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| Science |
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Mitochondrial dysfunction (Science, 2004,
307, 384) and metabolic overload of endoplasmic reticulum
(Science, 2004, 306, 425) are considered as primary causes
of insulin resistance.
The deficiency of NOS and heat shock protein functions are
also well documented in diabetes. Expression of constitutive
NOS is decreased in muscles of even well controlled diabetic
patients. Constitutive NOS derived NO has recently been
identified as a regulator of mitochondrial biogenesis. The
simultaneous cNOS deficiency and mitochondrial dysfunction
in diabetes suggests a linkage between the two mechanisms.
BGP-15 is designed to restore cNOS and inducible HSP
expression and function resulting in correction of damaged
mitochondrial and endoplasmic reticulum functions and
improved mitochondrial biogenesis. These combined actions
increase insulin sensitivity by affecting causal mechanisms
of insulin resistance. |
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