Serum amyloid A attenuates cellular insulin sensitivity by increasing JNK activity in 3T3-L1 adipocytes

Journal of Endocrinological Investigation

Volumn 32, Issue 7, 2009, Pages 568-575

  Ye, X Y ^a   Xue, Y M ^a   Sha, J P ^a   Li, C Z ^a   Zhen, Z J ^a  

^a FIRST MILITARY MEDICAL UNIVERSITY   (China)

Author keywords

3T3 L1 adipocytes; C Jun amino terminal kinases; Insulin resistance; Serum amyloid A

Indexed keywords

AMYLOID PROTEIN; DEXAMETHASONE DERIVATIVE; GLUCOCORTICOID DEXAMETHASONE; GLUCOSE; GLUCOSE TRANSPORTER 4; INSULIN; MESSENGER RNA; PHOSPHOTYROSINE; STRESS ACTIVATED PROTEIN KINASE; STRESS ACTIVATED PROTEIN KINASE INHIBITOR; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG;

ADIPOCYTE; ANIMAL CELL; ARTICLE; CONCENTRATION (PARAMETERS); CONTROLLED STUDY; DOWN REGULATION; ENZYME ACTIVITY; ENZYME LINKED IMMUNOSORBENT ASSAY; GENE EXPRESSION; GLUCOSE TRANSPORT; INSULIN RESISTANCE; INSULIN SENSITIVITY; MOUSE; NONHUMAN; PROTEIN BLOOD LEVEL; PROTEIN EXPRESSION; UPREGULATION;

3T3-L1 CELLS; ADIPOCYTES; ANIMALS; ENZYME ACTIVATION; GLUCOSE; GLUCOSE TRANSPORTER TYPE 4; HUMANS; INSULIN; INSULIN RESISTANCE; JNK MITOGEN-ACTIVATED PROTEIN KINASES; MICE; SERUM AMYLOID A PROTEIN; SIGNAL TRANSDUCTION; TUMOR NECROSIS FACTOR-ALPHA;

EID: 70949106129     PISSN: 03914097     EISSN: None     Source Type: Journal    
DOI: 10.3275/6111     Document Type: Article

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