Title : NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes.

Pub. Date : 2012 Dec

PMID : 22968630






8 Functional Relationships(s)
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Protein Name
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1 NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes. Metformin phosphotyrosine interaction domain containing 1 Homo sapiens
2 NYGGF4 (PID1) effects on insulin resistance are reversed by metformin in 3T3-L1 adipocytes. Metformin phosphotyrosine interaction domain containing 1 Homo sapiens
3 We aimed in the present study to further elucidate the effects of NYGGF4 on IR and the underlying mechanisms through using metformin treatment in 3T3-L1 adipocytes. Metformin phosphotyrosine interaction domain containing 1 Homo sapiens
4 Our data showed that the metformin pretreatment strikingly enhanced insulin-stimulated glucose uptake through increasing GLUT4 translocation to the PM in NYGGF4 overexpression adipocytes. Metformin phosphotyrosine interaction domain containing 1 Homo sapiens
5 NYGGF4 overexpression resulted in significant inhibition of tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, whereas incubation with metformin strongly activated IRS-1 and Akt phosphorylation in NYGGF4 overexpression adipocytes. Metformin phosphotyrosine interaction domain containing 1 Homo sapiens
6 The reactive oxygen species (ROS) levels in NYGGF4 overexpression adipocytes were strikingly enhanced, which could be decreased by the metformin pretreatment. Metformin phosphotyrosine interaction domain containing 1 Homo sapiens
7 Our data also showed that metformin increased the expressions of PGC1-alpha, NRF-1, and TFAM, which were reduced in the NYGGF4 overexpression adipocytes. Metformin phosphotyrosine interaction domain containing 1 Homo sapiens
8 These results suggest that NYGGF4 plays a role in IR and its effects on IR could be reversed by metformin through activating IRS-1/PI3K/Akt and AMPK-PGC1-alpha pathways. Metformin phosphotyrosine interaction domain containing 1 Homo sapiens