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 aquaculture. The lipopolysaccharide (LPS) endotoxin induces in mammals septic shock and the activation by LPS of hormone release through the hypothalamo-pituitary axis is well known. In crustaceans an increase in circulating Crustacean hyperglycemic hormone and hyperglycemia are reported to result from exposure to several environmental stressors but the metabolic and hormonal effects of LPS in vivo are undescribed. A sublethal 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 crangon 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. oculatus and a significant increase of 79% in M. rugosa up to 1300% in P. hirtellus over control levels was observed. The involvement of eyestalk hormones in this generalized response was tested on S. mantis, M. vernalis, and P. elegans; LPS injected into eyestalkless animals did not elicit a significant hyperglycemic response compared with saline-injected controls. Eyestalkless animals injected with one eyestalk equivalent homogenate in saline from untreated animals did show a change in color from red to normal likely due to red pigment concentrating hormone and a hyperglycemic response within 2 hr. Eyestalkless animals injected with homogenate from LPS-treated shrimps showed the change in color but not the hyperglycemic response. It is concluded that LPS directly, or cytokines circulated upon challenge by the endotoxin, may act on the medulla terminalis X-organ-sinus gland complex and release CHH selectively eliciting an hyperglycemic stress response, after which CHH stores become relatively depleted.