Fatty liver?

[Guest guest]

Just got the results of my annual checkup: have

something called a " fatty " or enlarged liver. This is

a condition seen among alcoholics and obese people -

but since I don't drink and I'm not obese, the doctors

are puzzled as why I have a " fatty " liver. (They're

running blood tests now to see if I've ever had

hepatitis).

The doctor I spoke with said this condition is not

really dangerous, and there is no cure. Anybody

familiar with this condition? Any dietary suggestions

for improving liver function? Found a few web sites on

the topic, but am unsure which offer solid info, and

which are by quacks.

Thanks,

__________________________________________________

[Guest guest]

----- Original Message -----

From: " Rand " <rand_peter2@...>

< >

Sent: Friday, July 06, 2001 6:56 PM

Subject: [ ] Fatty liver?

> Just got the results of my annual checkup: have

> something called a " fatty " or enlarged liver. This is

> a condition seen among alcoholics and obese people -

> but since I don't drink and I'm not obese, the doctors

> are puzzled as why I have a " fatty " liver. (They're

> running blood tests now to see if I've ever had

> hepatitis).

Hi ,

Suggest you checkout:

http://www.merck.com/pubs/mmanual_home/sec10/117.htm

Known Causes of Fatty Liver

Obesity

Diabetes

Chemicals and drugs (such as alcohol, corticosteroids, tetracyclines, valproic

acid, methotrexate, carbon tetrachloride,

and yellow phosphorus)

Malnutrition and a diet that is deficient in protein <<<<<<<<<<

Pregnancy

Vitamin A toxicity

Bypass surgery of the small intestine

Cystic fibrosis (most likely accompanied by malnutrition)

Hereditary defects in glycogen, galactose, tyrosine, or homocystine metabolism

Medium-chain aryldehydrogenase deficiency

Cholesterol esterase deficiency

Phytanic acid storage disease (Refsum's disease)

Abetalipoproteinemia

Reye's syndrome

http://www.merck.com/pubs/mmanual/section4/chapter39/39a.htm

Fatty liver (hepatic steatosis):

Excessive accumulation of lipid in hepatocytes, the most common response of the

liver to injury.

The liver occupies a central position in lipid metabolism. A small, rapidly used

pool of free fatty acids (FFAs),

absorbed from the diet or released into the blood from chylomicrons or fat

cells, accommodates almost all of the energy

requirements of a fasting animal. FFAs are taken up by the liver to join the

hepatic pool of FFA, a portion of which the

liver synthesizes. Some FFAs are oxidized to CO2 in the liver for energy, but

most are rapidly incorporated into complex

lipids (eg, triglycerides, phospholipids, glycolipids, cholesterol esters). Some

of these complex lipids enter a slowly

used pool that comprises the structural lipids of liver cells and their storage

site. Most triglycerides enter an active

pool where they combine with specific apoproteins to form lipoproteins (eg, very

low density lipoproteins [VLDLs]),

which are secreted into plasma. The liver is also responsible for lipid

degradation (eg, low density lipoproteins,

chylomicron remnants).

Fatty liver occurs when lipid accumulation exceeds the normal 5% of liver

weight. In the macrovesicular type, large fat

droplets balloon the liver cell, displacing the nucleus to the periphery of the

cell, like an adipocyte. Triglyceride

accumulates most commonly because it has the highest turnover rate of all

hepatic fatty acid esters. Liver uptake of FFA

from adipose tissue and the diet is unrestrained, whereas FFA disposition by

oxidation, esterification, and VLDL

secretion is limited.

In microvesicular fatty liver, small fat droplets accumulate, cells appear

foamy, and nuclei are central. Triglycerides

collect in subcellular organelles (eg, endoplasmic reticulum), reflecting

widespread metabolic disturbance.

Mitochondrial injury limits FFA oxidation, while apoprotein synthesis necessary

for VLDL secretion is depressed, leading

to triglyceride accumulation.

In phospholipidosis, phospholipids accumulate in association with certain drug

use (eg, amiodarone). Liver cells are

large and foamy.

http://www.cpmc.org/liver/topic_fat.htm

Nutritional causes of fatty liver include starvation, obesity, protein

malnutrition and intestinal bypass operations for

obesity. For obese patients, the fatty deposits can be accompanied by some

inflammatory changes and mild to severe

scarring of the liver.

http://www.ttuhsc.edu/pages/students/medscbu/MyRock/aametabolism.htm

Conversion of carnitine from lysine; inability to synthesize it leads to high

serum fatty acids without ketosis; fatty

liver and muscles

http://www.ttuhsc.edu/pages/students/medscbu/MyRock/knowbiochem.htm

Lysine is precursor of carnitine (shuttles FA into mitochondria)

Carnitine deficiency leads to high serum FA without ketosis and fatty liver and

muscles

Creatinine is spontaneously formed excretory product of creatine (CLINICALLY

IMPORTANT IN RENAL FUNCTION!!!)

Hope this helps,

Greg