Role of endoplasmic reticulum stress and c-Jun NH2-terminal kinase pathways in inflammation and origin of obesity and diabetes

Diabetes

Volumn 54, Issue SUPPL. 2, 2005, Pages

  Hotamisligil, Gökhan S ^a,b  

^a HARVARD SCHOOL OF PUBLIC HEALTH   (United States)

^b Bldg I ^*  (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADIPOCYTOKINE; C REACTIVE PROTEIN; CYTOKINE; INSULIN; INTERLEUKIN 6; STRESS ACTIVATED PROTEIN KINASE; TUMOR NECROSIS FACTOR ALPHA;

DIABETES MELLITUS; DIABETOGENESIS; DISEASE ASSOCIATION; ENDOPLASMIC RETICULUM; ENZYME ACTIVATION; HORMONE ACTION; HUMAN; IMMUNE RESPONSE; IMMUNE SYSTEM; INFLAMMATION; INSULIN DEPENDENT DIABETES MELLITUS; INSULIN RESISTANCE; METABOLIC DISORDER; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; OBESITY; PATHOGENESIS; PRIORITY JOURNAL; REVIEW; STRESS;

DIABETES MELLITUS; ENDOPLASMIC RETICULUM; HUMANS; INFLAMMATION; INSULIN; JNK MITOGEN-ACTIVATED PROTEIN KINASES; MODELS, BIOLOGICAL; OBESITY; STRESS;

EID: 33644750396     PISSN: 00121797     EISSN: 00121797     Source Type: Journal    
DOI: 10.2337/diabetes.54.suppl_2.S73     Document Type: Review

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