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alicefrolov.bsky.social
New visualization: Rewiring of nutrient-sensing phospho-signaling across the murine lifespan

I am sharing a figure summarizing how phosphorylation status across the insulin/IGF1–AKT–mTORC1.

#MTORC1 #AMPK #Phosphoproteomics #InsulinSignaling #IGF1 #NutrientSensing #HepaticMetabolism
New visualization: Rewiring of nutrient-sensing phospho-signaling across the murine lifespan I am sharing a figure summarizing how phosphorylation status across the insulin/IGF1–AKT–mTORC1 and AMPK axes remodels with hepatic aging. The subtitle reads: "Relative phosphorylation of key nodes in the insulin/IGF1-AKT-mTORC1 and AMPK axes in liver, young vs old." I want to emphasize at the outset that the underlying data are simulated; the visualization is constructed to illustrate a literature-grounded trend rather than to report primary measurements. The chart is a phospho-signaling connected dot matrix: nodes are arranged on a pathway lattice with node-link edges tracing canonical directional relationships (receptor engagement, PI3K–PDK1–AKT propagation, TSC1/2 regulation of RHEB, mTORC1 substrate phosphorylation, and the AMPK inhibitory arm). Each node is segmented into paired young-versus-old glyphs, encoding relative phosphostoichiometry at defined residues (e.g., AKT pT308/pS473, TSC2 pT1462, mTOR pS2448, S6K1 pT389, 4E-BP1, AMPKα pT172, ACC pS79, ULK1 pS757). The depicted trend reflects a recurrent motif in the literature: attenuated proximal insulin/IGF1 input coupled with paradoxical sustained or elevated distal mTORC1 substrate phosphorylation in aged liver, alongside blunted AMPK pT172 responsiveness. The connected-dot topology is intended to make the directionality of this dysregulation legible, foregrounding node-specific decoupling between receptor-proximal signaling and downstream effector output rather than uniform pathway suppression. Edge weighting and glyph saturation encode effect magnitude, so viewers can distinguish nodes exhibiting the strongest young-old divergence from those that remain comparatively stable. I would welcome methodological critique on residue selection, the choice of lattice layout, and whether the segmented-node encoding adequately conveys stoichiometric versus occupancy interpretations.
September 24, 2026 at 5:02 PM
ssteelab.bsky.social
Super interesting read : In Aldob-KO models, inhibiting lipogenesis reduces hepatic TGs but does not rescue the fasting phenotype. 🧬⬇️
Points to a defect beyond lipids: impaired nutrient sensing /signaling, not metabolism alone.
#HFI #Metabolism #LiverDisease #NutrientSensing
December 23, 2025 at 3:42 PM
sablesystems.bsky.social
Next week — Keystone Symposia #conference on #Diabetes and the #GutBrain Axis (Mar 16–19) in CO, USA! Experts from #neuroscience, #gutbiology, #metabolism, #nutrition, and #pharmacology will discuss the latest research & therapeutic applications.

buff.ly/cugH7ab

#Respirometry #NutrientSensing
Gut-Brain Axis | Keystone Symposia
Join us at the Keystone Symposia on Gut-Brain Axis, March 2026, in Breckenridge, with field leaders!
www.keystonesymposia.org
March 13, 2026 at 6:01 PM
alicefrolov.bsky.social
Sharing a phase-trajectory visualization from ongoing work on nutrient-sensing dynamics in skeletal muscle.

#mTORC1 #Autophagy #Proteostasis #SkeletalMuscle #Nutrientsensing #Anabolicresistance #TFEB #Autophagicflux
Sharing a phase-trajectory visualization from ongoing work on nutrient-sensing dynamics in skeletal muscle. Figure title: "mTORC1 signaling and autophagic flux trace opposing arcs during fasting-refeeding" Subtitle: "Young vs aged muscle: aging compresses the dynamic range of nutrient-sensing response" The plot maps mTORC1 activity (proxied by phospho-S6K1 Thr389 and phospho-4E-BP1) on the x-axis against autophagic flux (LC3-II accumulation under lysosomal inhibition, plus p62/SQSTM1 turnover) on the y-axis. Rather than plotting each variable against time separately, I rendered the coupled system as a looped time-course with directional arrows, so the reader traces the trajectory through the fasting-to-refeeding transition and back. Each arm of the loop corresponds to one metabolic phase: the fasting arm sweeps toward low mTORC1 and elevated flux, the refeeding arm reverses toward mTORC1 reactivation and flux suppression, consistent with ULK1 Ser757 phosphorylation dynamics and TFEB nuclear-cytoplasmic shuttling. Two trajectories are overlaid. The young-muscle loop encloses a large area, indicating robust reciprocal excursion between anabolic and catabolic states. The aged-muscle loop is markedly contracted, reflecting the central claim: aging compresses the dynamic range on both axes. mTORC1 shows elevated basal tone and blunted fasting-induced deactivation, while autophagic induction is attenuated, collapsing the phase space the system can traverse. I want to be explicit that these data are simulated. The values are not from a wet-lab cohort; they are generated to illustrate a trend that is well grounded in the literature on age-related anabolic resistance and impaired proteostatic flux. The visualization is intended as a conceptual and pedagogical instrument for reasoning about coupled signaling arms, not as an empirical result.
August 29, 2026 at 5:55 PM
stvanneste.bsky.social
Lysosomal membrane missing link in allosteric activation of mTORC1 kinase complex. #nutrientsensing, metabolic integration. Something similar going on in plants? 🤔
September 19, 2025 at 6:39 AM