Fatty Liver (cont.)
In this Article
What causes NAFLD and NASH?
The exact cause of NASH is still unknown. Strong
evidence, however, supports the concept that the process common to all stages of
primary fatty liver disease (NAFLD) is insulin-resistance. A number of other
factors may be involved as well in causing NAFLD and NASH and in progressing
through the stages of NAFLD.
What is insulin resistance and how does it relate to NAFLD?
Insulin
resistance is a state wherein normal signaling pathways that convey biochemical
messages between insulin and its target cells are disrupted. As a result, the
insulin does not exert its normal or full effects. Put another way, the body is
resistant to the effects of insulin.
What does insulin normally do? Well, the pancreas secretes varying amounts of
insulin during the day in response to food intake. Insulin works to maintain
blood sugar (glucose) at normal levels. Thus, insulin prevents blood glucose
from becoming too elevated. If insulin does not work in this way, high blood
sugars and diabetes would occur. Insulin is a hormone that acts on the receptors
of cells to trigger the complex biochemical reactions that control blood sugar.
The cells targeted by insulin are mainly the fat cells (adipocytes), muscle
cells (striated myocytes), and the liver cells (hepatocytes).
In insulin resistance, a defect in these insulin receptors causes insulin to
be less effective than it normally would be. Thus, the pancreas must produce
more insulin than normal in order to maintain normal blood glucose levels.
Initially in this process, the increased insulin levels are sufficient to
maintain normal blood glucose. In these patients, however, although the blood
glucose is normal, the condition of being overweight or obesity are still clues
that they are insulin resistant. At this juncture, only sophisticated blood
tests (such as the euglycemic clamp test) can detect insulin resistance at the
biochemical level.
As the insulin resistance progresses, even very high levels of insulin become
ineffective. This degree of insulin resistance leads to elevated blood sugars
and diabetes mellitus, type 2 (DM2). DM2 is usually managed by diet, exercise,
and medication (see treatment section) that increases insulin sensitivity (the
opposite of insulin resistance). If the process proceeds unchecked, however, the
pancreas can no longer secrete insulin. Then, the patients require insulin
injections, which condition is referred to as insulin-dependent DM2. Insulin
resistance and DM2 are very different from diabetes mellitus type 1 (DM1), which
is also called juvenile-onset diabetes. In DM1, a defect in insulin secretion
occurs early on in life and requires immediate and ongoing treatment with
insulin.
Insulin resistance can also surface early in life when it is due to
congenital genetic abnormalities in the insulin receptors. More often, however,
as described above, it becomes evident later in life as a result of acquired
obesity. A sedentary lifestyle and a diet rich in carbohydrates, sugars, and
fats also promote insulin resistance. Moreover, the degree of insulin resistance
increases with a greater BMI and abdominal fat (that is, big waists). Elevated
lipids (LDL cholesterol and triglycerides) are also associated with insulin
resistance.
Insulin resistance leads to changes in the processing (metabolism) of sugar
(glucose) and fat (lipid) in the liver, muscles, and fat cells (adipocytes). The
result of these changes is an increased uptake (infiltration and accumulation)
of triglyceride fat into the liver cells. The triglycerides are absorbed from
the diet as well as channeled from abdominal fat and peripheral muscles. These
large quantities of triglyceride fat are then stored in tiny sacs (vesicles)
inside the liver cells.
So, this is how a fatty liver develops. In fact, it has been shown that as
the BMI increases, so does the amount of fat in the liver.
Next: How does insulin resistance relate to NASH? »
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