Fig 1: NTS-NTSR2 signaling regulated the production of GDF15 via CerS2.a Expression level of Gdf15 upon NTS treatment in the primary adipocytes of WT mice (n = 3–4). b–d Expression levels of GDF15 protein upon CerS2 knockdown (b, n = 3–5), CerS2 overexpression (c, n = 6) and ceramide C22 treatment (d, n = 3–4) in primary adipocytes. e–g Serum concentrations of GDF15 (e, n = 6), mRNA expression levels of Gdf15 (f, n = 3) and GDF15 protein abundance in adipose tissues (g, n = 3) of control and CerS2+/– mice. *P < 0.05; **P < 0.01; ***P < 0.001.
Fig 2: NTS-NTSR2 signaling regulated ceramide metabolism in WATs.a A volcano plot of phospho-proteomics data. b Relative abundance of p-CerS2 (n = 3). c p-CerS2 levels detected by pull-down and western blot analysis in the primary adipocytes (n = 5–6). d, e Ceramide C16-C24 levels (d) or individual ceramide levels (e) in eWATs of control and Ntsr2 AKO mice (n = 6). f Individual ceramide levels in the serum of control and Ntsr2 AKO mice (n = 6). g Scheme of the establishment of CerS2+/– mouse strain. h, i Individual ceramide levels in the eWAT (h) and serum (i) of control and CerS2+/– mice (n = 3). j, k Food intake of control and CerS2+/– mice (j), and vehicle vs ceramide C22-treated mice (k); n = 6. l Food intake of control and Ntsr2 AKO mice with CerS2 knockdown (n = 4). *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.
Fig 3: NTS-NTSR2 signaling regulated UPR via CerS2.a–f Expression levels of UPR-related genes (a, b) and proteins (c–f, n = 3) in the adipose tissues of control and Ntsr2 AKO mice; n = 3–6. g Expression levels of UPR-related genes upon NTS treatment in vivo (n = 4). h, i Expression levels of UPR-related genes in the primary adipocytes upon the combinational treatment of NTS and RhoAa (h) or RhoAi (i); n = 4. j p-CerS2 levels in the primary adipocytes upon the combinational treatment of NTS and RhoAi or RhoAa (n = 2–3). k, l Expression levels of UPR-related genes in the primary adipocytes upon knockdown (k) or overexpression of CerS2 (l); n = 4–5. *P < 0.05; **P < 0.01; ***P < 0.001.
Fig 4: Decreasing GDF15 levels led to an increase in food intake in Ntsr2 AKO mice.a Expression levels of Gdf15 in the adipose tissues (n = 4–7). b–d GDF15 protein concentrations in the serum of control and Ntsr2 AKO mice fed by a chow diet (b, n = 8–11), HFD (c, n = 8–12) or treated by NTS (d, n = 5). e Illustration of the experimental design. f Food intake of control and Ntsr2 AKO mice with or without knockdown of Gfral (n = 8). g Food intake of mice treated by NTS in iWATs with Gfral knockdown (n = 5). *P < 0.05; ***P < 0.001; ns, not significant.
Fig 5: NTS-NTSR2 signaling in the adipose tissue regulated food intake.a Food intake of control and Ntsr2 AKO mice (n = 7–8). b–d Changes of body weight (b), GTT (c) and ITT (d) of mice pair-fed by HFD (n = 6–10). e Schematic diagram of local NTS treatment. f, g Food intake of WT lean (f) or obese (g) mice upon NTS treatment (n = 6–12). h Food intake of control and Ntsr2 AKO mice upon NTS treatment (n = 7–8). *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.
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