The inhibition of PP2A results in an acute worsening of
insulin resistance, indicating that PP2A activity is
required for insulin-stimulated glycogen storage.
Emerging evidence suggests hyperactivation of PP2A in liver,
muscle, retina and the pancreatic islet under the duress of
glucolipotoxicity and diabetes.
PP2A Regulation of Insulin Receptor Substrate 1 and Insulin
Studies of pancreatic cells indicate that impaired early
insulin secretion, which is a principal risk factor for
development of Type 2 diabetes in humans, could be secondary
to fatty acid-mediated increases in PP2A activity.
PP2A hyperactivity has been implicated in the pathogenesis
of insulin resistance and diabetes