Mahanta Anusree, Najar Sajad Ahmad, Hariharan Nivedita, Bhowmick Ajit, Rizvi Syed Iqra, Goyal Manisha, Parupalli Preethi, Subramanian Ramaswamy, Giangrande Angela, Palakodeti Dasaradhi, Mukherjee Tina
Institute for Stem Cell Science and Regenerative Medicine (inStem), GKVK post, Bellary Road, Bangalore, Karnataka, 560065, India.
The Shanmugha Arts, Science, Technology & Research Academy (SASTRA), Thanjavur, Tamil Nadu, 613401, India.
EMBO Rep. 2025 Sep 9. doi: 10.1038/s44319-025-00574-7.
Immune cells are increasingly recognized as nutrient sensors; however, their developmental role in regulating growth under homeostasis or dietary stress remains elusive. Here, we show that Drosophila larval macrophages, in response to excessive dietary sugar (HSD), reprogram their metabolic state by activating glycolysis, thereby enhancing TCA-cycle flux, and increasing lipogenesis-while concurrently maintaining a lipolytic state. Although this immune-metabolic configuration correlates with growth retardation under HSD, our genetic analyses reveal that enhanced lipogenesis supports growth, whereas glycolysis and lipolysis are growth-inhibitory. Notably, promoting immune-driven lipogenesis offsets early growth inhibition in imaginal discs caused by glycolytic and lipolytic immune-metabolic states. Our findings reveal a model of immune-metabolic imbalance, where growth-suppressive states (glycolysis, lipolysis) dominate over a growth-supportive lipogenic state, thereby impairing early organ size control and ultimately affecting adult size. Overall, this study provides important insights into dietary stress-induced immune-metabolic reprogramming and its link to organ size regulation and early developmental plasticity.
免疫细胞越来越被认为是营养传感器;然而,它们在稳态或饮食应激下调节生长的发育作用仍然难以捉摸。在这里,我们表明果蝇幼虫巨噬细胞在应对过量饮食糖分(高糖饮食,HSD)时,通过激活糖酵解来重新编程其代谢状态,从而增强三羧酸循环通量,并增加脂肪生成,同时维持脂解状态。尽管这种免疫代谢配置与高糖饮食下的生长迟缓相关,但我们的基因分析表明,增强的脂肪生成支持生长,而糖酵解和脂解则抑制生长。值得注意的是,促进免疫驱动的脂肪生成可抵消由糖酵解和脂解免疫代谢状态引起的成虫盘早期生长抑制。我们的研究结果揭示了一种免疫代谢失衡模型,其中生长抑制状态(糖酵解、脂解)超过生长支持性脂肪生成状态,从而损害早期器官大小控制并最终影响成虫大小。总体而言,本研究为饮食应激诱导的免疫代谢重编程及其与器官大小调节和早期发育可塑性的联系提供了重要见解。