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mouse recombinant leptin r leptin  (R&D Systems)


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    R&D Systems mouse recombinant leptin r leptin
    <t>r‐Leptin</t> and Fc‐Leptin characterization. (A) Comparison of r‐Leptin and Fc‐Leptin in vitro pSTAT3 functional activity with the human long‐form leptin receptor ( n = 2–4 independent experiments). (B) Comparison of r‐Leptin (10 mg/kg) and Fc‐Leptin (2 mg/kg) plasma exposure following a single SC dose administration in wildtype mice ( n = 3 mice per group). (C) Modelling of differences in pulsatile exposure following dosing with r‐Leptin (10 mg/kg SC BID) versus Fc‐Leptin (single 2 mg/kg dose). (D) Bodyweight in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 6. **** p < 0.0001, DF = 18, t ratio = −9.13. (E) Cumulative food intake (6 days) in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.07. (F) Body weight after a single Fc‐Leptin dose of 20 mg/kg in non‐obese mice ( n = 5 mice per group). Comparison shown is between vehicle and Fc‐Leptin each day. * p < 0.05, ** p < 0.01, DF = 8, t ratio = −3.85. (G) Cumulative food intake (6 days) in non‐obese mice that received a single Fc‐Leptin dose of 20 mg/kg ( n = 5 mice per group). *** p < 0.001, DF = 7.01, t ratio = 5.64. Values are shown as mean ± SEM.
    Mouse Recombinant Leptin R Leptin, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 162 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse recombinant leptin r leptin/product/R&D Systems
    Average 95 stars, based on 162 article reviews
    mouse recombinant leptin r leptin - by Bioz Stars, 2026-05
    95/100 stars

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    1) Product Images from "Evaluation of leptin treatment on maintenance of body weight loss in diet‐induced obese mice"

    Article Title: Evaluation of leptin treatment on maintenance of body weight loss in diet‐induced obese mice

    Journal: Diabetes, Obesity & Metabolism

    doi: 10.1111/dom.70207

    r‐Leptin and Fc‐Leptin characterization. (A) Comparison of r‐Leptin and Fc‐Leptin in vitro pSTAT3 functional activity with the human long‐form leptin receptor ( n = 2–4 independent experiments). (B) Comparison of r‐Leptin (10 mg/kg) and Fc‐Leptin (2 mg/kg) plasma exposure following a single SC dose administration in wildtype mice ( n = 3 mice per group). (C) Modelling of differences in pulsatile exposure following dosing with r‐Leptin (10 mg/kg SC BID) versus Fc‐Leptin (single 2 mg/kg dose). (D) Bodyweight in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 6. **** p < 0.0001, DF = 18, t ratio = −9.13. (E) Cumulative food intake (6 days) in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.07. (F) Body weight after a single Fc‐Leptin dose of 20 mg/kg in non‐obese mice ( n = 5 mice per group). Comparison shown is between vehicle and Fc‐Leptin each day. * p < 0.05, ** p < 0.01, DF = 8, t ratio = −3.85. (G) Cumulative food intake (6 days) in non‐obese mice that received a single Fc‐Leptin dose of 20 mg/kg ( n = 5 mice per group). *** p < 0.001, DF = 7.01, t ratio = 5.64. Values are shown as mean ± SEM.
    Figure Legend Snippet: r‐Leptin and Fc‐Leptin characterization. (A) Comparison of r‐Leptin and Fc‐Leptin in vitro pSTAT3 functional activity with the human long‐form leptin receptor ( n = 2–4 independent experiments). (B) Comparison of r‐Leptin (10 mg/kg) and Fc‐Leptin (2 mg/kg) plasma exposure following a single SC dose administration in wildtype mice ( n = 3 mice per group). (C) Modelling of differences in pulsatile exposure following dosing with r‐Leptin (10 mg/kg SC BID) versus Fc‐Leptin (single 2 mg/kg dose). (D) Bodyweight in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 6. **** p < 0.0001, DF = 18, t ratio = −9.13. (E) Cumulative food intake (6 days) in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.07. (F) Body weight after a single Fc‐Leptin dose of 20 mg/kg in non‐obese mice ( n = 5 mice per group). Comparison shown is between vehicle and Fc‐Leptin each day. * p < 0.05, ** p < 0.01, DF = 8, t ratio = −3.85. (G) Cumulative food intake (6 days) in non‐obese mice that received a single Fc‐Leptin dose of 20 mg/kg ( n = 5 mice per group). *** p < 0.001, DF = 7.01, t ratio = 5.64. Values are shown as mean ± SEM.

    Techniques Used: Comparison, In Vitro, Functional Assay, Activity Assay, Clinical Proteomics

    Leptin treatment after weight loss stabilization does not prevent weight regain. (A) Schematic representation of the 10% weight loss/weight maintenance model with a stabilization period in DIO mice fed a 60% HFD. (B) Plasma leptin concentration at baseline and after 21 days of 10% weight loss stabilization ( n = 5 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. ** p < 0.01, DF = 6.23, t ratio = 3.77. (C) Body composition at baseline and after 21 days of 10% weight loss stabilization ( n = 40 mice per group). * p < 0.05, **** p < 0.0001, DF = 3, f ratio = 238.7. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with vehicle, 2 mg/kg r‐Leptin, 20 mg/kg Fc‐Leptin, or 0.05 mg/kg Liraglutide ( n = 10 mice per group). Comparisons shown are between vehicle and liraglutide on day 39. ** p < 0.01, **** p < 0.0001, DF = 36, t ratio = −9.15. (F) Cumulative food intake (days 25 to 40) in DIO mice with treated with vehicle, 2 mg/kg r‐Leptin, 20 mg/kg Fc‐Leptin, or 0.05 mg/kg Liraglutide ( n = 5–10 mice per group). * p < 0.05, ** p < 0.01, DF = 3, f ratio = 4.89. (G) Body weight and (H) percent body weight change from baseline in DIO mice treated with pharmacological (2 mg/kg) and non‐pharmacological (0.2 and 0.02 mg/kg) doses of r‐Leptin or 0.05 mg/kg of Liraglutide ( n = 10 mice per group). Comparisons shown are between vehicle and liraglutide on day 44. ** p < 0.01, **** p < 0.0001, DF = 45, t ratio = −7.74. (I) Cumulative food intake (days 25 to 45) in DIO mice with treated with pharmacological (2 mg/kg) and non‐pharmacological (0.2 and 0.02 mg/kg) doses of r‐Leptin or 0.05 mg/kg of Liraglutide ( n = 10 mice per group). * p < 0.05, ** p < 0.01, DF = 4, f ratio = 5.25. (J) Fat mass and (K) lean mass of DIO mice treated with vehicle, 2 mg/kg r‐Leptin, or 0.05 mg/kg Liraglutide at the end of the weight maintenance phase ( n = 10 mice per group). *** p < 0.001, DF = 2, f ratio = 12.15. Values are shown as mean ± SEM. DIO, diet‐induced obesity; CR, caloric restriction; Wt, weight.
    Figure Legend Snippet: Leptin treatment after weight loss stabilization does not prevent weight regain. (A) Schematic representation of the 10% weight loss/weight maintenance model with a stabilization period in DIO mice fed a 60% HFD. (B) Plasma leptin concentration at baseline and after 21 days of 10% weight loss stabilization ( n = 5 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. ** p < 0.01, DF = 6.23, t ratio = 3.77. (C) Body composition at baseline and after 21 days of 10% weight loss stabilization ( n = 40 mice per group). * p < 0.05, **** p < 0.0001, DF = 3, f ratio = 238.7. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with vehicle, 2 mg/kg r‐Leptin, 20 mg/kg Fc‐Leptin, or 0.05 mg/kg Liraglutide ( n = 10 mice per group). Comparisons shown are between vehicle and liraglutide on day 39. ** p < 0.01, **** p < 0.0001, DF = 36, t ratio = −9.15. (F) Cumulative food intake (days 25 to 40) in DIO mice with treated with vehicle, 2 mg/kg r‐Leptin, 20 mg/kg Fc‐Leptin, or 0.05 mg/kg Liraglutide ( n = 5–10 mice per group). * p < 0.05, ** p < 0.01, DF = 3, f ratio = 4.89. (G) Body weight and (H) percent body weight change from baseline in DIO mice treated with pharmacological (2 mg/kg) and non‐pharmacological (0.2 and 0.02 mg/kg) doses of r‐Leptin or 0.05 mg/kg of Liraglutide ( n = 10 mice per group). Comparisons shown are between vehicle and liraglutide on day 44. ** p < 0.01, **** p < 0.0001, DF = 45, t ratio = −7.74. (I) Cumulative food intake (days 25 to 45) in DIO mice with treated with pharmacological (2 mg/kg) and non‐pharmacological (0.2 and 0.02 mg/kg) doses of r‐Leptin or 0.05 mg/kg of Liraglutide ( n = 10 mice per group). * p < 0.05, ** p < 0.01, DF = 4, f ratio = 5.25. (J) Fat mass and (K) lean mass of DIO mice treated with vehicle, 2 mg/kg r‐Leptin, or 0.05 mg/kg Liraglutide at the end of the weight maintenance phase ( n = 10 mice per group). *** p < 0.001, DF = 2, f ratio = 12.15. Values are shown as mean ± SEM. DIO, diet‐induced obesity; CR, caloric restriction; Wt, weight.

    Techniques Used: Clinical Proteomics, Concentration Assay

    Leptin treatment does not prevent weight regain after 10% weight loss and 30% lowering of circulating leptin. (A) Schematic representation of the 10% weight loss/weight maintenance model in DIO mice fed 60% HFD. (B) Plasma leptin concentration at baseline and after 10% weight loss ( n = 5 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. ** p < 0.01, DF = 7.9, t ratio = 4.47. (C) Body composition at baseline and after 10% weight loss ( n = 30 mice per group). *** p < 0.001, **** p < 0.0001, DF = 3, f ratio = 207.8. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with 2 mg/kg r‐Leptin after 10% weight loss ( n = 9–10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 14. * p < 0.05, DF = 17, t ratio = −2.12. (F) Cumulative food intake (days 3 to 14) in DIO mice with treated with 2 mg/kg r‐Leptin after 10% weight loss ( n = 9–10 mice per group). (G) Body weight and (H) percent of body weight change from baseline in DIO mice treated with 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). (I) Cumulative food intake (days 3 to 11) in DIO mice with treated with 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). Values are shown as mean ± SEM. DIO, diet‐induced obesity; CR, caloric restriction; Wt, weight.
    Figure Legend Snippet: Leptin treatment does not prevent weight regain after 10% weight loss and 30% lowering of circulating leptin. (A) Schematic representation of the 10% weight loss/weight maintenance model in DIO mice fed 60% HFD. (B) Plasma leptin concentration at baseline and after 10% weight loss ( n = 5 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. ** p < 0.01, DF = 7.9, t ratio = 4.47. (C) Body composition at baseline and after 10% weight loss ( n = 30 mice per group). *** p < 0.001, **** p < 0.0001, DF = 3, f ratio = 207.8. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with 2 mg/kg r‐Leptin after 10% weight loss ( n = 9–10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 14. * p < 0.05, DF = 17, t ratio = −2.12. (F) Cumulative food intake (days 3 to 14) in DIO mice with treated with 2 mg/kg r‐Leptin after 10% weight loss ( n = 9–10 mice per group). (G) Body weight and (H) percent of body weight change from baseline in DIO mice treated with 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). (I) Cumulative food intake (days 3 to 11) in DIO mice with treated with 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). Values are shown as mean ± SEM. DIO, diet‐induced obesity; CR, caloric restriction; Wt, weight.

    Techniques Used: Clinical Proteomics, Concentration Assay, Comparison

    Continuous high CNS leptin exposure does not prevent weight regain. (A) Schematic representation of the 10% weight loss/weight maintenance model induced by ICV and Alzet pump surgery in non‐obese or DIO mice fed a 60% HFD. (B) Body weight and (C) percent body weight change from baseline in non‐obese mice with continuous ICV aCSF or 8 nM infused r‐Leptin after 10% weight loss ( n = 10 mice per group). Comparisons shown are between aCSF and r‐Leptin (8 nM infused into CSF) on day 23. ** p < 0.01, **** p < 0.0001, DF = 18, t ratio = 5.35. (D) Cumulative food intake (days 4 to 23) in non‐obese mice with continuous ICV aCSF or 8 nM infused r‐Leptin after 10% weight loss ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.14. (E) Body weight and (F) percent body weight change from baseline in DIO mice with continuous ICV aCSF or r‐Leptin treatment (870 pM or 35 nM infused into CSF) after 10% weight loss ( n = 14 mice per group). (G) Cumulative food intake (days 4 to 23) in DIO mice with continuous ICV aCSF or r‐Leptin (870 pM or 35 nM infused into CSF) treatment after 10% weight loss ( n = 14 mice per group). (H) Plasma leptin concentration in DIO mice after 21 days of ICV aCSF or r‐Leptin infused into CSF ( n = 13–15 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. Values are shown as mean ± SEM. ICV, intracerebroventricular; aCSF, artificial cerebrospinal fluid; Wt, weight.
    Figure Legend Snippet: Continuous high CNS leptin exposure does not prevent weight regain. (A) Schematic representation of the 10% weight loss/weight maintenance model induced by ICV and Alzet pump surgery in non‐obese or DIO mice fed a 60% HFD. (B) Body weight and (C) percent body weight change from baseline in non‐obese mice with continuous ICV aCSF or 8 nM infused r‐Leptin after 10% weight loss ( n = 10 mice per group). Comparisons shown are between aCSF and r‐Leptin (8 nM infused into CSF) on day 23. ** p < 0.01, **** p < 0.0001, DF = 18, t ratio = 5.35. (D) Cumulative food intake (days 4 to 23) in non‐obese mice with continuous ICV aCSF or 8 nM infused r‐Leptin after 10% weight loss ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.14. (E) Body weight and (F) percent body weight change from baseline in DIO mice with continuous ICV aCSF or r‐Leptin treatment (870 pM or 35 nM infused into CSF) after 10% weight loss ( n = 14 mice per group). (G) Cumulative food intake (days 4 to 23) in DIO mice with continuous ICV aCSF or r‐Leptin (870 pM or 35 nM infused into CSF) treatment after 10% weight loss ( n = 14 mice per group). (H) Plasma leptin concentration in DIO mice after 21 days of ICV aCSF or r‐Leptin infused into CSF ( n = 13–15 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. Values are shown as mean ± SEM. ICV, intracerebroventricular; aCSF, artificial cerebrospinal fluid; Wt, weight.

    Techniques Used: Clinical Proteomics, Concentration Assay

    Leptin treatment does not prevent weight regain when circulating leptin is decreased to match non‐obese mice. (A) Schematic representation of the 20% weight loss/weight maintenance model in DIO mice fed a 60% HFD. (B) Plasma leptin concentration in DIO mice fed a 60% HFD at baseline and after 20% weight loss ( n = 15 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. **** p < 0.0001, DF = 18.4, t ratio = 9.43. (C) Body composition of DIO mice fed a 60% HFD at baseline and after 20% weight loss ( n = 15 mice per group). *** p < 0.001, **** p < 0.0001, DF = 3, f ratio = 141.3. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with vehicle or 2 mg/kg r‐Leptin after 20% weight loss ( n = 11 mice per group). (F) Cumulative food intake (days 43 to 46) during the weight maintenance phase in DIO mice treated with vehicle or 2 mg/kg r‐Leptin after 20% weight loss ( n = 5 mice per group). (G) Schematic representation of the 10% weight loss/weight maintenance model in DIO mice fed a 30% fat diet. (H) Plasma leptin concentration in DIO mice fed a 30% fat diet at baseline and after 10% weight loss ( n = 10 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. *** p < 0.001, DF = 18, t ratio = 4.05. (I) Body composition of DIO mice fed a 30% fat diet at baseline and after 10% weight loss ( n = 20 animals per group). **** p < 0.0001, DF = 3, f ratio = 320.8. (J) Body weight and (K) percent body weight change from baseline in DIO mice treated vehicle or 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). (L) Cumulative food intake (days 7 to 20) during the weight maintenance phase in DIO mice treated with vehicle or 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). Values are shown as mean ± SEM. CR, caloric restriction; DIO, diet‐induced obesity; Wt, weight.
    Figure Legend Snippet: Leptin treatment does not prevent weight regain when circulating leptin is decreased to match non‐obese mice. (A) Schematic representation of the 20% weight loss/weight maintenance model in DIO mice fed a 60% HFD. (B) Plasma leptin concentration in DIO mice fed a 60% HFD at baseline and after 20% weight loss ( n = 15 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. **** p < 0.0001, DF = 18.4, t ratio = 9.43. (C) Body composition of DIO mice fed a 60% HFD at baseline and after 20% weight loss ( n = 15 mice per group). *** p < 0.001, **** p < 0.0001, DF = 3, f ratio = 141.3. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with vehicle or 2 mg/kg r‐Leptin after 20% weight loss ( n = 11 mice per group). (F) Cumulative food intake (days 43 to 46) during the weight maintenance phase in DIO mice treated with vehicle or 2 mg/kg r‐Leptin after 20% weight loss ( n = 5 mice per group). (G) Schematic representation of the 10% weight loss/weight maintenance model in DIO mice fed a 30% fat diet. (H) Plasma leptin concentration in DIO mice fed a 30% fat diet at baseline and after 10% weight loss ( n = 10 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. *** p < 0.001, DF = 18, t ratio = 4.05. (I) Body composition of DIO mice fed a 30% fat diet at baseline and after 10% weight loss ( n = 20 animals per group). **** p < 0.0001, DF = 3, f ratio = 320.8. (J) Body weight and (K) percent body weight change from baseline in DIO mice treated vehicle or 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). (L) Cumulative food intake (days 7 to 20) during the weight maintenance phase in DIO mice treated with vehicle or 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). Values are shown as mean ± SEM. CR, caloric restriction; DIO, diet‐induced obesity; Wt, weight.

    Techniques Used: Clinical Proteomics, Concentration Assay

    Summary of the relationship between fat mass, leptin exposure, and functional activity. (A) In vitro pSTAT3 functional activity of r‐Leptin with the human long‐form leptin receptor annotated with concentrations achieved in this study and published clinical studies ( n = 2–4 independent runs). (B) Compilation of plasma leptin levels correlated to fat mass achieved in this study with different degrees of weight loss and dietary fat levels.
    Figure Legend Snippet: Summary of the relationship between fat mass, leptin exposure, and functional activity. (A) In vitro pSTAT3 functional activity of r‐Leptin with the human long‐form leptin receptor annotated with concentrations achieved in this study and published clinical studies ( n = 2–4 independent runs). (B) Compilation of plasma leptin levels correlated to fat mass achieved in this study with different degrees of weight loss and dietary fat levels.

    Techniques Used: Functional Assay, Activity Assay, In Vitro, Clinical Proteomics



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    R&D Systems 497 lr
    Fig. 2 | Activation of TGR5 by CCDC enhances <t>leptin-LepR-STAT3</t> signaling in <t>the</t> <t>NTS</t> to lower food intake. a Cumulative food intake of NTS CMC (n = 15; data replotted from Fig. 1b, h), leptin (n = 10; data replotted from Fig. 1h), CCDC (n = 10; data replotted from Fig. 1b) or CCDC+leptin (n = 11) HF rats 24 h after food was given back. b Representative western blot images of p-STAT3, t-STAT3, and GAPDH protein levels in NTS CCDC 5 min acute infusion, followed by a 3 h wait, then NTS CMC or leptin 5 min acute infusion, and a subsequent 30 min waiting time in HF rats. c Representative images (scale bar: 100 μm) of immunohistological staining for p-STAT3 with DAPI (top) and cFOS (bottom) in NTS CCDC 5 min acute infusion, followed by a 3 h wait, then NTS CMC or leptin 5 min acute infusion, and a sub- sequent 30 min waiting time in HF rats. d Relative NTS Tgr5 mRNA expression of NTS shMM (n = 6) or shTgr5 (n = 6) rats. e Relative NTS PKA activity of NTS CMC shMM (n = 6), CCDC shMM (n = 6), CMC shTgr5 (n = 6), or CCDC shTgr5 (n = 6) HF rats, measured 3 h after 5 min acute infusions. f Cumulative food intake of NTS CMC shMM (n = 5), CCDC+leptin shMM (n = 10), CMC shTgr5 (n = 5), or CCDC+leptin
    497 Lr, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/497 lr/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    497 lr - by Bioz Stars, 2026-05
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    hb6261 recombinant mouse leptin protein r d systems cat  (R&D Systems)
    95
    R&D Systems hb6261 recombinant mouse leptin protein r d systems cat
    Fig. 2 | Activation of TGR5 by CCDC enhances <t>leptin-LepR-STAT3</t> signaling in <t>the</t> <t>NTS</t> to lower food intake. a Cumulative food intake of NTS CMC (n = 15; data replotted from Fig. 1b, h), leptin (n = 10; data replotted from Fig. 1h), CCDC (n = 10; data replotted from Fig. 1b) or CCDC+leptin (n = 11) HF rats 24 h after food was given back. b Representative western blot images of p-STAT3, t-STAT3, and GAPDH protein levels in NTS CCDC 5 min acute infusion, followed by a 3 h wait, then NTS CMC or leptin 5 min acute infusion, and a subsequent 30 min waiting time in HF rats. c Representative images (scale bar: 100 μm) of immunohistological staining for p-STAT3 with DAPI (top) and cFOS (bottom) in NTS CCDC 5 min acute infusion, followed by a 3 h wait, then NTS CMC or leptin 5 min acute infusion, and a sub- sequent 30 min waiting time in HF rats. d Relative NTS Tgr5 mRNA expression of NTS shMM (n = 6) or shTgr5 (n = 6) rats. e Relative NTS PKA activity of NTS CMC shMM (n = 6), CCDC shMM (n = 6), CMC shTgr5 (n = 6), or CCDC shTgr5 (n = 6) HF rats, measured 3 h after 5 min acute infusions. f Cumulative food intake of NTS CMC shMM (n = 5), CCDC+leptin shMM (n = 10), CMC shTgr5 (n = 5), or CCDC+leptin
    Hb6261 Recombinant Mouse Leptin Protein R D Systems Cat, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hb6261 recombinant mouse leptin protein r d systems cat/product/R&D Systems
    Average 95 stars, based on 1 article reviews
    hb6261 recombinant mouse leptin protein r d systems cat - by Bioz Stars, 2026-05
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    Image Search Results


    r‐Leptin and Fc‐Leptin characterization. (A) Comparison of r‐Leptin and Fc‐Leptin in vitro pSTAT3 functional activity with the human long‐form leptin receptor ( n = 2–4 independent experiments). (B) Comparison of r‐Leptin (10 mg/kg) and Fc‐Leptin (2 mg/kg) plasma exposure following a single SC dose administration in wildtype mice ( n = 3 mice per group). (C) Modelling of differences in pulsatile exposure following dosing with r‐Leptin (10 mg/kg SC BID) versus Fc‐Leptin (single 2 mg/kg dose). (D) Bodyweight in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 6. **** p < 0.0001, DF = 18, t ratio = −9.13. (E) Cumulative food intake (6 days) in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.07. (F) Body weight after a single Fc‐Leptin dose of 20 mg/kg in non‐obese mice ( n = 5 mice per group). Comparison shown is between vehicle and Fc‐Leptin each day. * p < 0.05, ** p < 0.01, DF = 8, t ratio = −3.85. (G) Cumulative food intake (6 days) in non‐obese mice that received a single Fc‐Leptin dose of 20 mg/kg ( n = 5 mice per group). *** p < 0.001, DF = 7.01, t ratio = 5.64. Values are shown as mean ± SEM.

    Journal: Diabetes, Obesity & Metabolism

    Article Title: Evaluation of leptin treatment on maintenance of body weight loss in diet‐induced obese mice

    doi: 10.1111/dom.70207

    Figure Lengend Snippet: r‐Leptin and Fc‐Leptin characterization. (A) Comparison of r‐Leptin and Fc‐Leptin in vitro pSTAT3 functional activity with the human long‐form leptin receptor ( n = 2–4 independent experiments). (B) Comparison of r‐Leptin (10 mg/kg) and Fc‐Leptin (2 mg/kg) plasma exposure following a single SC dose administration in wildtype mice ( n = 3 mice per group). (C) Modelling of differences in pulsatile exposure following dosing with r‐Leptin (10 mg/kg SC BID) versus Fc‐Leptin (single 2 mg/kg dose). (D) Bodyweight in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 6. **** p < 0.0001, DF = 18, t ratio = −9.13. (E) Cumulative food intake (6 days) in non‐obese mice treated with r‐Leptin 2 mg/kg ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.07. (F) Body weight after a single Fc‐Leptin dose of 20 mg/kg in non‐obese mice ( n = 5 mice per group). Comparison shown is between vehicle and Fc‐Leptin each day. * p < 0.05, ** p < 0.01, DF = 8, t ratio = −3.85. (G) Cumulative food intake (6 days) in non‐obese mice that received a single Fc‐Leptin dose of 20 mg/kg ( n = 5 mice per group). *** p < 0.001, DF = 7.01, t ratio = 5.64. Values are shown as mean ± SEM.

    Article Snippet: Mouse recombinant leptin (r‐leptin) was purchased from R & D Systems (Minneapolis, MN).

    Techniques: Comparison, In Vitro, Functional Assay, Activity Assay, Clinical Proteomics

    Leptin treatment after weight loss stabilization does not prevent weight regain. (A) Schematic representation of the 10% weight loss/weight maintenance model with a stabilization period in DIO mice fed a 60% HFD. (B) Plasma leptin concentration at baseline and after 21 days of 10% weight loss stabilization ( n = 5 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. ** p < 0.01, DF = 6.23, t ratio = 3.77. (C) Body composition at baseline and after 21 days of 10% weight loss stabilization ( n = 40 mice per group). * p < 0.05, **** p < 0.0001, DF = 3, f ratio = 238.7. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with vehicle, 2 mg/kg r‐Leptin, 20 mg/kg Fc‐Leptin, or 0.05 mg/kg Liraglutide ( n = 10 mice per group). Comparisons shown are between vehicle and liraglutide on day 39. ** p < 0.01, **** p < 0.0001, DF = 36, t ratio = −9.15. (F) Cumulative food intake (days 25 to 40) in DIO mice with treated with vehicle, 2 mg/kg r‐Leptin, 20 mg/kg Fc‐Leptin, or 0.05 mg/kg Liraglutide ( n = 5–10 mice per group). * p < 0.05, ** p < 0.01, DF = 3, f ratio = 4.89. (G) Body weight and (H) percent body weight change from baseline in DIO mice treated with pharmacological (2 mg/kg) and non‐pharmacological (0.2 and 0.02 mg/kg) doses of r‐Leptin or 0.05 mg/kg of Liraglutide ( n = 10 mice per group). Comparisons shown are between vehicle and liraglutide on day 44. ** p < 0.01, **** p < 0.0001, DF = 45, t ratio = −7.74. (I) Cumulative food intake (days 25 to 45) in DIO mice with treated with pharmacological (2 mg/kg) and non‐pharmacological (0.2 and 0.02 mg/kg) doses of r‐Leptin or 0.05 mg/kg of Liraglutide ( n = 10 mice per group). * p < 0.05, ** p < 0.01, DF = 4, f ratio = 5.25. (J) Fat mass and (K) lean mass of DIO mice treated with vehicle, 2 mg/kg r‐Leptin, or 0.05 mg/kg Liraglutide at the end of the weight maintenance phase ( n = 10 mice per group). *** p < 0.001, DF = 2, f ratio = 12.15. Values are shown as mean ± SEM. DIO, diet‐induced obesity; CR, caloric restriction; Wt, weight.

    Journal: Diabetes, Obesity & Metabolism

    Article Title: Evaluation of leptin treatment on maintenance of body weight loss in diet‐induced obese mice

    doi: 10.1111/dom.70207

    Figure Lengend Snippet: Leptin treatment after weight loss stabilization does not prevent weight regain. (A) Schematic representation of the 10% weight loss/weight maintenance model with a stabilization period in DIO mice fed a 60% HFD. (B) Plasma leptin concentration at baseline and after 21 days of 10% weight loss stabilization ( n = 5 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. ** p < 0.01, DF = 6.23, t ratio = 3.77. (C) Body composition at baseline and after 21 days of 10% weight loss stabilization ( n = 40 mice per group). * p < 0.05, **** p < 0.0001, DF = 3, f ratio = 238.7. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with vehicle, 2 mg/kg r‐Leptin, 20 mg/kg Fc‐Leptin, or 0.05 mg/kg Liraglutide ( n = 10 mice per group). Comparisons shown are between vehicle and liraglutide on day 39. ** p < 0.01, **** p < 0.0001, DF = 36, t ratio = −9.15. (F) Cumulative food intake (days 25 to 40) in DIO mice with treated with vehicle, 2 mg/kg r‐Leptin, 20 mg/kg Fc‐Leptin, or 0.05 mg/kg Liraglutide ( n = 5–10 mice per group). * p < 0.05, ** p < 0.01, DF = 3, f ratio = 4.89. (G) Body weight and (H) percent body weight change from baseline in DIO mice treated with pharmacological (2 mg/kg) and non‐pharmacological (0.2 and 0.02 mg/kg) doses of r‐Leptin or 0.05 mg/kg of Liraglutide ( n = 10 mice per group). Comparisons shown are between vehicle and liraglutide on day 44. ** p < 0.01, **** p < 0.0001, DF = 45, t ratio = −7.74. (I) Cumulative food intake (days 25 to 45) in DIO mice with treated with pharmacological (2 mg/kg) and non‐pharmacological (0.2 and 0.02 mg/kg) doses of r‐Leptin or 0.05 mg/kg of Liraglutide ( n = 10 mice per group). * p < 0.05, ** p < 0.01, DF = 4, f ratio = 5.25. (J) Fat mass and (K) lean mass of DIO mice treated with vehicle, 2 mg/kg r‐Leptin, or 0.05 mg/kg Liraglutide at the end of the weight maintenance phase ( n = 10 mice per group). *** p < 0.001, DF = 2, f ratio = 12.15. Values are shown as mean ± SEM. DIO, diet‐induced obesity; CR, caloric restriction; Wt, weight.

    Article Snippet: Mouse recombinant leptin (r‐leptin) was purchased from R & D Systems (Minneapolis, MN).

    Techniques: Clinical Proteomics, Concentration Assay

    Leptin treatment does not prevent weight regain after 10% weight loss and 30% lowering of circulating leptin. (A) Schematic representation of the 10% weight loss/weight maintenance model in DIO mice fed 60% HFD. (B) Plasma leptin concentration at baseline and after 10% weight loss ( n = 5 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. ** p < 0.01, DF = 7.9, t ratio = 4.47. (C) Body composition at baseline and after 10% weight loss ( n = 30 mice per group). *** p < 0.001, **** p < 0.0001, DF = 3, f ratio = 207.8. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with 2 mg/kg r‐Leptin after 10% weight loss ( n = 9–10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 14. * p < 0.05, DF = 17, t ratio = −2.12. (F) Cumulative food intake (days 3 to 14) in DIO mice with treated with 2 mg/kg r‐Leptin after 10% weight loss ( n = 9–10 mice per group). (G) Body weight and (H) percent of body weight change from baseline in DIO mice treated with 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). (I) Cumulative food intake (days 3 to 11) in DIO mice with treated with 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). Values are shown as mean ± SEM. DIO, diet‐induced obesity; CR, caloric restriction; Wt, weight.

    Journal: Diabetes, Obesity & Metabolism

    Article Title: Evaluation of leptin treatment on maintenance of body weight loss in diet‐induced obese mice

    doi: 10.1111/dom.70207

    Figure Lengend Snippet: Leptin treatment does not prevent weight regain after 10% weight loss and 30% lowering of circulating leptin. (A) Schematic representation of the 10% weight loss/weight maintenance model in DIO mice fed 60% HFD. (B) Plasma leptin concentration at baseline and after 10% weight loss ( n = 5 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. ** p < 0.01, DF = 7.9, t ratio = 4.47. (C) Body composition at baseline and after 10% weight loss ( n = 30 mice per group). *** p < 0.001, **** p < 0.0001, DF = 3, f ratio = 207.8. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with 2 mg/kg r‐Leptin after 10% weight loss ( n = 9–10 mice per group). Comparison shown is between vehicle and r‐Leptin at day 14. * p < 0.05, DF = 17, t ratio = −2.12. (F) Cumulative food intake (days 3 to 14) in DIO mice with treated with 2 mg/kg r‐Leptin after 10% weight loss ( n = 9–10 mice per group). (G) Body weight and (H) percent of body weight change from baseline in DIO mice treated with 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). (I) Cumulative food intake (days 3 to 11) in DIO mice with treated with 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). Values are shown as mean ± SEM. DIO, diet‐induced obesity; CR, caloric restriction; Wt, weight.

    Article Snippet: Mouse recombinant leptin (r‐leptin) was purchased from R & D Systems (Minneapolis, MN).

    Techniques: Clinical Proteomics, Concentration Assay, Comparison

    Continuous high CNS leptin exposure does not prevent weight regain. (A) Schematic representation of the 10% weight loss/weight maintenance model induced by ICV and Alzet pump surgery in non‐obese or DIO mice fed a 60% HFD. (B) Body weight and (C) percent body weight change from baseline in non‐obese mice with continuous ICV aCSF or 8 nM infused r‐Leptin after 10% weight loss ( n = 10 mice per group). Comparisons shown are between aCSF and r‐Leptin (8 nM infused into CSF) on day 23. ** p < 0.01, **** p < 0.0001, DF = 18, t ratio = 5.35. (D) Cumulative food intake (days 4 to 23) in non‐obese mice with continuous ICV aCSF or 8 nM infused r‐Leptin after 10% weight loss ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.14. (E) Body weight and (F) percent body weight change from baseline in DIO mice with continuous ICV aCSF or r‐Leptin treatment (870 pM or 35 nM infused into CSF) after 10% weight loss ( n = 14 mice per group). (G) Cumulative food intake (days 4 to 23) in DIO mice with continuous ICV aCSF or r‐Leptin (870 pM or 35 nM infused into CSF) treatment after 10% weight loss ( n = 14 mice per group). (H) Plasma leptin concentration in DIO mice after 21 days of ICV aCSF or r‐Leptin infused into CSF ( n = 13–15 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. Values are shown as mean ± SEM. ICV, intracerebroventricular; aCSF, artificial cerebrospinal fluid; Wt, weight.

    Journal: Diabetes, Obesity & Metabolism

    Article Title: Evaluation of leptin treatment on maintenance of body weight loss in diet‐induced obese mice

    doi: 10.1111/dom.70207

    Figure Lengend Snippet: Continuous high CNS leptin exposure does not prevent weight regain. (A) Schematic representation of the 10% weight loss/weight maintenance model induced by ICV and Alzet pump surgery in non‐obese or DIO mice fed a 60% HFD. (B) Body weight and (C) percent body weight change from baseline in non‐obese mice with continuous ICV aCSF or 8 nM infused r‐Leptin after 10% weight loss ( n = 10 mice per group). Comparisons shown are between aCSF and r‐Leptin (8 nM infused into CSF) on day 23. ** p < 0.01, **** p < 0.0001, DF = 18, t ratio = 5.35. (D) Cumulative food intake (days 4 to 23) in non‐obese mice with continuous ICV aCSF or 8 nM infused r‐Leptin after 10% weight loss ( n = 10 mice per group). ** p < 0.01, DF = 17.8, t ratio = 3.14. (E) Body weight and (F) percent body weight change from baseline in DIO mice with continuous ICV aCSF or r‐Leptin treatment (870 pM or 35 nM infused into CSF) after 10% weight loss ( n = 14 mice per group). (G) Cumulative food intake (days 4 to 23) in DIO mice with continuous ICV aCSF or r‐Leptin (870 pM or 35 nM infused into CSF) treatment after 10% weight loss ( n = 14 mice per group). (H) Plasma leptin concentration in DIO mice after 21 days of ICV aCSF or r‐Leptin infused into CSF ( n = 13–15 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. Values are shown as mean ± SEM. ICV, intracerebroventricular; aCSF, artificial cerebrospinal fluid; Wt, weight.

    Article Snippet: Mouse recombinant leptin (r‐leptin) was purchased from R & D Systems (Minneapolis, MN).

    Techniques: Clinical Proteomics, Concentration Assay

    Leptin treatment does not prevent weight regain when circulating leptin is decreased to match non‐obese mice. (A) Schematic representation of the 20% weight loss/weight maintenance model in DIO mice fed a 60% HFD. (B) Plasma leptin concentration in DIO mice fed a 60% HFD at baseline and after 20% weight loss ( n = 15 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. **** p < 0.0001, DF = 18.4, t ratio = 9.43. (C) Body composition of DIO mice fed a 60% HFD at baseline and after 20% weight loss ( n = 15 mice per group). *** p < 0.001, **** p < 0.0001, DF = 3, f ratio = 141.3. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with vehicle or 2 mg/kg r‐Leptin after 20% weight loss ( n = 11 mice per group). (F) Cumulative food intake (days 43 to 46) during the weight maintenance phase in DIO mice treated with vehicle or 2 mg/kg r‐Leptin after 20% weight loss ( n = 5 mice per group). (G) Schematic representation of the 10% weight loss/weight maintenance model in DIO mice fed a 30% fat diet. (H) Plasma leptin concentration in DIO mice fed a 30% fat diet at baseline and after 10% weight loss ( n = 10 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. *** p < 0.001, DF = 18, t ratio = 4.05. (I) Body composition of DIO mice fed a 30% fat diet at baseline and after 10% weight loss ( n = 20 animals per group). **** p < 0.0001, DF = 3, f ratio = 320.8. (J) Body weight and (K) percent body weight change from baseline in DIO mice treated vehicle or 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). (L) Cumulative food intake (days 7 to 20) during the weight maintenance phase in DIO mice treated with vehicle or 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). Values are shown as mean ± SEM. CR, caloric restriction; DIO, diet‐induced obesity; Wt, weight.

    Journal: Diabetes, Obesity & Metabolism

    Article Title: Evaluation of leptin treatment on maintenance of body weight loss in diet‐induced obese mice

    doi: 10.1111/dom.70207

    Figure Lengend Snippet: Leptin treatment does not prevent weight regain when circulating leptin is decreased to match non‐obese mice. (A) Schematic representation of the 20% weight loss/weight maintenance model in DIO mice fed a 60% HFD. (B) Plasma leptin concentration in DIO mice fed a 60% HFD at baseline and after 20% weight loss ( n = 15 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. **** p < 0.0001, DF = 18.4, t ratio = 9.43. (C) Body composition of DIO mice fed a 60% HFD at baseline and after 20% weight loss ( n = 15 mice per group). *** p < 0.001, **** p < 0.0001, DF = 3, f ratio = 141.3. (D) Body weight and (E) percent body weight change from baseline in DIO mice treated with vehicle or 2 mg/kg r‐Leptin after 20% weight loss ( n = 11 mice per group). (F) Cumulative food intake (days 43 to 46) during the weight maintenance phase in DIO mice treated with vehicle or 2 mg/kg r‐Leptin after 20% weight loss ( n = 5 mice per group). (G) Schematic representation of the 10% weight loss/weight maintenance model in DIO mice fed a 30% fat diet. (H) Plasma leptin concentration in DIO mice fed a 30% fat diet at baseline and after 10% weight loss ( n = 10 mice per group). Mean plasma leptin concentration (nM) for each group is shown in parenthesis. *** p < 0.001, DF = 18, t ratio = 4.05. (I) Body composition of DIO mice fed a 30% fat diet at baseline and after 10% weight loss ( n = 20 animals per group). **** p < 0.0001, DF = 3, f ratio = 320.8. (J) Body weight and (K) percent body weight change from baseline in DIO mice treated vehicle or 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). (L) Cumulative food intake (days 7 to 20) during the weight maintenance phase in DIO mice treated with vehicle or 2 mg/kg Fc‐Leptin after 10% weight loss ( n = 10 mice per group). Values are shown as mean ± SEM. CR, caloric restriction; DIO, diet‐induced obesity; Wt, weight.

    Article Snippet: Mouse recombinant leptin (r‐leptin) was purchased from R & D Systems (Minneapolis, MN).

    Techniques: Clinical Proteomics, Concentration Assay

    Summary of the relationship between fat mass, leptin exposure, and functional activity. (A) In vitro pSTAT3 functional activity of r‐Leptin with the human long‐form leptin receptor annotated with concentrations achieved in this study and published clinical studies ( n = 2–4 independent runs). (B) Compilation of plasma leptin levels correlated to fat mass achieved in this study with different degrees of weight loss and dietary fat levels.

    Journal: Diabetes, Obesity & Metabolism

    Article Title: Evaluation of leptin treatment on maintenance of body weight loss in diet‐induced obese mice

    doi: 10.1111/dom.70207

    Figure Lengend Snippet: Summary of the relationship between fat mass, leptin exposure, and functional activity. (A) In vitro pSTAT3 functional activity of r‐Leptin with the human long‐form leptin receptor annotated with concentrations achieved in this study and published clinical studies ( n = 2–4 independent runs). (B) Compilation of plasma leptin levels correlated to fat mass achieved in this study with different degrees of weight loss and dietary fat levels.

    Article Snippet: Mouse recombinant leptin (r‐leptin) was purchased from R & D Systems (Minneapolis, MN).

    Techniques: Functional Assay, Activity Assay, In Vitro, Clinical Proteomics

    Fig. 2 | Activation of TGR5 by CCDC enhances leptin-LepR-STAT3 signaling in the NTS to lower food intake. a Cumulative food intake of NTS CMC (n = 15; data replotted from Fig. 1b, h), leptin (n = 10; data replotted from Fig. 1h), CCDC (n = 10; data replotted from Fig. 1b) or CCDC+leptin (n = 11) HF rats 24 h after food was given back. b Representative western blot images of p-STAT3, t-STAT3, and GAPDH protein levels in NTS CCDC 5 min acute infusion, followed by a 3 h wait, then NTS CMC or leptin 5 min acute infusion, and a subsequent 30 min waiting time in HF rats. c Representative images (scale bar: 100 μm) of immunohistological staining for p-STAT3 with DAPI (top) and cFOS (bottom) in NTS CCDC 5 min acute infusion, followed by a 3 h wait, then NTS CMC or leptin 5 min acute infusion, and a sub- sequent 30 min waiting time in HF rats. d Relative NTS Tgr5 mRNA expression of NTS shMM (n = 6) or shTgr5 (n = 6) rats. e Relative NTS PKA activity of NTS CMC shMM (n = 6), CCDC shMM (n = 6), CMC shTgr5 (n = 6), or CCDC shTgr5 (n = 6) HF rats, measured 3 h after 5 min acute infusions. f Cumulative food intake of NTS CMC shMM (n = 5), CCDC+leptin shMM (n = 10), CMC shTgr5 (n = 5), or CCDC+leptin

    Journal: Nature communications

    Article Title: Pharmacological and physiological activation of TGR5 in the NTS lowers food intake by enhancing leptin-STAT3 signaling.

    doi: 10.1038/s41467-025-60331-1

    Figure Lengend Snippet: Fig. 2 | Activation of TGR5 by CCDC enhances leptin-LepR-STAT3 signaling in the NTS to lower food intake. a Cumulative food intake of NTS CMC (n = 15; data replotted from Fig. 1b, h), leptin (n = 10; data replotted from Fig. 1h), CCDC (n = 10; data replotted from Fig. 1b) or CCDC+leptin (n = 11) HF rats 24 h after food was given back. b Representative western blot images of p-STAT3, t-STAT3, and GAPDH protein levels in NTS CCDC 5 min acute infusion, followed by a 3 h wait, then NTS CMC or leptin 5 min acute infusion, and a subsequent 30 min waiting time in HF rats. c Representative images (scale bar: 100 μm) of immunohistological staining for p-STAT3 with DAPI (top) and cFOS (bottom) in NTS CCDC 5 min acute infusion, followed by a 3 h wait, then NTS CMC or leptin 5 min acute infusion, and a sub- sequent 30 min waiting time in HF rats. d Relative NTS Tgr5 mRNA expression of NTS shMM (n = 6) or shTgr5 (n = 6) rats. e Relative NTS PKA activity of NTS CMC shMM (n = 6), CCDC shMM (n = 6), CMC shTgr5 (n = 6), or CCDC shTgr5 (n = 6) HF rats, measured 3 h after 5 min acute infusions. f Cumulative food intake of NTS CMC shMM (n = 5), CCDC+leptin shMM (n = 10), CMC shTgr5 (n = 5), or CCDC+leptin

    Article Snippet: Leptin (497-LR, R&D Systems) was dissolved firstly in 0.9% saline and thenwith/withoutCCDC (final CCDCconcentration 100μM) in 1% CMC to the concentration of 153μM (equivalent to 0.5μg/site) as this amount of leptin infused into the hypothalamus or NTS lowers food intake23,64,65.

    Techniques: Activation Assay, Western Blot, Staining, Expressing, Activity Assay

    Fig. 3 | Activation of TGR5 decreases inflammation and leptin signaling sup- pressor in the NTS. Relative NTS Cd68 (a), Il6 (b), Tnfa (c), LepRb (d), Ptp1b (e), and Socs3 (f) mRNA expression of NTS CMC (n = 8) or CCDC (n = 6) chow rats and NTS CMC (n = 8 for a–d; n = 7 for e, f) or CCDC (n = 8 for a–d; n = 7 for e, f) HF rats, measured 24 h after food was given back following 5 min acute infusion. g Representative images (scale bar: 100 μm; 25 μm for the digital zoomed-in ima- ges) showing FISH for Tgr5, Aif1, and DAPI or LepR, Aif1, and DAPI in the NTS of HF rats 30 min after CMC 5 min acute infusion. Digital zooms of the boxed regions are shown to the left. Arrowheads indicate cells co-expressing Tgr5 or LepR and Aif1. h Left: Proportion of Aif1+ microglia in the NTS that are Tgr5+ or Tgr5- and LepR+ or LepR- (pie chart). Right: Percentage of Aif1+ microglia expressing Tgr5or LepR in the NTS (n = 3 per group). i Representative images (scale bar: 100 μm; 25 μm for the digital zoomed-in images) showing FISH for Tgr5, Rbfox3, and DAPI or LepR, Rbfox3, and DAPI in the NTS of HF rats 30 min after CMC 5 min acute infusion.

    Journal: Nature communications

    Article Title: Pharmacological and physiological activation of TGR5 in the NTS lowers food intake by enhancing leptin-STAT3 signaling.

    doi: 10.1038/s41467-025-60331-1

    Figure Lengend Snippet: Fig. 3 | Activation of TGR5 decreases inflammation and leptin signaling sup- pressor in the NTS. Relative NTS Cd68 (a), Il6 (b), Tnfa (c), LepRb (d), Ptp1b (e), and Socs3 (f) mRNA expression of NTS CMC (n = 8) or CCDC (n = 6) chow rats and NTS CMC (n = 8 for a–d; n = 7 for e, f) or CCDC (n = 8 for a–d; n = 7 for e, f) HF rats, measured 24 h after food was given back following 5 min acute infusion. g Representative images (scale bar: 100 μm; 25 μm for the digital zoomed-in ima- ges) showing FISH for Tgr5, Aif1, and DAPI or LepR, Aif1, and DAPI in the NTS of HF rats 30 min after CMC 5 min acute infusion. Digital zooms of the boxed regions are shown to the left. Arrowheads indicate cells co-expressing Tgr5 or LepR and Aif1. h Left: Proportion of Aif1+ microglia in the NTS that are Tgr5+ or Tgr5- and LepR+ or LepR- (pie chart). Right: Percentage of Aif1+ microglia expressing Tgr5or LepR in the NTS (n = 3 per group). i Representative images (scale bar: 100 μm; 25 μm for the digital zoomed-in images) showing FISH for Tgr5, Rbfox3, and DAPI or LepR, Rbfox3, and DAPI in the NTS of HF rats 30 min after CMC 5 min acute infusion.

    Article Snippet: Leptin (497-LR, R&D Systems) was dissolved firstly in 0.9% saline and thenwith/withoutCCDC (final CCDCconcentration 100μM) in 1% CMC to the concentration of 153μM (equivalent to 0.5μg/site) as this amount of leptin infused into the hypothalamus or NTS lowers food intake23,64,65.

    Techniques: Activation Assay, Expressing