Mitochondrial dysfunction and type 2 diabetes
BB Lowell, GI Shulman - Science, 2005 - science.org
BB Lowell, GI Shulman
Science, 2005•science.orgMaintenance of normal blood glucose levels depends on a complex interplay between the
insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion
by pancreatic β cells. Defects in the former are responsible for insulin resistance, and
defects in the latter are responsible for progression to hyperglycemia. Emerging evidence
supports the potentially unifying hypothesis that both of these prominent features of type 2
diabetes are caused by mitochondrial dysfunction.
insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion
by pancreatic β cells. Defects in the former are responsible for insulin resistance, and
defects in the latter are responsible for progression to hyperglycemia. Emerging evidence
supports the potentially unifying hypothesis that both of these prominent features of type 2
diabetes are caused by mitochondrial dysfunction.
Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion by pancreatic β cells. Defects in the former are responsible for insulin resistance, and defects in the latter are responsible for progression to hyperglycemia. Emerging evidence supports the potentially unifying hypothesis that both of these prominent features of type 2 diabetes are caused by mitochondrial dysfunction.
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