4-Hydroxyisoleucine ameliorates fatty acid-induced insulin resistance and inflammatory response in skeletal muscle cells

4-Hydroxyisoleucine from Fenugreek (Trigonella foenum-graecum): Effects on Insulin Resistance Associated with Obesity

“…The basal phosphorylation of Akt (Ser-473) increased after treatment with 4-OHIle, but mRNA expression of total Akt, IRS-1, GLUT-4, and glycogen synthase kinase-3β (GSK-3β) was unchanged. Treatment of L6 myotubes with 4-OHIle decreased IR induced by FFAs [104]. In fact, 4-OHIle restored glucose uptake and GLUT-4 translocation to the plasma membrane after palmitate treatment via insulin induction of IRS-1 phosphorylation.…”

“…Increased insulin receptor substrate-1 tyrosine phosphorylation (pIRS-1), increased PI3K, increased pAkt, decreased reactive oxygen species (ROS), decreased NF-kB, decreased c-Jun N-terminal kinase 1/2 (JNK), decreased p38 MAPK [104] Insulin-resistant 3T3-L1 adipocytes Decreased TNF-α, increased glucose uptake [105] Insulin-resistant HepG2 cells…”

Raspberry Supplementation Improves Insulin Signaling and Promotes Brown‐Like Adipocyte Development in White Adipose Tissue of Obese Mice

“…The insulin signaling is mediated by IRS‐1 tyrosine phosphorylation, which further activates the downstream phosphatidylinositol 3‐kinase/Akt pathway to stimulate expression and translocation of GLUT4 . However, increased serine phosphorylation of IRS‐1 antagonizes its tyrosine phosphorylation by the insulin receptor, leading to insulin resistance . Supportively, inflammation elicited by tumor necrosis factor‐α increases phosphorylation of IRS‐1 at Ser307 in 3T3‐L1 pre‐adipocytes which inhibits glucose uptake .…”

Fucosylated chondroitin sulphate from sea cucumber reduces hepatic endoplasmic reticulum stress-associated inflammation in obesity mice

“…Dong et al (2015) recently reported that reduction in hepatic NO production in mice, which suffered carbon tetrachloride-induced acute liver injury, was associated with the lowered expression of proinflammatory cytokines and the inactivation of NFκB and JNK pathways. Meanwhile, overloaded FFA and proinflammatory cytokines, such as IL-1β and TNF-α, can induce ROS and NO products, which results in activation of NFκB and JNK signalling and blocking insulin signal cascade (Guo, Lin, Liu, Lin, & Liu, 2010;Maurya et al, 2014). HFSD-fed insulin resistant mouse model showed significant high levels of serum and hepatic ROS and NO, and interestingly, the elevation was lowered by Am-CHS.…”