Islet amyloid polypeptide (amylin)-deficient mice develop a more severe form of alloxan-induced diabetes

American Journal of Physiology - Endocrinology and Metabolism

Volumn 278, Issue 4 41-4, 2000, Pages

  Mulder, Hindrik ^a,d   Gebre Medhin, Samuel ^a,c   Betsholtz, Christer ^c   Sundler, Frank ^a   Ahrén, Bo ^b  

^a LUND UNIVERSITY   (Sweden)

^b LUND UNIVERSITY HOSPITAL   (Sweden)

^c UNIVERSITY OF GOTHENBURG   (Sweden)

^d UNIVERSITY OF TEXAS AT DALLAS   (United States)

Author keywords

Gene knockout; Glucose tolerance; Glucose transporter 2; Insulin messenger ribonucleic acid; cell mass

Indexed keywords

AMYLIN; GLUCOSE TRANSPORTER; INSULIN; MESSENGER RNA;

ALLOXAN DIABETES MELLITUS; ANIMAL CELL; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; DIABETOGENESIS; GENE EXPRESSION; GLUCOSE TOLERANCE; KNOCKOUT GENE; MOUSE; NONHUMAN; PANCREAS ISLET BETA CELL; PANCREAS ISLET CELL FUNCTION; PRIORITY JOURNAL;

EID: 0034003559     PISSN: 01931849     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajpendo.2000.278.4.e684     Document Type: Article

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