, oxidative stress, and lipid peroxidation. The results indicated that Makoi downregulated the expression of fatty acid synthase, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase), and sterol regulatory element-binding proteins (SREBPs) through the AMP-activated protein kinase (AMPK) pathway and upregulated the expression of carnitine palmitoyltransferase 1 (CPT1) and peroxisome proliferator-activated receptor alpha.
Makoi & Chitrak help excretion of fecal cholesterol and phospholipids and prevent accumulation of cholesterol and triglycerides in liver and aorta. It's also lower down the Serum LDL, VLDL & total Cholesterol and also Cholesterol-phospholipid ratio. It brings progressive improvement in normalizing biochemical parameters (SGOT, SGPT, Serum cholesterol), exerts antiviral & immunomodulatory action.
Anti-oxidant plays an important role in protecting the vital organs including liver at subcellular level and by exerting free radical scavenging effect. Picroliv from Kutaki, Amla, Makoi, Kalmegh, and Tulsi show anti-oxidant activity by protecting hepatocytes against free radical-mediated inhibition of anti- oxidant enzymes.
Chitrak & kalmegh and punernava has pronounced choleretic effect stimulates secretion of bile juices thereby, bringing improvement in process of digestion of fat and fulfills the requirements of the nutrition required by the body.
Realizing this dire need Aimil pharmaceutical has launched a revolutionary formulation which fulfills all the objectives of management and prevention of liver disease. Amlycure D.S. is the desired strength, comprehensive polyherbal formulation with antioxidants and micronutrients Which gives pronounced effect in fatty liver, Lack of appetite, Hyperbillirubinaemia, Viral hepatitis (acute & chronic), Hepatotoxicity induced by Hepatotoxic drugs such as ATT & Chemotherapy Poor Liver Function Tests (LFT’s), Chronic alcoholism and Compromised immunity.