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

Rac1 and AMPK Account for the Majority of Muscle Glucose Uptake Stimulated by Ex Vivo Contraction but Not In Vivo Exercise

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Genetic Studies of Leptin Concentrations Implicate Leptin in the Regulation of Early Adiposity

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. The Role of Glucagon in the Acute Therapeutic Effects of SGLT2 Inhibition

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. No detectable remodelling in adult human menisci: an analysis based on the C14 bomb pulse

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Glucagon-Like Peptide-2 Analogue ZP1849 Augments Colonic Anastomotic Wound Healing

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  • Lykke Sylow
  • Lisbeth Møller
  • Maximilian Kleinert
  • Gommaar D'Hulst
  • Estelle De Groote
  • Peter Schjerling
  • Gregory R Steinberg
  • Thomas Jensen
  • Erik Richter
Vis graf over relationer
Exercise bypasses insulin resistance to increase glucose uptake in skeletal muscle and therefore represents an important alternative to stimulate glucose uptake in insulin-resistant muscle. Both Rac1 and AMPK have been shown to partly regulate contraction-stimulated muscle glucose uptake, but whether those two signaling pathways jointly account for the entire signal to glucose transport is unknown. We therefore studied the ability of contraction and exercise to stimulate glucose transport in isolated muscles with AMPK loss of function combined with either pharmacological inhibition or genetic deletion of Rac1.
Muscle-specific knockout (mKO) of Rac1, a kinasedead a2 AMPK (a2KD), and double knockout (KO) of b1 and b2 AMPK subunits (b1b2 KO) each partially decreased contraction-stimulated glucose transport in mouse soleus and extensor digitorum longus (EDL) muscle. Interestingly, when pharmacological Rac1 inhibition was combined with either AMPK b1b2 KO or a2KD, contraction-stimulated glucose transport was almost completely inhibited. Importantly, a2KD+Rac1 mKO double-transgenic mice also displayed severely impaired
contraction-stimulated glucose transport, whereas exercise-stimulated glucose uptake in vivo was only partially reduced by Rac1 mKO with no additive effect
of a2KD. It is concluded that Rac1 and AMPK together account for almost the entire ex vivo contraction response in muscle glucose transport, whereas only Rac1, but not a2 AMPK, regulates muscle glucose uptake during submaximal exercise in vivo.
OriginalsprogEngelsk
TidsskriftDiabetes
Vol/bind66
Sider (fra-til)1548-1559
Antal sider12
ISSN0012-1797
DOI
StatusUdgivet - jun. 2017

ID: 52759439