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JOURNAL the Problem of Fatty Liver Disease

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JOURNAL the Problem of Fatty Liver Disease ISSN: 2277- 7695 CODEN Code: PIHNBQ ZDB-Number: 2663038-2 Received: 21-12-2012 IC Journal No: 7725 Accepted: 26-02-2013 Vol. 2 No. 1 2013 Online Available at www.thepharmajournal.com THE PHARMA INNOVATION - JOURNAL The Problem of Fatty Liver Disease (FLD ) in Diabetics Dr Seema Mishra 1* 1. Professor, Department of Clinical Nutrition, Govt Bilasa Girls’s College, Bilaspur Chhattisgarh, India [E-mail: [email protected]] The diabetics are 50% more likely to develop liver disease. Particularly fatty liver disease. Fatty liver disease is incredibly common in overweight people (type II diabetics); nearly everyone with excess weight on their abdomen has some degree of fatty liver. Diabetics, specially Type II are prone to carrying excess weight on their abdomen, but even slim diabetics often have a fatty liver. The liver relevant all biochemical parameters were measured in diabetics and compared with the estimated parameters of non diabetics, a significant differences were noticed among both groups in relation with the enzymatic profile and hepato-proteins etc. It was concluded by this work that diabetics are extremely prone to develop fatty liver disease. Keyword: Steatohepatitis, Syndrome X, Hepatic enzymes, Prothrombin time, Albumin Introduction higher, insulin loses its ability to control blood It is well known that diabetes increases the risk of sugar levels. Therefore the blood sugar level kidney disease, nerve damage, blood vessel creeps upwards, eventually getting high enough damage, infections, blindness and heart disease, to qualify as diabetes. The vast majority of but even today it is not realized that diabetes have diabetics have a fatty liver. One do not need to be terrible adverse effects on the liver. Insulin overweight to have a fatty liver; the condition is resistance (syndrome X) is the driving force very common in slim people even. behind the development of fatty liver. Type 1 diabetes usually develops in childhood, although The Hepato-damaging Effect of Diabetes: The by the time they are in their mid 30s, most type 1 liver plays a central and crucial role in the diabetics have developed insulin resistance as regulation of carbohydrate metabolism. Its well in India. People with insulin resistance have normal functioning is essential for the high levels of insulin in their bloodstream. Insulin maintenance of blood glucose levels and of a signals to ones liver to manufacture fat, especially continued supply to organs that require a glucose triglycerides and cholesterol. This promotes the energy source. This central role for the liver in accumulation of fat inside the liver, inside other glucose homeostasis offers a clue to the organs, inside arteries and as general body fat pathogenesis of glucose intolerance in liver stores. As insulin levels become higher and `Vol. 2 No. 1 2013 www.thepharmajournal.com Page | 89 The Pharma Innovation - Journal diseases but little insight into the mechanisms of by first-pass extraction in the liver. Insulin liver disease in diabetes mellitus. promotes glycogen synthesis (glycogenesis) The liver uses glucose as a fuel and also has in the liver and inhibits its breakdown the ability to store it as glycogen and (glycogenolysis). It promotes protein, synthesize it from non carbohydrate cholesterol, and triglyceride synthesis and precursors (gluconeogenesis). stimulates formation of very-low-density Glucose absorbed from the intestinal tract is lipoprotein cholesterol. It also inhibits hepatic transported via the portal vein to the liver. gluconeogenesis, stimulates glycolysis, and Although the absolute fate of this glucose is inhibits ketogenesis. The liver is the primary still controversial, some authors suggest that target organ for glucagon action, where it most of the absorbed glucose is retained by promotes glycogenolysis, gluconeogenesis, the liver so that the rise in peripheral glucose and ketogenesis. concentration reflects only a minor Glucose that is taken up by a cell may be component of postprandial absorbed glucose. oxidized to form energy (glycolysis). It is Therefore, it is possible that the liver plays a oxidized to pyruvate in the cytosol, and more significant role than does peripheral electrons generated from this process are tissue in the regulation of systemic blood transferred to the mitochondria. Pyruvate glucose levels following a meal. generated by this Emden-Meyerhof pathway Many cells in the body, including fat, liver, is oxidized to acetyl CoA in the mitochondria, and muscle cells, have specific cell membrane which in turn undergoes further oxidation by insulin receptors, and insulin facilitates the the Krebs tricarboxylic acid cycle. Nearly 36 uptake and utilization of glucose by these moles of high energy phosphate are generated cells. Glucose rapidly equilibrates between from each molecule of glucose by aerobic the liver cytosol and the extracellular fluid. glycolysis. Transport into certain cells, such as resting If oxygen not be available, pyruvate is muscle, is tightly regulated by insulin, converted to lactate by the action of lactate whereas uptake into the nervous system is not dehydrogenase. Lactate is a potential fuel, or insulin-dependent. it may be converted back to glucose. The Glucose can be used as a fuel or stored in a formation of glucose from lactate and various macromolecular form as polymers: starch in non carbohydrate precursors is known as plants and glycogen in animals. Glycogen gluconeogenesis and occurs mainly in the storage is promoted by insulin, but the liver and kidneys. capacity within tissues is physically limited The liver, kidney, intestine, and platelets because it is a bulky molecule. contain the enzyme glucose-6-phosphatase, Insulin is formed from a precursor molecule, which produces glucose from glucose-6- pre-insulin, which is then cleaved to pro- phosphate and is the final step in the insulin. Further maturation results in the production of glucose via gluconeogenesis. conversion of proinsulin into insulin and a This enzyme is absent in other tissues. smaller peptide called C-peptide. Glucose that is metabolized peripherally may A small amount of pro-insulin enters the therefore be converted back to glucose or to circulation. It has a half-life 3–4 times longer hepatic glycogen via gluconeogenesis with than that of insulin because it is not lactate as the primary substrate. This is known metabolized by the liver. However, pro- as the Cori cycle. insulin has <10% of the biological activity of In type 2 diabetes, excessive hepatic glucose insulin. output contributes to the fasting Insulin is metabolized by insulinase in the hyperglycemia. Increased gluconeogenesis is liver, kidney, and placenta. About 50% of the predominant mechanism responsible for insulin secreted by the pancreas is removed this increased glucose output, while Vol. 2 No. 1 2013 www.thepharmajournal.com Page | 90 The Pharma Innovation - Journal glycogenolysis has not been shown to be have reported the combination also in obese increased in patients with type 2 patients. diabetes. Hyperglucagonemia has been shown Patients showing solely excessive glycogen to augment increased rates of hepatic glucose deposition may exhibit hepatomegaly and output, probably through enhanced liver enzyme abnormalities and may have gluconeogenesis. abdominal pain and even nausea and vomiting and rarely ascites. All these abnormalities Liver Disease Occurring as a Consequence of may improve with sustained glucose control. Diabetes Mellitus Fatty Liver, Steatohepatitis-Hepatic fat Glycogen-Deposition -Excess glycogen accumulation is a well-recognized accumulation in the liver is seen in 80% of complication of diabetes with a reported diabetic patients. Glycogen synthesis in the liver frequency of 40–70%. Unfortunately, is impaired in diabetes due to defective activation associated obesity is a frequently occurring of glycogen synthase. However, studies attesting confounding variable. Type 1 diabetes is not to this were usually performed on animals with associated with fat accumulation if glycemia recently induced diabetes. In patients with is well controlled, but type 2 diabetes may chronic diabetes, glycogen accumulation is seen, have a 70% correlation regardless of blood and it is postulated that long-standing insulin glucose control. deficiency may actually facilitate synthase Fat is stored in the form of triglyceride and activity. This and enhanced gluconeogenesis may may be a manifestation of increased fat account for the net accumulation of glycogen in transport to the liver, enhanced hepatic fat diabetes. synthesis, and decreased oxidation or removal The mechanism of cytoplasmic glycogen of fat from the liver. The steatosis may be deposition is uncertain but is perhaps related micro-vesicular or macro-vesicular and may to the large variations in glucose progress to fibrosis and cirrhosis. The degree concentration and frequent insulin dosing. No of glycaemic control does not correlate with correlation between hepatic glycogen content the presence or absence of fat. The most and fasting blood glucose levels has been common clinical presentation is demonstrated. There is also no demonstrable hepatomegaly, and most patients have normal association between the type of diabetes or or only mildly abnormal transaminases and the fat content of the hepatocytes and the normal bilirubin. presence of glycogen. The mechanism for nuclear glycogen Complications of Diabetes Therapy: Insulin deposition is also unclear, with the stored therapy may increase
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