TYPE 2 DIABETES FATTY LIVER The liver lies at the nexus of food energy storage and production. After absorption through the intestines, portal circulation delivers nutrition’s direct to the liver.
No wonder that, since body fat is essentially a method of food energy storage, diseases of fat storage involve the liver intimately.
Remember that all fats are not created equal. Excess dietary fat bypasses the liver and can be stored anywhere in the body. Fat carried under the skin(subcutaneous fat) contributes to overall weight and body mass index but has minimal health consequences. It is cosmetically undesirable but seems to be otherwise metabolically innocuous.
Excess dietary carbohydrates and protein are stored first in the liver as glycogen. Once glycogen stores are full, *DNL converts glucose to fat, which can then be exported out of the liver to the rest of the body, including to fat stores in and around the abdominal organs. When *DNL exceeds the export capacity of the liver, fat accumulates in the liver, where it contributes to central obesity and has dangerous health consequences. Too much sugar and insulin, over too long a period of time, leads to fatty liver.
Eventually, the overfilled, fatty liver becomes unable to accept any more glucose and starts becoming insulin resistant.
The cycle proceeds as follows:
Hyperinsulinemia causes fatty liver
Fatty liver causes insulin resistance
Insulin resistance leads to compensatory hyperinsulinemia
Fat inside the liver, rather than overall obesity, is the crucial stepping stone toward insulin resistance and diabetes. Fatty liver is associated at all stages of insulin resistance from obesity to pre-diabetes to full-blown diabetes. And that relationship holds in all racial groups and ethnicities.
Fatty liver is the clearest sign that hyperinsulinemia and insulin resistance is developing, and one of the earliest. Fatty liver precedes the clinical diagnosis of type 2 diabetes by ten years or more. As the liver slowly accumulates fat it becomes increasingly insulin resistant. Fatty liver can be diagnosed by ultrasound, but an increased waist circumference or waist-to-height ratio is an important clue to its presence. Blood markers of liver damage also often mirror that slow rise, and this phase has been termed “the long, silent scream from the liver”.
Two main types of fatty liver exist:
- alcohol-related liver disease
- non-alcoholic fatty liver disease.
The first is associated, as the name suggests, with drinking too much alcohol. Since most alcohol is metabolized solely in the liver, too much too often forces the body to deal with the overflow. The result is a fatty liver. But a lot of people who develop fatty liver disease and diabetes are not alcoholics, and it’s only recently that scientists have begun to understand the connection.
Read more about >> Non-alcoholic fatty liver disease (NAFLD)
How fatty liver develops
“ Here’s a startling fact: I can give you fatty liver. Actually, I can give anybody fatty liver”
What is the scariest part? This crucial first step toward type 2 diabetes only takes three weeks.
Excessive glucose and insulin drive new fat production *DNL. If this occurs faster than the liver can export it out to the adipocytes (fat cells), fat accumulates in the liver. This condition can be achieved simply by overeating sugary snacks. Hey presto, fatty liver disease.
Researchers fed overweight volunteers an extra thousand calories of sugary snacks daily in addition to their regular food consumption. This sounds like a lot, but it only means ingesting an extra two small bags of candy, a glass of juice, and two cans of Coca-Cola per day. After three weeks, body weight increased by a relatively insignificant 2%. However, liver fat increased by a whopping 27%, caused by an identical increase in the rate of DNL. This fatty liver was far from benign, as blood markers of liver damage increased by a similar 30%.
But all was not lost. When volunteers returned to their usual diets, their weight, liver fat, and markers of liver damage all completely reversed. A mere 4% decrease in body weight reduced their liver fat by 25%.
Fatty liver is a completely reversible process. Emptying the liver of its surplus glucose and dropping insulin levels returns the liver to normal. Hyperinsulinemia drives DNL, which is the primary determinant of fatty liver disease. Normalizing insulin levels reverses the fatty liver. Refined carbohydrates, which cause a large increase in insulin, are far more sinister than dietary fat. High carbohydrate intake can increase DNL tenfold, whereas high-fat consumption, with correspondingly low carbohydrate intake, does not change hepatic fat production noticeably.
Specifically, the sugar fructose, rather than glucose, is the main culprit, even though fructose does not produce insulin response. In one of my next posts, I will explain why in more detail.
Producing fatty liver in animals is simple, too. The delicacy known as foie gras is the fatty liver of a duck or a goose. Geese naturally develop large fatty livers to store energy in preparation for the long migration ahead, but more than a thousand years ago the Egyptians developed a technique known as gavage. Originally done by hand, this deliberate overfeeding is now administered using more modern and efficient methods. A large amount of high-starch corn mash is fed directly into goose or duck’s digestive system several times per day through a tube called an embuc. In just ten to fourteen days, the liver becomes fatty and enlarged.
Producing foie gras in animals and fatty liver in humans is basically the same process. Deliberate carbohydrate overfeeding provokes the high insulin levels necessary to develop fatty liver. In 1977, the Dietary Guidelines for Americans strongly advised people to eat less fat and more carbohydrates, such as bread and pasta. The result? Dramatically increased insulin levels. Little did they know that they were, in essence, making human foie gras.
Fatty liver is the harbinger of insulin resistance, but it is only the beginning. The fat within organs, including the skeletal muscles and the pancreas, also plays a leading role in this disease.