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Fatty liver disease, also known as nonalcoholic hepatosteatosis, is a disease one-quarter of the entire population of the earth has but very few people have ever heard of. It is a major reason for liver transplantation and cause of heart to heart disease.

Here's an important question for diabetics. When you use insulin or insulin-stimulating drugs to get your blood sugar levels down, do you know where the blood sugar goes? Much of it gets stored as fat in your liver, and eventually fatty liver can cause its own health problems.

Medical researchers have come to realize that about one out of every four people in the entire world has nonalcoholic hepatosteatosis, also known as NASH, the accumulation of fat deposits in the liver that is not triggered by alcoholism. One of the liver's major contributions to the body's overall functions is energy storage. Your body keeps the equivalent of about 1000 to 2000 calories of ready energy in the form of glycogen. The liver combines glucose with water to make glycogen, and when the body needs energy and you can't eat, it turns the glycogen back into glucose with the release of water. Your muscles do the same thing. Without this storage mechanism, we would have to eat 24 hours a day. People who suffer a defect of this storage mechanism can literally die if they do not get to eat in the middle of the night.

There are limits to how much energy your liver can store as glycogen. After the liver sets aside an emergency store of ready energy, it turns sugars into fatty acids and fatty acids into triglycerides. In a way, the liver is acting as a fire extinguisher. Too much glucose in the bloodstream can interact with metals (copper, for instance) and become a kind of sticky "caramel" that coats red blood cells and neurons. If you are a diabetic, you probably get regular tests for this; it's called glycosylated hemoglobin. To keep this caramel from gunking up cells all over your body, your liver turns sugar into fatty acids and fatty acids into fat. However, not all fatty acids are equal. Here's the problem:

  • When your liver senses that your body isn't making (or, if you are a diabetic, you aren't injecting) a lot of insulin, it breaks down stored triglycerides into droplets of fatty acids that can escape through pores in the membranes of the cells that stored them. This gives your muscles a second source of energy when sugars run low.
  • When your liver senses a high level of insulin in your bloodstream, it locks triglycerides in place so your bloodstream won't be flooded with potentially "combustible" substances. it cannot break down these stored fats into droplets that are small enough to escape your cells.

Of course, the same thing happens with your body fat. The explanation of fatty liver causes is a little long, but here is the common problem in both obesity and fatty liver disease.

  • Fighting famine is the reason your liver cells and your body fat cells are programmed to hang on to triglycerides until the body absolutely, positively has to use them for energy. Fat cells and liver cells won't give up their fatty acids if they get hormonal signals that the body actually has more energy than it needs. In fact, the triglycerides inside fat cells are so bulky that they can't pass across the cell membrane to get back into the bloodstream to circulate to the muscles that would burn them.
  • The signaling chemical for fat cells is insulin. As long as there are high levels of insulin (the hormone the body uses to transport sugar into cells for energy), fat cells are more responsive an enzyme called lipoprotein lipase, commonly abbreviated LPL. This hormone activates a series of processes that literally make them suck fatty acids out of the bloodstream for storage.
  • At the same time LPL is changing the chemistry of fat cells so that they take fat out of the bloodstream and store it as triglycerides, insulin makes the muscles, which actually burn fat, less able to absorb fatty acids. LPL tells the body to burn sugar first. Fat cells don't actually respond to blood sugar levels (at least in this regard). They respond to blood insulin levels.
  • If your insulin levels are high, your body is poised to store every extra calorie as fat and your fat cells won't let fatty acids go. That is, unless something changes the balance of fatty acid storage and fatty acid release. Is all of this a little hard to follow? Here's the bottom line.
  • Anything that increases your insulin levels, like eating sugary foods, keeps fat locked in your fat cells until you have gone long enough without eating that your body absolutely, positively has to use body fat for energy. The more sugar you eat, the longer the effect lasts. And if you are a diabetic who takes medications that increase your body's production of insulin or you inject large amounts of insulin, you naturally tend to get fatter and fatter. Your liver will get fattier and fattier, too.

Why should you care?

Continue reading after recommendations

  • Chow WC, Tai ES, Lian SC, Tan CK, Sng I, Ng HS. Significant non-alcoholic fatty liver disease is found in non-diabetic, pre-obese Chinese in Singapore. Singapore Med J. 2007 Aug. 48(8):752-7. [Medline].
  • Park JW, Jeong G, Kim SJ, Kim MK, Park SM. Predictors reflecting the pathological severity of non-alcoholic fatty liver disease: comprehensive study of clinical and immunohistochemical findings in younger Asian patients. J Gastroenterol Hepatol. 2007 Apr. 22(4):491-7.
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