LIPOPOLYSACCHARIDE-INDUCED HYPERGLYCEMIA IS MEDIATED BY CHH RELEASE IN CRUSTACEANS

Septicemia in crustaceans may occur occasionally due to Gram-negative opportunistic bacteria, especially under conditions of intensive aquac ulture. The lipopolysaccharide (LPS) endotoxin induces in mammals sept ic shock and the activation by LPS of hormone release through the hypo thalamo-pituitary axis is well known. In crustaceans an increase in ci rculating Crustacean hyperglycemic hormone and hyperglycemia are repor ted to result from exposure to several environmental stressors but the metabolic and hormonal effects of LPS in vivo are undescribed. A subl ethal dose of LPS (Sigma, Escherichia coli 0111:B4) was injected into at least five individuals of species representative of crustacean taxa and life habits: Squilla mantis (Stomatopoda); the Decapoda Crangon c rangon and Palaemon elegans (Caridea), Nephrops norvegicus (Astacidea) , Munida rugosa and Paguristes oculatus (Anomura), Pilumnus hirtellus, Macropipus vernalis, Parthenope massena, and Ilia nucleus (Brachyura) . Within 3 hr an increase in blood sugar developed ranging from 26.00 +/- 8.37 sd mg/dl in M. rugosa to 201.50 +/- 95.91 sd mg/dl in P. ocul atus and a significant increase of 79% in M. rugosa up to 1300% in P. hirtellus over control levels was observed. The involvement of eyestal k hormones in this generalized response was tested on S. mantis, M. ve rnalis, and P. elegans; LPS injected into eyestalkless animals did not elicit a significant hyperglycemic response compared with saline-inje cted controls. Eyestalkless animals injected with one eyestalk equival ent homogenate in saline from untreated animals did show a change in c olor from red to normal likely due to red pigment concentrating hormon e and a hyperglycemic response within 2 hr. Eyestalkless animals injec ted with homogenate from LPS-treated shrimps showed the change in colo r but not the hyperglycemic response. It is concluded that LPS directl y, or cytokines circulated upon challenge by the endotoxin, may act on the medulla terminalis X-organ-sinus gland complex and release CHH se lectively eliciting an hyperglycemic stress response, after which CHH stores become relatively depleted. (C) 1997 Academic Press.