Defects in beta cell Ca2+ signalling, glucose metabolism and insulin secretion in a murine model of KATP channel-induced neonatal diabetes mellitus

Diabetologia

Volumn 54, Issue 5, 2011, Pages 1087-1097

  Benninger, R K P ^a   Remedi, M S ^b   Head, W S ^a   Ustione, A ^a   Piston, D W ^a   Nichols, C G ^b  

^a VANDERBILT UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Beta cell; Calcium; Gap junctions; KATP channel; Neonatal diabetes mellitus; Transgenic mice

Indexed keywords

ADENOSINE TRIPHOSPHATE SENSITIVE POTASSIUM CHANNEL; CALCIUM ION; GLUCOSE; INSULIN; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR6.2; POTASSIUM CHLORIDE; SULFONYLUREA DERIVATIVE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CALCIUM CELL LEVEL; CALCIUM SIGNALING; CONTROLLED STUDY; DIABETES MELLITUS; DISORDERS OF MITOCHONDRIAL FUNCTIONS; ELECTROSTIMULATION; GAP JUNCTION; GLUCOSE METABOLISM; HYPERGLYCEMIA; HYPOINSULINEMIA; INSULIN RELEASE; MOUSE; NEWBORN DIABETES MELLITUS; NONHUMAN; OXIDATION REDUCTION STATE; PANCREAS ISLET BETA CELL DYSFUNCTION; PANCREAS ISLET CELL FUNCTION; PANCREAS ISLET DISEASE; PANCREAS ISLET TRANSPLANTATION; PATHOPHYSIOLOGY; PRIORITY JOURNAL; PROTEIN EXPRESSION;

ANIMALS; ANIMALS, NEWBORN; CALCIUM; CALCIUM SIGNALING; DIABETES MELLITUS; GLUCOSE; INSULIN; KATP CHANNELS; MICE; MICE, TRANSGENIC; POTASSIUM CHANNELS, INWARDLY RECTIFYING;

EID: 79954633671     PISSN: 0012186X     EISSN: 14320428     Source Type: Journal    
DOI: 10.1007/s00125-010-2039-7     Document Type: Article

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