SwePub
Sök i LIBRIS databas

  Utökad sökning

WFRF:(Musi G)
 

Sökning: WFRF:(Musi G) > Metformin increases...

Metformin increases AMP-activated-protein-kinase activity in skeletal of subjects with type 2 diabetes

Musi, N. (författare)
Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States
Hirschman, M. F. (författare)
Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States
Nygren, J. (författare)
Karolinska Institutet
visa fler...
Svanfeldt, M. (författare)
Karolinska Institutet
Båvenholm, P. (författare)
Division of Medicine, Karolinska Hospital and Institute, Stockholm, Sweden; Department of Emergency and Cardiovascular Medicine, Karolinska Hospital and Institute, Stockholm, Sweden
Rooyackers, O. (författare)
Karolinska Institutet
Zhou, G. (författare)
Department of Meta Bolic Disorders, Merck Research Laboratories, Rahway, NJ, United States
Williamsson, J. M. (författare)
Department of Meta Bolic Disorders, Merck Research Laboratories, Rahway, NJ, United States
Ljungqvist, Olle, 1954- (författare)
Örebro universitet,Institutionen för medicinska vetenskaper,Region Örebro län,Karolinska Institute, Centre of Gastrointestinal Disease, Ersta Hospital, Stockholm, Sweden; Department of Surgery, Huddinge University Hospital, Huddinge, Sweden
Efendic, S. (författare)
Division of Molecular Medicine, Karolinska Hospital and Institute, Stockholm, Sweden; Department of Endocrinology, Karolinska Hospital and Institute, Stockholm, Sweden
Moller, D. E. (författare)
Department of Meta Bolic Disorders, Merck Research Laboratories, Rahway, NJ, United States
Thorell, A. (författare)
Karolinska Institutet
Goodyear, L. J. (författare)
Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States; Research Division, Joslin Diabetes Center, One Joslin Place, Boston, United States
visa färre...
 (creator_code:org_t)
Alexandra, VA, USA : American Diabetes Association Inc. 2002
2002
Engelska.
Ingår i: Diabetes. - Alexandra, VA, USA : American Diabetes Association Inc.. - 0012-1797 .- 1939-327X. ; 51:7, s. 2074-2081
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Metformin is an effective hypoglycemic drug that lowers blood glucose concentrations by decreasing hepatic glucose production and increasing glucose disposal in skeletal muscle; however, the molecular site of metformin action is not well understood. AMP-activated protein kinase (AMPK) activity increases in response to depletion of cellular energy stores, and this enzyme has been implicated in the stimulation of glucose uptake into skeletal muscle and the inhibition of liver gluconeogenesis. We recently reported that AMPK is activated by metformin in cultured rat hepatocytes, mediating the inhibitory effects of the drug on hepatic glucose production. In the present study, we evaluated whether therapeutic doses of metformin increase AMPK activity in vivo in subjects with type 2 diabetes. Metformin treatment for 10 weeks significantly increased AMPK α2 activity in the skeletal muscle, and this was associated with increased phosphorylation of AMPK on Thr172 and decreased acetyl-CoA carboxylase-2 activity. The increase in AMPK α2 activity was likely due to a change in muscle energy status because ATP and phosphocreatine concentrations were lower after metformin treatment. Metformin-induced increases in AMPK activity were associated with higher rates of glucose disposal and muscle glycogen concentrations. These findings suggest that the metabolic effects of metformin in subjects with type 2 diabetes may be mediated by the activation of AMPK α2.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)

Publikations- och innehållstyp

ref (ämneskategori)
art (ämneskategori)

Hitta via bibliotek

  • Diabetes (Sök värdpublikationen i LIBRIS)

Till lärosätets databas

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy