Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Insulin-stimulated glucose uptake partly relies on p21-activated kinase (PAK)2, but not PAK1, in mouse skeletal muscle

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. A physiological model of the inflammatory-thermal-pain-cardiovascular interactions during an endotoxin challenge

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Regulation of plasma volume in male lowlanders during 4 days of exposure to hypobaric hypoxia equivalent to 3500 m altitude

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Heterogeneity in subcellular muscle glycogen utilisation during exercise impacts endurance capacity in men

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. KATP channels modulate cerebral blood flow and oxygen delivery during isocapnic hypoxia in humans

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. The impact of loading, unloading, ageing and injury on the human tendon

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  • Lisbeth L V Møller
  • Merna Jaurji
  • Rasmus Kjøbsted
  • Giselle A Joseph
  • Agnete B Madsen
  • Jonas Roland Knudsen
  • Anne-Marie Lundsgaard
  • Nicoline Resen Andersen
  • Peter Schjerling
  • Thomas E Jensen
  • Robert S Krauss
  • Lykke Sylow
Vis graf over relationer
The group I p21-activated kinase (PAK) isoforms PAK1 and PAK2 are activated in response to insulin in skeletal muscle and PAK1/2 signalling is impaired in insulin-resistant mouse and human skeletal muscle. Interestingly, PAK1 has been suggested to be required for insulin-stimulated glucose transporter 4 translocation in mouse skeletal muscle. Therefore, the present study aimed to examine the role of PAK1 in insulin-stimulated muscle glucose uptake. The pharmacological inhibitor of group I PAKs, IPA-3 partially reduced (-20%) insulin-stimulated glucose uptake in isolated mouse soleus muscle (P < 0.001). However, because there was no phenotype with genetic ablation of PAK1 alone, consequently, the relative requirement for PAK1 and PAK2 in whole-body glucose homeostasis and insulin-stimulated muscle glucose uptake was investigated. Whole-body respiratory exchange ratio was largely unaffected in whole-body PAK1 knockout (KO), muscle-specific PAK2 KO and in mice with combined whole-body PAK1 KO and muscle-specific PAK2 KO. By contrast, glucose tolerance was mildly impaired in mice lacking PAK2 specifically in muscle, but not PAK1 KO mice. Moreover, while PAK1 KO muscles displayed normal insulin-stimulated glucose uptake in vivo and in isolated muscle, insulin-stimulated glucose uptake was slightly reduced in isolated glycolytic extensor digitorum longus muscle lacking PAK2 alone (-18%) or in combination with PAK1 KO (-12%) (P < 0.05). In conclusion, glucose tolerance and insulin-stimulated glucose uptake partly rely on PAK2 in glycolytic mouse muscle, whereas PAK1 is dispensable for whole-body glucose homeostasis and insulin-stimulated muscle glucose uptake.
OriginalsprogEngelsk
TidsskriftThe Journal of physiology
ISSN0022-3751
StatusUdgivet - dec. 2020

ID: 61777648