Fatty liver - liver disorder

1. PRESENTED BY:
BINDU JACOB

2. INTRODUCTION
•Normal liver contains 4% as total lipids,
three-fourths of which is phospholipids
(PL) and one-fourths of which as neutral
fats (TG).
•This amount of lipid content in the liver
is the resultant of several influences,
some acting in conjuction with and some
in opposition to other.

3. FACTORS REGULATING FAT CONTENT
OF LIVER

4. • Normal levels of Lipids in the Liver are the result
of maintenance of a proper balance between
the above mentioned factors.
• A relative increase or decrease in the rate of
one or other of these processes can result in
accumulation of abnormal quantity of lipids in
the Liver, producing FATTY LIVER.

6. TYPES OF FATTY LIVER
• Type-1 Overfeeding of fat
• Type-2 Oversynthesis of fats from carbohydrates
• Type-3 Over mobilisation from depots to liver
• Type-4 Under mobilisation from liver to depots
• Type-5 Under utilisation in the liver

7. • Overfeeding of fats produce increase in circulating
chylomicrons:
• Liver can take up by pinocytosis, leading to increased TG in
Liver cells.
• Circulating chylomicrons are acted by Lipoprotein lipase,
which produces increase in FFA by hydrolysis of TG of
chylomicrons. Leads to influx of FFA in liver, synthesis of TG
is enhanced and formation and secretion of more VLDL.
• Lipids deposited in type-1, reflects the composition of
dietary Lipids.

8. Ingestion of carbohydrates in excess of caloric requirement, overloads the capacity
of the cells which normally store glycogen. Surplus carbohydrates are channeled to
synthesis of FA and TG (lipogenesis) in Liver and adipose tissue.
Plasma lipids: Increase in plasma TG ↑ and VLDL ↑, which in turn increases LDL level.
Causes: Oversynthesis from carbohydrates can result from:
1. Forced overfeeding of carbohydrates,
2. Experimentally,
• By administration of excessive amounts of certain B-vitamins viz. thiamine, riboflavin and biotin, and
• Administration of amino acid cystine.

9. • This type of fatty liver is referred as physiological fatty liver. This represents an
exaggeration of normal process, excessive mobilisation of FFA from depot to Liver. Liver
responds to increase synthesis of TG and VLDL and increases the plasma level of LDL.
• Causes: Fatty liver of this type develops in conditions involving greatly increased
utilisation of fats as “fuel” and where there is interference with oxidation of
carbohydrates. (Non-utilisation of carbohydrates for energy). Thus, it occurs in:
• Diabetes mellitus: Human or experimental of thehypoinsulin, hyperpituitary or
hyperadreno cortical type,
• Starvation and
• Carbohydrate deprivation.
• Owing to the non-utilisation of carbohydrates, adipose tissue cannot esterify FFA due to
lack of α-glycero-P, thus aggravating the hyperlipaemia. In addition to fatty liver and
hyperlipaemia, this condition is characterised by ketosis and in advanced cases acidosis.

10. • Fatty Liver of this type is designated as Pathological fatty liver. It is accompanied
by a decrease↓ in plasma lipids (hypolipaemia), which affects mainly PL and Ch-esters.
• The pattern of liver lipids is also abnormal, Fatty Livers of this type, if not treated,
eventuates in cirrhosis liver and there may be associated haemorrhagic lesions in
the kidneys.
• Causes: They appear to be caused by agents or conditions, which produce either
absolute or a relative deficiency in certain of the ingredients used by the Liver for
synthesis of VLDL. Such as the:
• Protein: Apoprotein itself or
• The building blocks of its structural lipid moieties, such as cholesterol esters and
PL viz. Inositol phosphatides, choline and the polyunsaturated FA
• Factors interfering with secretory mechanism.

11. • Causative agents: Fatty livers of Type-4 may be
roughly classified according to the causative
agent or phenomenon as follows:
• 1. Deficiency of EFA
• 2. Imbalance of Vitamin-B Complex Group

12. Type 5: Underutilisation in the Liver
1. It is possible that the fatty livers of pantothenic acid
deficiency are of this type, i.e underutilisation. Deficiency
of pantothenic acid leads to decrease↓ in availability of
CoA-SH. Hence, activation of FA and its oxidation suffers.
2. Poisoning by salts of rare earth elements (e.g. Cerium)
also appears to cause underutilisation, by inhibition of the
mitochondrial system which oxidises FA.

13. SYMPTOMS
Fatigue
Abdominal
discomfort
Poor appetite
Weakness
Tiredness

14. DIAGNOSIS
• Physical Exam
If the liver has become inflamed, your physician can detect it by examining the abdomen. An
extensive history may reveal fatigue or loss of appetite as well. A thorough history will include
alcohol use and other medications or supplements.
• Blood Tests
Higher than normal liver enzymes may be found on a routine blood test. This does not confirm a
diagnosis of fatty liver. Further analysis will look for the cause of inflammation.
• Ultrasound
The fat on your liver will show up as a white area on the image. Other imaging studies may be done
as well such as a CT (computed tomography) scan or MRI (magnetic resonance imaging). Imaging
studies can detect fat in the liver, but will not be able to confirm any further damage.
• Liver Biopsy
A needle is inserted into the liver to remove a piece of tissue for examination (after giving a local
anesthetic to lessen the pain). This is the only way to know for certain if you have fatty liver. The
biopsy will also help your doctor learn the exact cause.

15. TREATMENT