Pellerin, A. | bioRxiv Science

bioRxiv2026

Fatty acids from adipocyte lipolysis stimulate insulin secretion

White adipose tissue and pancreatic islets play central roles in the regulation of metabolic homeostasis. Although ectopic lipid accumulation is established as a driver of impaired insulin secretion, the acute contribution of adipocyte lipolysis to islet function remains poorly documented. Here, we investigated a mouse model with inducible adipocyte-specific deletion of both adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), which leads to defective adipocyte lipolysis. Despite preserved ex vivo islet function, these mice displayed a marked reduction in insulin secretion in response to stimulation of adipocyte {beta}3-adrenoceptors, as well as following glucose and arginine challenges. Mechanistically, we identified non-esterified fatty acids as critical mediators of lipolysis-driven insulin secretion, engaging pancreatic signaling of the free fatty acid receptors FFAR4 (a.k.a. GPR120) and FFAR1 (a.k.a. GPR40). The regulation of insulin secretion by adipocyte lipolysis was preserved in high-fat diet-induced obesity. These findings identify an underappreciated adipose-islet crosstalk that couples adipocyte lipolysis to insulin secretion and links lipid and glucose metabolism.

physiology↗

bioRxiv2023

Emiliania huxleyi virus arrests host calcification and nutrient consumption, and triggers shifts in organic stoichiometry

Blooms of the coccolithophore Emiliania huxleyi are routinely infected by a specific lytic virus (EhV), which rapidly kills host cells triggering bloom termination and organic and inorganic carbon export. However, the impact of EhV on the dynamic of resource acquisition and cellular stoichiometry remains unknown, limiting the current understanding of the ecological and biogeochemical significance of E. huxleyi blooms. To tackle this knowledge gap, we used algal and EhV cultures to determine over the course of infections the dynamics of alkalinity, modulated by calcification, nitrate and phosphate consumption and organic matter stoichiometry. We found that within 24hr alkalinity concentration stabilized and nutrient uptake declined to background levels. In parallel, the stoichiometric ratio of carbon to nitrogen was about 15% higher and the nitrogen to phosphorus ratio was about 12% lower during infections relative to controls. These variations likely resulted from lipid accumulation required for viral replication and the differential retention of phosphorus-rich macromolecular pools in decaying cells, respectively. Finally, after host population decay a progressive enrichment in phosphorus relative to nitrogen and carbon was detected in the remaining cell lysates. We estimate that this stoichiometric shift post-infection was driven by the progressive accumulation of heterotrophic bacteria involved in the degradation of organic material. Viral-mediated cell remodeling and consequent shifts in biomass stoichiometry likely impacts the patterns of nutrient cycling and biological carbon pump efficiency during large-scale blooms in the oceans.

microbiology↗