What
Happens in Gestational Diabetes Mellitus?
Women who develop GDM enter
pregnancy with a chronic defect in
function that leads to abnormal blood glucose levels |
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GDM
results when the supply of insulin is inadequate to
meet the tissue demands for normal blood glucose
control during pregnancy.
The
Causes of GDM
Autoimmune
β-cell dysfunction
Damage
& destruction of β-cell function
Evolving
type 1 diabetes
Commonly
called Maturity-Onset Diabetes of the Young (MODY)
Autosomal
dominant inherited pattern
IR
is a condition in which cells resist the
action of insulin in facilitating the passage of
glucose into cells
Most
women who develop GDM have chronic β-cell
dysfunction on a background of chronic insulin
resistance
Women who have GDM & Autoimmune β cell dysfunction
suffer from inadequate insulin secretion resulting
from:
circulating
antibodies to the β-cells,
Which
in turn causes autoimmune damage to, &
destruction of, pancreatic β cell function
In
the pancreas, it is the β cells that produce
insulin.
These
women are often lean & rapidly progress to overt
type 1 diabetes after pregnancy
Now lets discuss GDM & Monogenic Diabetes. They are
commonly referred to as Maturity Onset Diabetes of
the Young. There is a genetic abnormality in the
regulation of β-cell mass &/or function that is
severe enough to cause hyperglycemia. There are
other forms of genetic mutations besides the
abnormality of β-cells such as the genetic mutations
of the enzymes necessary for insulin regulation in
the mitochondria.
Interestingly, these patients tend not to be obese
or insulin resistant.
And it should be noted that insulin resistance
appears in most women who develop GDM.
Insulin Resistance
Obesity is a common cause of chronic IR
Common causes of IR that occur
in obesity have been identified
in women with GDM
Increased levels of leptin
Increased inflammatory markers
Decreased levels of adiponectin
Increased visceral adiposity
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Leptin is a protein secreted by fat cells that
decrease appetite, increase energy expenditures, &
increase the secretion of other hormones. It is has
been observed that obese individuals have high
levels of leptin; therefore, obesity leads to
resistance to the action of leptin.
Typical inflammatory markers are tumor necrosis
factor-α (TNF) and C-reactive protein.
Adiponectin is a hormone that modulates glucose
regulation and fatty acid metabolism. Adiponectin is
secreted by fat tissues into the bloodstream.
Adiponectin is decreased in obesity. Some of the
functions of adiponectin are increased glucose
uptake by cells, decreased gluconeogenesis, improved
insulin sensitivity, control of energy metabolism,
fat catabolism, and protection from endothelial
dysfunction. Hypoadiponectinemia is an independent
risk factor for developing diabetes and metabolic
syndrome.