Partial inactivation of Ankrd26 causes diabetes with enhanced insulin responsiveness of adipose tissue in mice

Diabetologia

Volumn 54, Issue 11, 2011, Pages 2911-2922

  Raciti, G A ^a   Bera, T K ^a   Gavrilova, O ^b   Pastan, I ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES   (United States)

Author keywords

Ankrd26; Diabetes; Energy intake restriction; Insulin sensitivity; Obesity; WAT

Indexed keywords

INSULIN; INSULIN RECEPTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANKRD26 GENE; ARTICLE; BODY WEIGHT; CONTROLLED STUDY; DIABETES MELLITUS; DIET RESTRICTION; GENE; GENE INACTIVATION; GLUCOSE HOMEOSTASIS; GLUCOSE TOLERANCE; INSULIN RESISTANCE; INSULIN RESPONSE; INSULIN SENSITIVITY; MALE; MOUSE; MUTANT; NONHUMAN; OBESITY; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; RISK FACTOR; WHITE ADIPOSE TISSUE;

ADIPOSE TISSUE, WHITE; ANIMALS; APPETITE REGULATION; CALORIC RESTRICTION; DIABETES MELLITUS, TYPE 2; DISEASE MODELS, ANIMAL; DNA-BINDING PROTEINS; GLUCOSE INTOLERANCE; INSULIN; INSULIN RESISTANCE; MALE; MICE; MICE, INBRED C57BL; MICE, MUTANT STRAINS; MUTANT PROTEINS; OBESITY; ORGAN SPECIFICITY; PHOSPHORYLATION; PROTEIN PROCESSING, POST-TRANSLATIONAL; RANDOM ALLOCATION; RECEPTOR, INSULIN; SIGNAL TRANSDUCTION; TRANSCRIPTION FACTORS;

EID: 80054695640     PISSN: 0012186X     EISSN: 14320428     Source Type: Journal    
DOI: 10.1007/s00125-011-2263-9     Document Type: Article

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