2019 Fiscal Year Annual Research Report
Elucidation of energy homeostasis of corpora cardiaca and corpora allata in insect
| Project/Area Number |
18J22078
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| Research Institution | The University of Tokyo |
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Principal Investigator |
ZHOU YIJUN 東京大学, 新領域創成科学研究科, 特別研究員(DC1)
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| Project Period (FY) |
2018-04-25 – 2021-03-31
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| Keywords | CCAP / Myosuppressin / Energy homeostasis |
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| Outline of Annual Research Achievements |
The elucidation of the counteractive regulation of two neuropeptides, CCAP and MS, in energy homeostasis CCAP and MS regulated energy homeostasis counteractively, with alteration on food intake, excretion, carbohydrate and lipid level in the hemolymph.
Knockdown of AKH receptor and Insulin receptor substrate inhibited the function of MS, indicating that function of MS on energy homeostasis is dependent of AKH/Insulin signals, whereas CCAP is independent. Glucose in circulation increased the expression of CCAP in central nervous system and dietary glucose decreased the expression of CCAP in Intestine. Both circulating and dietary trehalose increased expression of MS in CNS and intestine.
(CCAP: Crustacean cardioactive peptide; MS: Myosuppressin; AKH: Adipokinetic hormone)
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| Current Status of Research Progress |
Current Status of Research Progress
2: Research has progressed on the whole more than it was originally planned.
Reason
The elucidation of effects of CCAP and MS on energy homeostasis is the most important part in this research, due to both of them were reported as the upstream signals of AKH, a predominant regulator that only expressed in corpora cardiaca.
After confirming the neurosecretory cells or CCAP- and MS- expressing neurons in central nervous system or intestine, this part is able to be published.
Also, for the entire study, confirmation of endocrine signals from pheripheral organs to corpora cardiaca is important for understanding the role of feedback signal in energy homeostais regulation, which is a clue for adaptive feeding behavior.
(CCAP: Crustacean cardioactive peptide; MS: Myosuppressin; AKH: Adipokinetic hormone)
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| Strategy for Future Research Activity |
(1) Confirmation of the neurosecretory cells or expressing neurons of CCAP and MS and discuss the possibility of colocalization
(2) Screening of the endocrine factor that from peripheral organs, such as fatbody or intestine, to terminate at corpora cardiaca
(3) Elucidation of the mechanism of (2), and figure out what adaptive alteration would cause and how these peripheral endocrine factors result in the adaptive feeding behavior.
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