scholarly journals The insulin signalling pathway

2002 ◽  
Vol 12 (7) ◽  
pp. R236-R238 ◽  
Author(s):  
Jose M. Lizcano ◽  
Dario R. Alessi
Keyword(s):  
Insulin Signalling ◽  
Signalling Pathway ◽  
Insulin Signalling Pathway

Effect of food restriction on the insulin signalling pathway in rat skeletal muscle and adipose tissue

2005 ◽  
Vol 16 (10) ◽  
pp. 602-609 ◽  
Author(s):  
Ana Alonso ◽  
Yolanda Fernández ◽  
Rebeca Fernández ◽  
Patricia Ordóñez ◽  
María Moreno ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Food Restriction ◽  
Insulin Signalling ◽  
Signalling Pathway ◽  
Rat Skeletal Muscle ◽  
Insulin Signalling Pathway ◽  
Effect Of Food

scholarly journals Mulberry leaf reduces inflammation and insulin resistance in type 2 diabetic mice by TLRs and insulin Signalling pathway

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Simin Tian ◽  
Min Wang ◽  
Chenyue Liu ◽  
Hongbin Zhao ◽  
Baosheng Zhao
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Insulin Signalling ◽  
Signalling Pathway ◽  
Inflammatory Factor ◽  
Diabetic Mice ◽  
Mulberry Leaf ◽  
Insulin Signalling Pathway ◽  
Tnf Α ◽  
Necrosis Factor

Abstract Background It has been testified that Diabetes mellitus (DM) has a close association with chronic inflammation and Toll-like Receptors (TLRs), and DM could be prevented by mulberry leaf. Therefore, a hypothesis came into being that mulberry leaf could ameliorate proinflammation and insulin resistance (IR) through TLRs and insulin signalling pathways. Methods Water extracts of mulberry leaf (WEM) was given to diabetic mice by gavage for 10 weeks, and the diabetic mice was injected with low-dose streptozocin, fed with high-fat and high-sugar diet. Oral glucose tolerance tests (OGTTs) were conducted. At the same time, homeostasis model assessment of insulin (HOMA-IR) and the level of the inflammatory factor, tumour necrosis factor-α (TNF-α) was measured. The expressions of critical nodes of TLRs and insulin signalling pathway were also examined. Results WEM contributed to a significant decrease in fasting blood glucose, AUC from the investigation of OGTTs and HOMA-IR. The levels of the inflammatory factor, tumour necrosis factor-α (TNF-α) also declined. Moreover, WEM suppressed the expression of TLR2, myeloid differentiation primary-response protein 88 (MyD88), tumour-necrosis-factor receptor-associated factor 6 (TRAF6), nuclear factor kappa B (NF-κB) in the skeletal muscle. WEM could up-regulate the expression of insulin receptor (InsR) and insulin receptor substrate 1 (IRS1), and down-regulate the phosphorylation of IRS1 in adipose tissue. Conclusion Through this study, a conclusion could be made that WEM mitigates hyperglycemia, IR, and inflammation through the interactions among TLR2 signalling pathway, insulin signalling pathway and TNF-α.

scholarly journals S-resistin, a non secretable resistin isoform, impairs the insulin signalling pathway in 3T3-L1 adipocytes

2015 ◽  
Vol 71 (3) ◽  
pp. 381-390 ◽  
Author(s):  
María Rodríguez ◽  
Eduardo Moltó ◽  
Lidia Aguado ◽  
Nilda Gallardo ◽  
Antonio Andrés ◽  
...  
Keyword(s):  
Insulin Signalling ◽  
Signalling Pathway ◽  
Insulin Signalling Pathway

scholarly journals Mir-338-3p Mediates Tnf-A-Induced Hepatic Insulin Resistance by Targeting PP4r1 to Regulate PP4 Expression

2017 ◽  
Vol 41 (6) ◽  
pp. 2419-2431 ◽  
Author(s):  
Lin Dou ◽  
Shuyue Wang ◽  
Libo Sun ◽  
Xiuqing Huang ◽  
Yang Zhang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Phosphatase ◽  
Insulin Signalling ◽  
Critical Role ◽  
Transcriptional Regulator ◽  
Signalling Pathway ◽  
Hepatic Insulin Resistance ◽  
Luciferase Assay ◽  
Insulin Signalling Pathway ◽  
Tnf Α

Objective: Insulin resistance is a critical factor contributing to the pathogenesis of type 2 diabetes and other metabolic diseases. Recent studies have indicated that miR-338-3p plays an important role in cancer. Here, we investigated whether miR-338-3p mediates tumour necrosis factor-α (TNF-α)-induced hepatic insulin resistance. Methods: The activation of the insulin signalling pathway and the level of glycogenesis were examined in the livers of the db/db and high fat diet (HFD)-fed mice and in HEP1-6 cells transfected with miR-338-3p mimic or inhibitor. Computational prediction of microRNA target, luciferase assay and Western blot were used to assess the miR-338-3p target. Chromatin immunoprecipitation (ChIP) assay was used to determine the transcriptional regulator of miR-338-3p. Results: miR-338-3p was down-regulated in the livers of the db/db, HFD-fed and TNF-α-treated C57BL/6J mice, as well as in mouse HEP1-6 hepatocytes treated with TNF-α. Importantly the down-regulation of miR-338-3p induced insulin resistance, as indicated by impaired glucose tolerance and insulin tolerance. Further research showed that the down-regulated miR-338-3p resulted in the impaired AKT/ glycogen synthase kinase 3 beta (GSl·Gβ) signalling pathway and glycogen synthesis. In contrast, hepatic over-expression of miR-338-3p rescued the TNF-α-induced insulin resistance. Moreover, protein phosphatase 4 regulator subunit 1 (PP4R1) was identified as a direct target of miR-338-3p that mediated hepatic insulin signalling by regulating protein phosphatase 4 (PP4). Finally we identified hepatic nuclear factor 4 alpha (HNF-4α) as the transcriptional regulator of miRNA-338-3p. Conclusions: Our studies provide novel insight into the critical role and molecular mechanism by which miR-338-3p is involved in TNF-α-induced hepatic insulin resistance. miR-338-3p might mediate TNF-α-induced hepatic insulin resistance by targeting PP4R1 to regulate PP4 expression.

Sign in / Sign up

Export Citation Format

Share Document