scholarly journals Oleic Acid Stimulates Glucose Uptake Into Adipocytes by Enhancing Insulin Receptor Signaling

2014 ◽  
Vol 126 (4) ◽  
pp. 337-343 ◽  
Author(s):  
Ayako Tsuchiya ◽  
Hisao Nagaya ◽  
Takeshi Kanno ◽  
Tomoyuki Nishizaki
BMC Cancer ◽  
2007 ◽  
Vol 7 (1) ◽  
Author(s):  
Kiyosumi Shibata ◽  
Hiroaki Kajiyama ◽  
Kazuhiko Ino ◽  
Akihiro Nawa ◽  
Seiji Nomura ◽  
...  

2002 ◽  
Vol 92 (2) ◽  
pp. 736-744 ◽  
Author(s):  
Christine Y. Christ ◽  
Desmond Hunt ◽  
Joe Hancock ◽  
Rebeca Garcia-Macedo ◽  
Lawrence J. Mandarino ◽  
...  

Exercise training improves skeletal muscle insulin sensitivity in the obese Zucker rat. The purpose of this study was to investigate whether the improvement in insulin action in response to exercise training is associated with enhanced insulin receptor signaling. Obese Zucker rats were trained for 7 wk and studied by using the hindlimb-perfusion technique 24 h, 96 h, or 7 days after their last exercise training bout. Insulin-stimulated glucose uptake (traced with 2-deoxyglucose) was significantly reduced in untrained obese Zucker rats compared with lean controls (2.2 ± 0.17 vs. 5.4 ± 0.46 μmol · g−1 · h−1). Glucose uptake was normalized 24 h after the last exercise bout (4.9 ± 0.41 μmol · g−1 · h−1) and remained significantly elevated above the untrained obese Zucker rats for 7 days. However, exercise training did not increase insulin receptor or insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, phosphatidylinositol 3-kinase (PI3-kinase) activity associated with IRS-1 or tyrosine phosphorylated immunoprecipitates, or Akt serine phosphorylation. These results are consistent with the hypothesis that, in obese Zucker rats, adaptations occur during training that lead to improved insulin-stimulated muscle glucose uptake without affecting insulin receptor signaling through the PI3-kinase pathway.


Diabetes ◽  
2006 ◽  
Vol 55 (6) ◽  
pp. 1581-1591 ◽  
Author(s):  
S. C. Martinez ◽  
C. Cras-Meneur ◽  
E. Bernal-Mizrachi ◽  
M. A. Permutt

Author(s):  
Anni M. Y. Zhang ◽  
Jenny C. C. Yang ◽  
Twan J. J. de Winter ◽  
David F. Schaeffer ◽  
Janel L. Kopp ◽  
...  

Aging Cell ◽  
2020 ◽  
Vol 19 (10) ◽  
Author(s):  
Hilaree N. Frazier ◽  
Katie L. Anderson ◽  
Adam O. Ghoweri ◽  
Ruei-Lung Lin ◽  
Tara R. Hawkinson ◽  
...  

2019 ◽  
Vol 316 (4) ◽  
pp. E660-E673 ◽  
Author(s):  
Katrine D. Galsgaard ◽  
Marie Winther-Sørensen ◽  
Jens Pedersen ◽  
Sasha A. S. Kjeldsen ◽  
Mette M. Rosenkilde ◽  
...  

Glucagon and insulin are important regulators of blood glucose. The importance of insulin receptor signaling for alpha-cell secretion and of glucagon receptor signaling for beta-cell secretion is widely discussed and of clinical interest. Amino acids are powerful secretagogues for both hormones, and glucagon controls amino acid metabolism through ureagenesis. The role of insulin in amino acid metabolism is less clear. Female C57BL/6JRj mice received an insulin receptor antagonist (IRA) (S961; 30 nmol/kg), a glucagon receptor antagonist (GRA) (25-2648; 100 mg/kg), or both GRA and IRA (GRA + IRA) 3 h before intravenous administration of similar volumes of saline, glucose (0.5 g/kg), or amino acids (1 µmol/g) while anesthetized with isoflurane. IRA caused basal hyperglycemia, hyperinsulinemia, and hyperglucagonemia. Unexpectedly, IRA lowered basal plasma concentrations of amino acids, whereas GRA increased amino acids, lowered glycemia, and increased glucagon but did not influence insulin concentrations. After administration of GRA + IRA, insulin secretion was significantly reduced compared with IRA administration alone. Blood glucose responses to a glucose and amino acid challenge were similar after vehicle and GRA + IRA administration but greater after IRA and lower after GRA. Anesthesia may have influenced the results, which otherwise strongly suggest that both hormones are essential for the maintenance of glucose homeostasis and that the secretion of both is regulated by powerful negative feedback mechanisms. In addition, insulin limits glucagon secretion, while endogenous glucagon stimulates insulin secretion, revealed during lack of insulin autocrine feedback. Finally, glucagon receptor signaling seems to be of greater importance for amino acid metabolism than insulin receptor signaling.


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