Gene family-level endocrine compensation and metabolic reprogramming preserve growth homeostasis under sustained insulin-like peptide suppression in Litopenaeus vannamei.

Authors

Jiawei Liu, Zijie Liu, Xiaowei Song, Su Liu, Lin Song, Yi Gao

Published in

Frontiers in endocrinology. Volume 17. Pages 1842807. Epub Jun 08, 2026.

Abstract

Insulin-like peptide (ILP) signaling is a critical endocrine axis governing growth, metabolism, and reproduction in crustaceans. In decapods, the ILP family has diversified into four subtypes through gene duplication, yet the functional coordination among these ligands to buffer endocrine perturbations remains poorly understood. Building on our previous identification of insulin-type ILP (LvIns) as a key regulator of growth and glucose metabolism in Litopenaeus vannamei, we investigated the long-term physiological consequences of sustained LvIns suppression. Surprisingly, prolonged knockdown did not result in progressive growth deterioration or elevated mortality. Instead, shrimp exhibited a notable recovery of growth and metabolic performance, revealing a dynamic adaptive response to chronic endocrine perturbation. Notably, this recovery coincided with robust up-regulation of the gonadulin-type ILP LvGon, another ILP family member. In vivo glucose challenge and exogenous insulin assays, together with in vitro primary hepatopancreas cell experiments, demonstrated that LvGon is rapidly induced by hyperglycemia and suppressed by insulin, placing it within a glucose-insulin regulatory loop. LvGon also exhibited broad tissue distribution similar to LvIns, sharing conserved insulin-like structural features and predicted insulin receptor-binding potential. Transcriptomic analysis further revealed coordinated metabolic reprogramming, including up-regulation of glycolysis, fatty acid oxidation/ketogenesis, and the tricarboxylic acid cycle, as well as activation of growth-associated Wnt and MAPK/ERK pathways. Collectively, these findings support a multilevel compensatory framework, in which ligand-level substitution (LvGon up-regulation), metabolic remodeling, and growth signaling activation converge to restore growth homeostasis under sustained disruption of insulin-like signaling, providing mechanistic insight into endocrine redundancy and network plasticity in crustaceans.

PMID:
42339088
Bibliographic data and abstract were imported from PubMed on 24 Jun 2026.

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