The prevalent Glu23Lys polymorphism in the potassium inward rectifier 6.2 (KIR6.2) gene is associated with impaired glucagon suppression in response to hyperglycemia

Diabetes

Volumn 51, Issue 9, 2002, Pages 2854-2860

  Tschritter, Otto ^a   Stumvoll, Michael ^a   Machicao, Fausto ^a   Holzwarth, Martin ^a   Weisser, Melanie ^a   Maerker, Elke ^a   Teigeler, Anna ^a   Häring, Hans ^a   Fritsche, Andreas ^a  

^a UNIVERSITY HOSPITAL TÜBINGEN   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ARGININE; C PEPTIDE; GLUCAGON; GLUCAGON LIKE PEPTIDE 1; GLUCOSE; GLUTAMIC ACID; INSULIN; LYSINE; POTASSIUM CHANNEL;

ADULT; ARTICLE; CELL FUNCTION; CONTROLLED STUDY; FEMALE; GENE; GENETIC POLYMORPHISM; GLUCAGON BLOOD LEVEL; GLUCAGON RELEASE; GLUCOSE METABOLISM; HUMAN; HYPERGLYCEMIA; INSULIN SENSITIVITY; KIR6.2 GENE; MAJOR CLINICAL STUDY; MALE; NON INSULIN DEPENDENT DIABETES MELLITUS; ORAL GLUCOSE TOLERANCE TEST; PANCREAS ISLET ALPHA CELL; PANCREAS ISLET BETA CELL; PATHOGENESIS; PRIORITY JOURNAL;

EID: 0036724723     PISSN: 00121797     EISSN: None     Source Type: Journal    
DOI: 10.2337/diabetes.51.9.2854     Document Type: Article

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