ArticleJournal of advanced research2026
Nutritional and hormonal regulation of mitochondrial biogenesis drives fat body remodeling for reproductive competence.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Mitochondria-targeted phototherapeutic system enabling spatiotemporal-controlled NADH depletion for keloid intervention.Materials today. Bio · 2026Article
- Beyond Fuel: Exercise-Induced Lactate as a Metabolic-Epigenetic Regulator in Central Nervous System Health and Disease.Biomolecules · 2025Review
- Exercise orchestrates systemic metabolic and neuroimmune homeostasis via the brain-muscle-liver axis to slow down aging and neurodegeneration: a narrative review.European journal of medical research · 2025Review
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8 authors.
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Abstract
introductionInsect fat body serves as a central hub for energy mobilization and protein synthesis. During larval metamorphosis, fat body undergoes programmed cell death and tissue disassembly. Following adult eclosion, fat body reconstructs with cell proliferation and becomes competent for large-scale vitellogenin (Vg) synthesis required for the maturation of dozens of eggs.
objectivesThis study aims to uncover the molecular mechanisms underlying the remodeling of fat body in acquisition of competence for massive Vg production.
methodsRNA-seq and metabolomics were used for identification of differentially expressed genes and metabolites. RNAi was applied for gene knockdown. Transmission electron microscope, MitoTracker staining, mitochondrial DNA quantification, ATP and citrate synthase assays were employed for examining mitochondrial biogenesis. Dual-luciferase reporter assay and EMSA were performed for transcriptional regulation. qRT-PCR and western blot were performed for measuring Vg synthesis.
resultsTranscriptomic and metabolomic analyses revealed significant upregulation of genes and metabolites involved in mitochondrial biogenesis in the fat body of adult locusts. PGC-1α was highly expressed in adult fat body. Knockdown of PGC-1α reduced mitochondrial biogenesis, fat body cell number, Vg synthesis and ovarian development. CREBB bound to PGC-1α promoter and activated its transcription. CREBB depletion impaired mitochondrial biogenesis and fat body remodeling. Moreover, loss of TORC1 function suppressed CREBB function and PGC-1α expression, subsequently disrupting mitochondrial biogenesis and fat body remodeling. Juvenile hormone (JH) deprivation also decreased CREBB function and PGC-1α expression, which was reversible with JH treatment. Our results suggest that TORC1 and JH coordinate CREBB-upregulated PGC-1α expression, which promotes mitochondrial biogenesis and fat body remodeling for Vg synthesis and egg production.
conclusionThe findings provide new insights into the molecular mechanisms of post-metamorphic fat body development, and highlight the role of JH/TORC1/CREBB/PGC-1α/mitochondrial biogenesis axis in insect reproduction. The data also offer potential targets for insect pest control.
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