Comprehensive Insulin Receptor Phosphorylation Dynamics Profiled by Mass Spectrometry

FEBS Journal ◽  
2021 ◽  
Author(s):  
Zhongping Liao ◽  
Chen Zhang ◽  
Liyun Ding ◽  
Julie S. Moyers ◽  
Jason X. Tang ◽  
...  

Metabolism ◽  
2008 ◽  
Vol 57 (11) ◽  
pp. 1545-1551 ◽  
Author(s):  
April J. Stull ◽  
John P. Thyfault ◽  
Mark D. Haub ◽  
Richard E. Ostlund ◽  
Wayne W. Campbell


2017 ◽  
Vol 27 (2) ◽  
pp. 120-131 ◽  
Author(s):  
Katarzyna Głombik ◽  
Joanna Ślusarczyk ◽  
Ewa Trojan ◽  
Katarzyna Chamera ◽  
Bogusława Budziszewska ◽  
...  




2020 ◽  
Vol 21 (15) ◽  
pp. 5469 ◽  
Author(s):  
Marco Raffaele ◽  
Maria Licari ◽  
Sherif Amin ◽  
Ragin Alex ◽  
Hsin-hsueh Shen ◽  
...  

Aim: Obesity is associated with metabolic syndrome, hypertension, dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and type 2 diabetes. In this study, we investigated whether the dietary supplementation of pomegranate seed oil (PSO) exerted a protective effect on liver lipid uptake, fibrosis, and mitochondrial function in a mouse model of obesity and insulin resistance. Method: In this in vivo study, eight-week-old C57BL/6J male mice were fed with a high fat diet (HFD) for 24 weeks and then were divided into three groups as follows: group (1) Lean; group (n = 6) (2) HF diet; group (n = 6) (3) HF diet treated with PSO (40 mL/kg food) (n = 6) for eight additional weeks starting at 24 weeks. Physiological parameters, lipid droplet accumulation, inflammatory biomarkers, antioxidant biomarkers, mitochondrial biogenesis, insulin sensitivity, and hepatic fibrosis were determined to examine whether PSO intervention prevents obesity-associated metabolic syndrome. Results: The PSO group displayed an increase in oxygen consumption, as well as a decrease in fasting glucose and blood pressure (p < 0.05) when compared to the HFD-fed mice group. PSO increased both the activity and expression of hepatic HO-1, downregulated inflammatory adipokines, and decreased hepatic fibrosis. PSO increased the levels of thermogenic genes, mitochondrial signaling, and lipid metabolism through increases in Mfn2, OPA-1, PRDM 16, and PGC1α. Furthermore, PSO upregulated obesity-mediated hepatic insulin receptor phosphorylation Tyr-972, p-IRB tyr1146, and pAMPK, thereby decreasing insulin resistance. Conclusions: These results indicated that PSO decreased obesity-mediated insulin resistance and the progression of hepatic fibrosis through an improved liver signaling, as manifested by increased insulin receptor phosphorylation and thermogenic genes. Furthermore, our findings indicate a potential therapeutic role for PSO in the prevention of obesity-associated NAFLD, NASH, and other metabolic disorders.





1983 ◽  
Vol 214 (2) ◽  
pp. 361-366 ◽  
Author(s):  
W E Plehwe ◽  
P F Williams ◽  
I D Caterson ◽  
L C Harrison ◽  
J R Turtle

Phosphorylation of the insulin receptor of isolated rat adipocytes in response to insulin has been studied. Immunoprecipitation of adipocyte membrane protein demonstrated increased incorporation of 32P after exposure to insulin for 15 min, but this was dependent on the presence of physiological concentrations of Ca2+ and Mg2+. Autoradiography of solubilized immunoprecipitated membrane protein after sodium dodecyl sulphate/polyacrylamide-gel electrophoresis revealed that most of the 32P incorporation occurred in a band corresponding to Mr 95 000, which has been identified previously as the beta-subunit of the insulin receptor. 32P incorporation was inhibited by 2,4-dinitrophenol and trifluoperazine. It is suggested that insulin-receptor phosphorylation is an energy-requiring process that is Ca2+-dependent and may be modulated by calmodulin. Phosphorylation may proceed independently of glucose transport.



Endocrinology ◽  
1990 ◽  
Vol 127 (1) ◽  
pp. 481-487 ◽  
Author(s):  
VINCENT DURONIO ◽  
STEVEN JACOBS


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