Signaling
How the adipocyte talks: leptin, adiponectin, insulin, and the beta-adrenergic pathway that turns white fat brown.
Efthymiou V et al. 2026. snRNA-seq of human WAT identifies adipocyte subpopulations; a low-maturation subset linked to TSHZ3-mediated transcriptional suppression is associated with metabolic disease severity.
Kitto ES et al. 2026. snRNA-seq and spatial transcriptomics reveal previously unappreciated adipocyte subpopulations across depots and disease states; cross-species comparisons clarify conserved vs. human-specific subsets.
Grothen JER et al. 2026. NPY receptor 1 (NPY1R) identified as a cell-autonomous brake on adipocyte lipolysis; expression is inversely correlated with BMI and rises after weight loss, implicating neuropeptide Y signaling in direct lipolysis control.
Sahin C et al. 2026. Heterogeneous adipose progenitor subsets are characterized; specific subpopulations are required for thermogenic adipocyte generation and healthy remodeling, with implications for browning strategies.
Zhang et al. 1994. Leptin identified as the ob gene product, a 16-kDa adipocyte-secreted hormone that acts centrally via the hypothalamus to suppress appetite and regulate energy expenditure.
Scherer et al. 1995. Adiponectin (Acrp30) discovered as a second major adipokine, induced 100-fold during adipocyte differentiation, now known to improve insulin sensitivity via AdipoR1/R2.
Hotamisligil et al. 1993. Adipose tissue secretes TNF-alpha in obesity; it serine-phosphorylates IRS-1 via JNK1, blocking insulin receptor interaction. The founding paper on fat as an inflammatory organ.
Sano et al. 2003. The molecular step between Akt activation and GLUT4 appearance at the plasma membrane in adipocytes, completing the insulin-signaling cascade to glucose uptake.
Yamauchi et al. 2002. Mechanism by which adiponectin, the adipocyte-derived insulin sensitizer, acts on its target organs; explains why its loss in obesity worsens metabolic control.
Nicholls 1976. UCP1 mechanism established: purine nucleotides inhibit inner membrane conductance; long-chain fatty acids relieve this inhibition and drive proton leak as heat. The founding UCP1 paper.
Wu et al. 2012. Cold and beta-adrenergic stimulation recruit UCP1-positive beige adipocytes in white depots via a distinct developmental pathway from classical brown fat.
Kitamura T et al. 1999. Insulin's anti-lipolytic action in adipocytes traced to PDE3B activation downstream of Akt, lowering cAMP and inactivating PKA and HSL.
Summers 2006. Excess saturated fatty acids generate ceramide, which activates PP2A and PKCzeta to block Akt membrane translocation, impairing insulin signaling in adipocytes.
Gual P et al. 2005. Review of the serine phosphorylation sites on IRS-1 that block insulin receptor interaction, including the TNF/JNK1 and ceramide pathways. [removed fabricated PNAS DOI; replaced with verified PMID]
Leptolin identified as a novel adipokine positively correlated with exercise and inversely with BMI; it boosts energy expenditure in animal models, a candidate add to the adipokine output panel.
Curated review collection on adipokine biology and signaling, useful as a current overview of which adipokines are considered established versus candidate.
Reviews macrophage heterogeneity in adipose tissue: M1/M2 simplification is inadequate; single-cell data reveal multiple activation states with distinct metabolic roles.
Oya M et al. 2026. Adipocyte-specific AM knockout mice fed HFD developed higher systolic blood pressure than controls; circulating AM was lower and renal dopaminergic responses were blunted. The fat cell secretes adrenomedullin that buffers hypertension during chronic metabolic stress -- another adipokine axis the kidney depends on.
Curtin MC, Jackson AE et al. 2026. Lean mammary adipocytes secrete 9S-HODE, an oxylipin that induces ferroptosis in breast cancer cells by disrupting iron homeostasis; obesity suppresses this secretion. The fat cell as tumor suppressor when healthy -- mechanism is iron-dependent lipid peroxidation, not immune recruitment.