Increased β-cell apoptosis prevents adaptive increase in β-cell mass in mouse model of type 2 diabetes: Evidence for role of islet amyloid formation rather than direct action of amyloid

Diabetes

Volumn 52, Issue 9, 2003, Pages 2304-2314

  Butler, Alexandra E ^a   Janson, Juliette ^b   Soeller, Walter C ^c   Butler, Peter C ^a  

^a UNIVERSITY OF SOUTHERN CALIFORNIA   (United States)

^b KAROLINSKA INSTITUTE   (Sweden)

^c PFIZER GLOBAL RESEARCH AND DEVELOPMENT   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLIN; AMYLOID;

ADAPTATION; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL DIVISION; CELL LOSS; CONCENTRATION RESPONSE; CONTROLLED STUDY; DISEASE ASSOCIATION; GLUCOSE BLOOD LEVEL; INNER CELL MASS; INSULIN RESISTANCE; MOUSE; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; OBESITY; PANCREAS ISLET BETA CELL; PATHOGENESIS; PRIORITY JOURNAL; REGULATORY MECHANISM;

AMYLOID; AMYLOIDOSIS; ANIMALS; APOPTOSIS; BLOOD GLUCOSE; BODY WEIGHT; DIABETES MELLITUS; DIABETES MELLITUS, TYPE 2; DISEASE MODELS, ANIMAL; HUMANS; INSULIN; ISLETS OF LANGERHANS; MICE; MICE, TRANSGENIC; OBESITY; TRANSGENES;

EID: 0042822112     PISSN: 00121797     EISSN: None     Source Type: Journal    
DOI: 10.2337/diabetes.52.9.2304     Document Type: Article

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