Insulin stimulates GLUT4 translocation in the semitendinosus muscle of Shetland ponies

Insulin Resistance Selectively Alters Cell‐Surface Glucose Transporters but not their Total Protein Expression in Equine Skeletal Muscle

“…Similarly, we have demonstrated previously no increase in crude membrane GLUT4 content despite a substantial increase in insulin availability in athletic horses after administration of IV glucose infusion or consumption of large amount of highly soluble carbohydrate 25,27,31 . In addition, it was recently shown that insulin minimally stimulates GLUT4 translocation in the semitendinosus muscle of healthy ponies, even with supraphysiological insulin concentrations 32 . However, in this recent study of ponies, 32 GLUT4 translocation was only estimated by measuring total GLUT4 protein content in partially purified plasma membranes obtained by conventional subfractionation technique, which does not accurately quantify active cell‐surface GLUT4 protein content.…”

“…In addition, it was recently shown that insulin minimally stimulates GLUT4 translocation in the semitendinosus muscle of healthy ponies, even with supraphysiological insulin concentrations 32 . However, in this recent study of ponies, 32 GLUT4 translocation was only estimated by measuring total GLUT4 protein content in partially purified plasma membranes obtained by conventional subfractionation technique, which does not accurately quantify active cell‐surface GLUT4 protein content. Indeed, in the present study we reported different results regarding GLUT4 protein content in the labeled cell‐surface fractions (measured by biotinylation cell‐surface assay) versus in plasma membrane‐enriched fractions (measured by Western blot), similar to other reports 13 .…”

AICAR administration affects glucose metabolism by upregulating the novel glucose transporter, GLUT8, in equine skeletal muscle

“…Thus, the fact that skeletal muscle 304 protein expression of GLUT1, a basal transporter, was not affected by AICAR 305 infusion was not unexpected. The failure of GLUT4 translocation to increase in post-306 AICAR treated muscle samples is consistent with the fact that GLUT4 is primarily 307 translocated via an insulin-dependent mechanism, and thus would not necessarily be 308 targeted by an insulin-independent mechanism, such as AMPK phosphorylation 309 (Duehlmeier et al, 2010). Surprisingly, we did not observe an upregulation of GLUT4 310 protein to the cell membrane in response to the transient hyperinsulinaemia following 311 AICAR infusion and this may be a function of sample timing because insulin 312 concentration had returned to between reference range values at the time of biopsy 313 collection.…”

“…Prior studies have shown that GLUT1 does not appear to be a key GLUT in 302 equine skeletal muscle, and this is consistent with its insulin-independent action 303 (Duehlmeier et al, 2010;de Laat et al, 2014). Thus, the fact that skeletal muscle 304 protein expression of GLUT1, a basal transporter, was not affected by AICAR 305 infusion was not unexpected.…”

PID1 alters antilipolytic action of insulin and increases lipolysis via Inhibited the activation of AKT/PKA Pathway

“…Guo et al found that PID1 which contain a phosphotyrosine binding (PTB) domain canbind to phosphorylated tyrosine residuesand impair insulin signal transduction. And increased expression of PID1 leads to a reduction in insulinstimulatedglucose uptake and impaired insulin-stimulated GLUT4translocation in mature adipocytes [9], but whether PID1 alsoinfluencessignaling pathway of insulin regulates lipid metabolism still needs to be confirmed by further investigations.…”