TY - JOUR
T1 - Cell signaling
T2 - IP3 receptor types 2 and 3 mediates exocrine secretion underlying energy metabolism
AU - Futatsugi, Akira
AU - Nakamura, Takeshi
AU - Yamada, Maki K.
AU - Ebisui, Etsuko
AU - Nakamura, Kyoko
AU - Uchida, Kelko
AU - Kitaguchi, Tetsuya
AU - Takashi-Iwanaga, Hiromi
AU - Noda, Tetsuo
AU - Aruga, Jun
AU - Mikoshiba, Katsuhiko
PY - 2005/9/30
Y1 - 2005/9/30
N2 - Type 2 and type 3 inositol 1,4,5-trisphosphate receptors (IP3R2 and IP3RB) are intracellular calcium-release channels whose physiological roles are unknown. We show exocrine dysfunction in IP 3R2 and IP3R3 double knock-out mice, which caused difficulties in nutrient digestion. Severely impaired calcium signaling in acinar cells of the salivary glands and the pancreas in the double mutants ascribed the secretion deficits to a lack of intracellular calcium release. Despite a normal caloric intake, the double mutants were hypoglycemic and lean. These results reveal IP3R2 and IP3R3 as key molecules in exocrine physiology underlying energy metabolism and animal growth.
AB - Type 2 and type 3 inositol 1,4,5-trisphosphate receptors (IP3R2 and IP3RB) are intracellular calcium-release channels whose physiological roles are unknown. We show exocrine dysfunction in IP 3R2 and IP3R3 double knock-out mice, which caused difficulties in nutrient digestion. Severely impaired calcium signaling in acinar cells of the salivary glands and the pancreas in the double mutants ascribed the secretion deficits to a lack of intracellular calcium release. Despite a normal caloric intake, the double mutants were hypoglycemic and lean. These results reveal IP3R2 and IP3R3 as key molecules in exocrine physiology underlying energy metabolism and animal growth.
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U2 - 10.1126/science.1114110
DO - 10.1126/science.1114110
M3 - Article
C2 - 16195467
AN - SCOPUS:25844462280
SN - 0036-8075
VL - 309
SP - 2232
EP - 2234
JO - Science
JF - Science
IS - 5744
ER -