Glucotoxicity and α cell dysfunction: Involvement of the PI3K/Akt pathway in glucose-induced insulin resistance in rat islets and clonal αtC1-6 cells

Endocrine Research

Volumn 37, Issue 1, 2012, Pages 12-24

  Shen, Xiao Xia ^a   Li, Hong Liang ^b   Pan, Lin ^b   Hong, Jing ^b   Xiao, Juan ^b   Hermansen, Kjeld ^c   Jeppesen, Per Bendix ^c   Li, Guang Wei ^a  

^a FUWAI HOSPITAL   (China)

^b CHINA JAPAN FRIENDSHIP HOSPITAL   (China)

^c AARHUS UNIVERSITY HOSPITAL   (Denmark)

Author keywords

Cell; High glucose; Insulin resistance; PI3K Akt pathway

Indexed keywords

GLUCAGON; GLUCOSE; INSULIN; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; WORTMANNIN;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL FUNCTION; CELL LINE; CHRONIC TOXICITY; CLONAL VARIATION; CONTROLLED STUDY; GENE EXPRESSION; GLUCAGON RELEASE; INSULIN RESISTANCE; MALE; NONHUMAN; PANCREAS ISLET ALPHA CELL; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; RAT; WESTERN BLOTTING;

ANIMALS; CELLS, CULTURED; GLUCAGON; GLUCAGON-SECRETING CELLS; GLUCOSE; INSULIN; INSULIN RESISTANCE; ISLETS OF LANGERHANS; MALE; PHOSPHATIDYLINOSITOL 3-KINASES; PROTO-ONCOGENE PROTEINS C-AKT; RATS; RATS, SPRAGUE-DAWLEY; SIGNAL TRANSDUCTION;

EID: 84255167476     PISSN: 07435800     EISSN: 15324206     Source Type: Journal    
DOI: 10.3109/07435800.2011.610855     Document Type: Article

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