Fatty Liver. Fatty liver is an abnormal condition characterized by increasing deposition of lipids, mainly T.G. in the liver cells.

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1 Fatty Liver Fatty liver is an abnormal condition characterized by increasing deposition of lipids, mainly T.G. in the liver cells. When accumulation of lipid becomes chronic, fibrotic changes occur in the cells, which progress to cirrhosis and impaired liver function.

2 Fatty Liver Normal fat content of the liver is about 5% of its weight and is mainly phospholipids but in fatty liver it may reach 20-30% and is mainly in the form of neutral fat.

3 Causes of fatty liver: 1. Increased fat in diet, increased uptake of fats by liver if this exceeds the capacity of thr liver to synthesis VLDL fatty liver. 2. Over feeding carbohydrate (COH) overload the capacity of the liver to store it as glycogen converts CHO to TG, if this exceed the capacity of the liver to synthesize VLDL fatty liver.

4 3. Decreased oxidation of FA directs fatty acids to esterification (TG). This decreases fatty acid oxidation occurs in the following condition. i. Deficiency of pantothenic acid. ii. iii. Deficiency of carnitine (choline deficiency). Alcoholism, alcoholic fatty liver is caused by:

5 A. Decreased FA oxidation as a result of oxidation of ethanol to acetaldehyde leading to NADH/NAD ratio. B. Increased fatty acid synthesis. Alcohol dehydrogenase CH 3 CH 2 OH ethanol CH 3 CHO Acetaldehyde NAD NADH+H +

6 4. Increased mobilization of fat from adipose tissue to liver cell. This occurs in conditions characterized by decrease carbohydrate utilization e.g. D.M., starvation. 5. Decreased mobilization of fat from liver to blood. TG synthesized in the liver are normally mobilized to blood by VLDL. Failure to synthesize VLDL may be caused by decreased protein synthesis (apolipoprotein), failure in conjugation or failure in secretory mechanism. Decreased mobilization associated with deficiency of lipotropic factors. 4. Liver poisons e.g. chloroform puromycin and carbon tetrachloride decreased protein synthesis.

7 Lipotropic Factors: These are substances that protect against and cure fatty liver. They include mainly the substances essential for phospholipids synthesis. Phospholipids are easily mobilized from liver and less liable to deposition in liver cell.

8 These substances are: 1. Choline lecithin, choline plasmalogen, sphingomyleine. 2. Methionine required for choline synthesis. 3. Folic acid and B12 transfer of CH3 group (transmethylation). 4. Inositol phosphatidyl inositol.

9 4. Essential FA required in position 2 of phosphoglyceride. Deficiency of essential FA results from intake of excess cholesterol. 4. Vitamin E & selenium: Protect FFA against oxidation and peroxide formation. 4. Adequate diet provides high protein, essential and vitamins.

10 Role of Adipose Tissue in Lipid Metabolism

11 Role of Adipose Tissue in Lipid Metabolism Adipose tissues carry all metabolic process of any active tissues. Calories are stored in it as triglycerides. The triglycerides of adipose tissue are continually undergoing hydrolysis (Lipolysis) and reesterification.

12 Role of Adipose Tissue in Lipid Metabolism The resultant of these two processes determines the amount of FFA released from adipose tissue into blood. The glycerol liberated from the hydrolysis can not be utilized by fat cell due to deficiency of glycerol kinase enzyme so it passes to blood.

13 Thus insulin and a diet rich in carbohydrates help the reesterification of FAA and decrease their release into the blood by increasing the uptake and oxidation of glucose by adipose tissue. Fasting glucagon, adrenaline glucocorticoids and growth hormone have the opposite effect.

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15 Insulin and a diet rich in carbohydrates and fat Fasting glucagon, adrenaline, glucocorticoids and growth hormone have the opposite effect.

16 Metabolism of adipose tissue The hydrolysis of triacylglycerol (lipolysis) is under the control of the enzyme hormone-sensitive triacylglycerol lipase. This enzyme may exist in one of two forms: An active form lipase a which is phosphorylated, and an inactive form lipase b which is dephosphorylated.

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18 camp

19 activated by adrenaline, noradrenaline glucagons, ACTH, TSH, MSH Thyroxine increases the sensitivity of adenyl cyclase to hormones by increasing the membrane receptors. Increasing Lipolysis Growth hormone (GH) augmenting the synthesis of adenyl cyclase

20 inhibited by insulin, prostaglandin E, and nicotinic acid. camp is hydrolyzed to 5 AMP by the enzyme phosphodiesterase.

21 inhibited by insulin, prostaglandin E, nicotinic acid. activated by adrenaline, noradrenaline glucagons, ACTH, TSH, MSH,thyroxine, growth H.

22 Hormones that Regulate fat Mobilization: The rate of release of FFA from adipose tissue is affected by many hormones that influence either rate of esterification or rate of lipolysis. Insulin reduces the output of FFA from adipose tissue by: A. Help reesterification of FA released in adipose tissue. B. Inhibit activity of hormone- sensitive triglyceride lipase reduce release of FFA and glycerol.

23 Insulin enhances lipogenesis and synthesis of triglycerides by: A. It increases transport of glucose into the cell (e.g. in adipose tissue) and stimulates glycolysis pyruvic, glycerol 3 PO4, also stimulates HMP shunt NADPH+H+. B. Insulin increase activity of pyruvate dehydrogenase, acetyl-coa carboxylase and glycerol-phosphate acyl transferase, these three enzymes are regulated by covalent modification i.e. by phosphorylationdephosphorylation mechanism.

24 Several hormones promote lipolysis, these include epinephrine, norepinephrine, glucagons, ACTH, MSH, TSH, GH.

25 Role of liver in Lipid Metabolism facilitating the digestion and absorption of fats by the production of the bile salts. Plays a central role in the metabolism of various types of TG, steroids, phospholipids, plasma lipoproteins and fat soluble vitamin.

26 A. Role in triglyceride and fatty acid metabolism: Uptake: After meals, the liver takes up about 30% of the free fatty acids and most glycerol of absorbed fat. Synthesis: A carbohydrate- rich meal, the liver converts part of the absorbed sugar into triglycerides. The liver reesterifies the free fatty acid, released from adipose tissue or resulting from the hydroysis of absorbed fats during fasting and after feeding of fat, into triacylglycerol.

27 Mobilization: Triacylglycerols synthesized in the liver are mobilized to the blood in the form of VLDL. Oxidation: The FFA and glycerol are partly oxidized by the liver to supply energy. Ketogenesis: During starvation, FFA are released from adipose tissue, are taken up by the liver (30%) oxidized to acetyl-coa which is largely converted to ketone bodies. Ketone bodies go via blood to extra hepatic tissues where they become oxidized to CO2 and H2O.

28 Desaturation: Liver is the main site of desaturation of FA. Gluconeogenesis: The glycerol released into the blood from adipose tissue or resulting from the hydrolysis of absorbed fats is largely to taken up by the liver where it is converted to glucose. The terminal 3 C of odd chain FA are also converted to glucose in the liver.

29 B. Role in phospholipids metabolism: The liver is the principle organ, which adds and removes phospholipids from the blood plasma. This function is related to the secretion and uptake of the plasma lipoprotein HDL, LDL and VLDL.

30 C. Role in steroid metabolism: The liver is a major site for cholesterol synthesis and important source of plasma cholesterol. It also removes cholesterol from the blood and converts cholesterol to 7 dehydrocholesterol (for further conversion to vitamin D3) and to bile acids (for secretion into bile). C. Role in metabolism of plasma lipoproteins The liver plays a very important role in the metabolism of different types of plasma lipoproteins.

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