Diminished glucagon suppression after β-cell reduction is due to impaired α-cell function rather than an expansion of α-cell mass

American Journal of Physiology - Endocrinology and Metabolism

Volumn 300, Issue 4, 2011, Pages 717-723

  Meier, Juris J ^a   Ueberberg, Sandra ^b   Korbas, Simone ^b   Schneider, Stephan ^b  

^a ST JOSEF HOSPITAL   (Germany)

^b RUHR UNIVERSITY BOCHUM   (Germany)

Author keywords

Hyperglucagonemia; Intraislet insulin; Streptozotocin; Type 2 diabetes

Indexed keywords

GLUCAGON; GLUCOSE; INSULIN; STREPTOZOCIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL DIVISION; CELL EXPANSION; CONTROLLED STUDY; DRUG TREATMENT FAILURE; GLUCAGON BLOOD LEVEL; GLUCAGON RELEASE; GLUCOSE BLOOD LEVEL; GLUCOSE TOLERANCE TEST; HYPERGLUCAGONEMIA; HYPERGLYCEMIA; IMMUNOHISTOCHEMISTRY; INSULIN BLOOD LEVEL; MOUSE; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; PANCREAS ISLET ALPHA CELL; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; STATISTICAL SIGNIFICANCE; UPREGULATION;

ANIMALS; BLOOD GLUCOSE; CELL COUNT; CELL PROLIFERATION; DIABETES MELLITUS, EXPERIMENTAL; DIABETES MELLITUS, TYPE 2; DOWN-REGULATION; GLUCAGON; GLUCAGON-SECRETING CELLS; GLUCOSE TOLERANCE TEST; INFUSIONS, PARENTERAL; INSULIN; INSULIN-SECRETING CELLS; MICE; STREPTOZOCIN;

EID: 79955153811     PISSN: 01931849     EISSN: 15221555     Source Type: Journal    
DOI: 10.1152/ajpendo.00315.2010     Document Type: Article

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