The Xu study found an incredible amount of glycation, the hallmark of
"diabetes," with arachidonic acid. I've posted it many times before.
There was a sciencedaily.com report today (below) about diabetes and
mitochondrial dysfunction. The mitochondria damage ususally occurs
with excessive oxidative stress, usually due to too much dietary
polyunsaturated fatty acids. If the milk is homogenized, there will be
more oxidative stress. If you heat it too much, there will be more
oxidative stress, if you don't buy whole milk, there will be more
oxidative stress, and so on. But it's the highly unsaturated oils and
meats cooked while exposed to air that are probably doing much more
damage than anything else. Why don't these snake oil salesmen (who are
now mostly fish oil salesmen) tell you this? Because it's a bit more
complicated than the average person can handle, these chanlatans need
something simpler, so they generate these phrases that have no
scientific merit whatsoever. I, on the other hand, want to see the
scientific foundation for any claim. If you go to pubmed.com and
search for arachidonic inflammation, for example, you will see what is
probably the biggest problem in health today (in nations like the USA).
That is, the highly unstable arachidonic acid is at terribly high
levels in most peoples' tissues, leading to the "epidemics" of "chronic
disease" we are witnessing these days.
8/24/2005
Type 2 Diabetes: Problems In The Furnace
A detectable decline in energy production by mitochondria - the
organelles that are the cell's furnace for energy production - seems
to be a key problem leading to insulin resistance, and thus to type 2
diabetes, according to studies by Howard Hughes Medical Institute
researchers.
The research team said that insulin resistance - an impaired response
to the presence of insulin - is detectable as early as 20 years
before the symptoms of diabetes become evident. In fact, insulin
resistance is now seen as the best predictor that type 2 diabetes will
eventually develop, said the study's senior author, Gerald I. Shulman,
a Howard Hughes Medical Institute investigator at the Yale University
School of Medicine.
In the new study examining how insulin interacts with the
energy-producing mitochondria inside living cells, Shulman and his
colleagues found that the rate of insulin-stimulated energy production
by mitochondria is significantly reduced in the muscles of lean,
healthy young adults who have already developed insulin resistance and
who are at increased risk of developing diabetes later in life.
"This is further evidence that people who are prone to develop
diabetes have signs of mitochondrial dysfunction," Shulman said in an
interview. This is important because mitochondria are the "energy
factories" inside cells and produce most of the chemical power needed
to sustain life.
The new research, which is published in the September 2005 issue of the
open-access journal PLoS Medicine, indicates that a decreased ability
to burn sugars and fats efficiently is an early and central part of the
diabetes problem. Their new data also suggest the basic defect lies
within the mitochondria, which exist in almost every cell.
The young adults studied by the research team are the offspring of
parents who have type 2 diabetes, adding support to the idea that the
risk can be inherited, and that the problem begins well before diabetes
symptoms become evident. In an earlier research study published in the
journal Science, Shulman and his colleagues had also found that
healthy, lean older individuals have a major reduction in mitochondrial
energy production that leads to accumulation of fat inside muscle cells
resulting in insulin resistance. "These data may explain the
increased prevalence of type 2 diabetes that occurs with aging"
Shulman said.
In the new studies, Shulman and his Yale colleagues - Kitt Falk
Petersen and Sylvie Dufour - discovered that the mitochondria in
muscle cells respond poorly to insulin stimulation. Normal mitochondria
react to insulin by boosting production of an energy-carrying molecule,
ATP, by 90 percent. But the mitochondria from the insulin-resistant
people they tested only boosted ATP production by 5 percent.
"These data demonstrate that insulin-stimulated rates of ATP
synthesis are reduced in the insulin-resistant offspring of parents
with Type 2 diabetes," the researchers wrote in their report. Their
work offers new insight into the early steps in the development of
insulin resistance, and offers important clues to where the problem
lies.
Among their findings was also evidence for a severe reduction in the
amount of insulin stimulated phosphorus transport into the muscle cells
of the insulin-resistant participants. This also points to a dramatic
defect in insulin signaling and may explain the observed abnormalities
in insulin-stimulated power production in the insulin-resistant study
subjects, since phosphorus is a key element in the mitochondrion's
complex energy-production process, the oxidative-phosphorylation
pathway.
"Type 2 diabetes affects about 171 million people worldwide, and the
number of people likely to be affected by diabetes is expected to
double by 2030," Shulman and his colleagues added. "Type 2 Diabetes
develops when resistance to insulin action is combined with impaired
insulin secretion," resulting in a severe oversupply of sugars and
fats in the blood. "Studies have demonstrated the presence of insulin
resistance in virtually all patients with type 2 diabetes," Shulman
added. Diabetes is the leading cause of blindness, end stage kidney
disease and non-traumatic loss of limb, and has associated health care
costs that exceed $130 billion a year in the United States.
Such fundamental research is important because the problem of diabetes
is growing rapidly worldwide, and effective drugs are needed to halt or
even reverse the disease process. Understanding how the cell's internal
energy system is controlled by the hormone, insulin, and how the
mitochondria behave, may eventually lead to improved ways to overcome
or prevent diabetes.
