IP3 receptor types 2 and 3 mediate exocrine secretion underlying energy metabolism

被引:263
作者
Futatsugi, A [1 ]
Nakamura, T
Yamada, MK
Ebisui, E
Nakamura, K
Uchida, K
Kitaguchi, T
Takahashi-Iwanaga, H
Noda, T
Aruga, J
Mikoshiba, K
机构
[1] Japan Sci & Technol Agcy, Calcium Oscillat, Int Cooperat Res Project, Tokyo 1080071, Japan
[2] RIKEN, Brain Sci Inst, Dev Neurobiol Lab, Brain Dev Res Grp, Saitama 3510198, Japan
[3] Univ Tokyo, Inst Med Sci, Div Mol Neurobiol, Tokyo 1088639, Japan
[4] Hokkaido Univ, Sch Med, Dept Anat, Sapporo, Hokkaido 0608638, Japan
[5] Japanese Fdn Canc Res, Inst Canc, Dept Cell Biol, Tokyo 1708455, Japan
关键词
D O I
10.1126/science.1114110
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Type 2 and type 3 inositol 1,4,5-trisphosphate receptors (IP3 R2 and IP(3)R3) are intracellular calcium-release channels whose physiological roles are unknown. We show exocrine dysfunction in IP3 R2 and IP3 R3 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 tack of intracellular calcium release. Despite a normal caloric intake, the double mutants were hypoglycemic and lean. These results reveal IP3 R2 and IP3 R3 as key molecules in exocrine physiology underlying energy metabolism and animal growth.
引用
收藏
页码:2232 / 2234
页数:3
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