Activation of fat body glycogen phosphorylase in the eastern lubber grasshopper (Romalea microptera) by the endogenous neuropeptides Ro I and Ro II
✍ Scribed by Gäde, Gerd ;Spring, Jeffrey H.
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- English
- Weight
- 976 KB
- Volume
- 250
- Category
- Article
- ISSN
- 0022-104X
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✦ Synopsis
Romalea corpus cardiacum (CC) contains large quantities of two neuropeptides, named Ro I and Ro 11, that are capable of eliciting strong hyperlipemic (locusts) and hypertrehalosemic (cockroaches) responses in test species (Spring and Gade: Journal of Experimental Zoology 241:41-50, 1987). Although clearly members of the locust adipokinetic hormone/crustacean red pigment-concentrating hormone (AKH/RPCH) family of peptides (Gade:
Zeitschrift fur Naturforschung, Section C 41:315-320, 19861, these neuropeptides have no discernible effect on hemolymph lipids or carbohydrates in RomaZea itself, and neither do large doses of synthetic locust AKH I (1,000 pmol) nor stick insect hypertrehalosemic factor I1 (HTF 11: 500 pmol). Injections of its own CC are capable of stimulating Romalea fat body glycogen phosphorylase in a dose-dependent manner, and this effect can be mimicked by Ro I and Ro 11. Neither extracts of pars intercerebralis nor subesophageal ganglion have any significant effect on phosphorylase activation. Using synthetic peptides, we determined doseresponse curves for phosphorylase activation. Ro I is the more effective in stimulating phosphorylase, with a maximum activation of 70%, compared to 50% for Ro 11. Ro I1 is more potent, however, producing a significant activation with 0.1 pmol, compared to 0.5 pmol of Ro I.
Although these peptides are powerful activators of endogenous fat body glycogen phosphorylase in Romalea, this function does not explain the enormous quantities of neuropeptide (2,800 pmol Ro I; 650 pmol Ro 11) found in the CC. Glycogen phosphorylase is also activated by starvation, and this effect is reversed by feeding. It is not clear at present whether the starvation-induced activation is hormonally controlled.