Abstract:

Using the corpora cardiaca (CC) of Drosophila melanogaster as the central focus, this review establishes a four-dimensional framework—development, secretion, regulation, and function—to systematically summarize the pivotal role of the CC in glucose homeostasis. We first emphasize that Drosophila, owing to its sophisticated genetic toolkit and extensive gene homology with humans, constitutes an ideal model for studying energy balance. The CC and the insulin-producing cells (IPCs) are considered functional counterparts of the vertebrate pancreatic α- and β-cells, respectively, and jointly modulate haemolymph glucose and trehalose levels via the counter-regulatory hormones adipokinetic hormone (AKH) and Drosophila insulin-like peptides (DILPs). We begin by detailing CC ontogeny: the structure originates in the head mesoderm, undergoes embryonic specification, larval expansion, pupal remodelling, and adult fusion, ultimately forming a bilobed organ encircling the oesophagus. Precise spatiotemporal signalling by sine oculis, glass, Notch, dpp, and hh is required; loss-of-function mutations at any of these loci can lead to CC absence or severe functional defects. The CC integrates external inputs that converge from nutrient status, the intestine, and the brain. Under starvation, surface glucose sensors detect hypoglycaemia and increase AKH secretion. Enteroendocrine cells release peptides such as AstA, Bursicon α, and NPF, exerting positive or negative feedback on the CC. Dopaminergic neurons, pigment-dispersing factor (PDF), and DILP1/2 from the brain create a neuro-endocrine antagonistic network that finely tunes AKH release. The CC secretes three principal molecular classes: (1) AKH, which, via the AKHR–cAMP–PKA pathway, mobilises glycogen and triacylglycerol in the fat body; (2) Limostatin (Lst) , which, acting through its receptor, suppresses DILP release from IPCs; and (3) the insulin antagonist protein Imaginal morphogenesis protein-Late 2 (ImpL2) , which antagonises DILPs and inhibits the TOR pathway, thereby coupling nutrient status to developmental progression. The AKH/AKHR axis drives carbohydrate and lipid mobilisation and foraging hyperactivity under starvation, high-fat diet, or thermal stress. Prothoracicotropic hormone (PTTH) and ImpL2 mediate CC–prothoracic-gland signalling to ensure proper ecdysteroid function after attainment of the critical weight. CC axons innervate the crop, modulating its emptying rate, and the AKH-FoxO-s-LNv circuit prevents starvation-induced sleep loss, thereby maintaining circadian homeostasis. By integrating CC developmental mechanisms, hormone secretion pathways, and interactions with other tissues, this review not only advances our understanding of insect energy homeostasis but also provides novel perspectives and molecular targets for studies of metabolic disorders and related diseases in vertebrates.

Key words: Drosophila melanogaster, Metabolism, Corpora Cardiaca, Adipokinetic hormone