Oxidative stress and calcium dysregulation by palmitate in type 2 diabetes.

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Annotation Summary

Term Occurence Count Dictionary
Insulin 1 endocrinologydiseasesdrugs
cholic acid 1 endocrinologydiseasesdrugs
hyperglycemia 1 endocrinologydiseases
obesity 4 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 30245 connection in mitochondrial dysfunction and β-cell failure by palmitate deserves further investigation. Insulin resistance in target tissuesIt is well-known that palmitate induces insulin resistance by disrupting
cholic acid 15766 using the chemical chaperone 4-phenylbutyric acid.[80], [81], [82], [83] Taurine-conjugated ursodeoxy cholic acid (TUDCA) has also been tested as a chaperone to protect hepatocytes from palmitate-induced ER stress
Select Disease Character Offset Disease Term Instance
hyperglycemia 33416 traditionally been attributed to long-term exposure to high glucose. The four classical pathways of hyperglycemia -induced complications include (1) increased polyol pathway flux, (2) increased intracellular formation
obesity 7468 consequence of impaired oxidative metabolism.[25] The disruption of the CD36 gene, however, protects from obesity -associated steatosis and insulin resistance.[26] In diabetic animals, a lack of CD36 attenuates NADPH
obesity 17729 death.[92]ER proteome analysis in the liver of ob/ob mice shows a fundamental shift in ER function in obesity from protein synthesis to lipid synthesis and metabolism.[93] One important factor inducing ER calcium
obesity 17853 synthesis to lipid synthesis and metabolism.[93] One important factor inducing ER calcium depletion in obesity is the increased phosphatidylcholine/phosphatidylethanolamine ratio, which disrupts ER calcium refilling
obesity 25574 release and apoptotic cell death (Figure 2).[116]Accumulating evidence suggests that human subjects with obesity or insulin resistance exhibit reduced oxygen consumption rates, decreased expression of mitochondrial

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