We studied glucose transporter-4 (GLUT-4) insulin receptor substrate-1
(IRS-1), Insulin receptor (IR), Phosphoenolpyrovate carboxykinase (PEPCK), Sterol regulatory element binding protein-1c (SREBP-1c), Fatty acid synthase (FAS), Peroxisome proliferator-activated receptor-a (PPAR-a), Peroxisome proliferator-activated receptor-g (PPAR-g) and tumor necrosis factor-a (TNF-a) in hepatic, skeletal muscle and adipose tissue.
The excess of FFA leads per se to insulin-resistance by inactivation of key enzymes such as pyruvate dehydrogenase (PDH) or by decreasing glucose transport activity, which may be a consequence of altered insulin signaling through decreased insulin receptor substrate-1
(IRS-1) associated PI3 kinase activity .
Moreover, CPEC and its two triterpenoids not only enhanced glucose uptake in an insulin-independent manner, but also restored insulin-mediated protein kinase B (Akt) phosphorylation by reducing the activation of IKK[beta] and regulating insulin receptor substrate-1
(IRS-1) serine/tyrosine phosphorylation.
C-reactive protein induces phosphorylation of insulin receptor substrate-1
on Ser307 and Ser612 in L6 myocytes thereby impairing the insulin signalling pathway that promotes glucose transport.
In fact, the insulin receptor substrate-1
Gly972Arg variant is widely studied in terms of its relationship to diabetes mellitus.
29] have shown that tyrosine nitration of the insulin receptor substrate-1
reduces insulin stimulated glucose uptake.
These effects were associated with significant reduction in IGF-I secretion; inhibition of IGF-I-induced cell cycle progression and insulin receptor substrate-1
(IRS-1) tyrosine phosphorylation, along with an increase in sub-G1 peak by apigenin.
Insulin stimulates PKCzeta-mediated phosphorylation of insulin receptor substrate-1
Muscular Insulin receptor, Insulin receptors phosphorylation, insulin receptor substrate-1
, serine/thereonine kinase.
Insulin receptor substrate-1
gene mutations in NIDDM; implications for the study of polygenic disease.
In tissue from people with Alzheimer's disease and mild cognitive impairment (MCI), researchers found that changes to a protein called insulin receptor substrate-1
(IRS-1 pS636/639 and pS616) in brain cells were linked to the severity of memory impairments regardless of age, sex, diabetes history, or apolipoprotein E (APOE) gene status.
Interleukin-1B inhibits insulin signaling with phosphorylating insulin receptor substrate-1
on serine residues in 3T3-L1 adipocytes.