Like two peas in a pod, the obesity and type 2 diabetes epidemics
have joined forces in an attempt to ravage America's health ...
and it's working, as hundreds of millions of people have been significantly
affected by this deadly pair.
But how are these two epidemics intertwined? Popular belief is
that if one eats too much sugar, they'll get fat and develop diabetes;
and, if they don't get diabetes it's merely because their body is
producing enough insulin to keep up with the sugar. However, researchers
have discovered evidence that there's more to the obesity-diabetes
connection than this classic way of thinking: The missing link?
Leptin.
Mice Studies Shed Light on the Subject
Research on mice has suggested that leptin is the key, as it regulates
blood sugar through two different brain-body passageways:
- One: Responsible for controlling appetite and fat storage
- Two: Responsible for telling the liver what to do with its stored
glucose
While it was previously found that disrupting the appetite-controlling
passageway leads to obesity (which significantly increases the risk
of diabetes), results of the study indicated that it likely takes
disruptions in both of leptin's passageways to trigger full-blown
diabetes.
Mice used in the study were genetically modified to disable what
is known as the leptin-STAT3 cell-signaling passageway that leads
from the brain to the body. This s/s strain of mice was still able
to produce leptin and the receptor it attaches to when sending STAT3
signals in the body. Further, after eating too much and becoming
obese, s/s mice did not develop diabetes; however, other strains
of mice that did not produce leptin or have receptors became obese,
developed diabetes and died.
Therefore, even when disrupting the leptin-STAT3 signal, the s/s
mice were still able to keep their glucose under control, suggesting
the likelihood of a brain-liver signaling passageway responsible
for regulating blood sugar.
Cell
Metabolism
March 2005; Vol 1, 169-178 (Free Full-Text Article)
Newswise
Mar 16, 2005
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