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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

 

 

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

•Monogenic diabetes

•Commonly called “Maturity-Onset Diabetes of the Young” (MODY)

•Autosomal dominant inherited pattern

•Insulin resistance (IR)

•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 let’s 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

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.

 

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