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ghrelin  (MedChemExpress)


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    Structured Review

    MedChemExpress ghrelin
    Ghrelin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 67 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ghrelin/%CE%B2-Amyloid/pm42185568-121-34-24
    Average 96 stars, based on 67 article reviews
    ghrelin - by Bioz Stars, 2026-09
    96/100 stars

    Images

    Related Articles

    Control:

    Article Title: Ghrelin Improves Glucolipotoxicity-Induced Pancreatic β-Cellular Dysfunction and Apoptosis by Inhibiting Endoplasmic Reticulum Stress-Induced IRE1/JNK Pathway
    Article Snippet: Copyright: © 2024 The Author(s).. Published by Discovery Medicine.. This is an open access article under the CC BY 4.0 license.

    Cell Culture:

    Article Title: Ghrelin Improves Glucolipotoxicity-Induced Pancreatic β-Cellular Dysfunction and Apoptosis by Inhibiting Endoplasmic Reticulum Stress-Induced IRE1/JNK Pathway
    Article Snippet: Copyright: © 2024 The Author(s).. Published by Discovery Medicine.. This is an open access article under the CC BY 4.0 license.

    Incubation:

    Article Title: Ghrelin Improves Glucolipotoxicity-Induced Pancreatic β-Cellular Dysfunction and Apoptosis by Inhibiting Endoplasmic Reticulum Stress-Induced IRE1/JNK Pathway
    Article Snippet: Copyright: © 2024 The Author(s).. Published by Discovery Medicine.. This is an open access article under the CC BY 4.0 license.

    Article Title: Ghrelin Ameliorates Alzheimer's Disease-Associated Astrocyte Dysfunction via UCP2-Mediated Inhibition of FOXO1 Nuclear Translocation.
    Article Snippet: Alzheimer’s disease (AD) is associated with mitochondrial dysfunction and impaired energy metabolism in astrocytes.. Although ghrelin is known to exert neuroprotective effects, the mechanisms through which it modulates astrocyte bioenergetics under AD-like conditions remain incompletely defined.. In primary astrocytes treated with Aβ25-35 oligomers, ghrelin attenuated mitochondrial damage, reducing ROS and enhancing mitochondrial membrane potential (ΔΨm) and respiratory complex activities.

    other:

    Article Title: Ghrelin attenuates metabolic dysfunction-associated steatotic liver disease by activating glutamine metabolism via inhibition of the IRE1α-XBP-1 pathway.
    Article Snippet: Metabolic dysfunction-associated steatotic liver disease (MASLD) encompasses a complex interplay of metabolic and cellular stress pathways.. Disruptions in several metabolic processes, including endoplasmic reticulum (ER) stress, glutamine metabolism, and ferroptosis, are key in the initiation and progression of MASLD.. Although ghrelin confers protective effects against MASLD, its mechanism of action remains unclear.

    Article Title: Famsin, a novel gut-secreted hormone, contributes to metabolic adaptations to fasting via binding to its receptor OLFR796.
    Article Snippet: The intestine is responsible for nutrient absorption and orchestrates metabolism in different organs during feeding, a process which is partly controlled by intestine-derived hormones.. However, it is unclear whether the intestine plays an important role in metabolism during fasting.. Here we have identified a novel hormone, famsin, which is secreted from the intestine and promotes metabolic adaptations to fasting.

    Microscopy:

    Article Title: Ghrelin inhibits NLRP3 inflammasome activation by upregulating autophagy to improve Alzheimer's disease.
    Article Snippet: Nod-like receptor protein 3 (NLRP3) inflammasome, autophagy, and the aggregation of β-amyloid (Aβ) are key factors in Alzheimer’s disease (AD) development.. Ghrelin has shown promise in providing neuroprotection for AD.. However, the mechanism underlying ghrelin’s ability to improve AD by modulating autophagy and the NLRP3 inflammasome requires further clarification.



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    Changes in adipokine and gut hormone levels after 24 weeks of dulaglutide treatment. Values are presented as mean±standard error (SE). (A) Leptin, (B) adiponectin, (C) obestatin, (D) <t>ghrelin,</t> and (E) resistin. Statistical significance is indicated as follows: a P <0.01, b P <0.001 vs. baseline (week 0).
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    Changes in adipokine and gut hormone levels after 24 weeks of dulaglutide treatment. Values are presented as mean±standard error (SE). (A) Leptin, (B) adiponectin, (C) obestatin, (D) <t>ghrelin,</t> and (E) resistin. Statistical significance is indicated as follows: a P <0.01, b P <0.001 vs. baseline (week 0).
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    Changes in adipokine and gut hormone levels after 24 weeks of dulaglutide treatment. Values are presented as mean±standard error (SE). (A) Leptin, (B) adiponectin, (C) obestatin, (D) <t>ghrelin,</t> and (E) resistin. Statistical significance is indicated as follows: a P <0.01, b P <0.001 vs. baseline (week 0).
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    Hello Bio Inc ghrelin
    Mice containing activating DREADDs in Glp1r/Trh neurons were treated with saline or CNO at the onset of the dark cycle (a), during refeeding following an overnight fast (b), or prior to <t>ghrelin</t> treatment (c). a , Cumulative dark-cycle food intake at 0, 1, 2, and 3 hours following IP CNO or saline in a within-subject crossover design (n=5).. b , Cumulative post-fast food intake at 0, 1, 2, 4, 6, and 8 hours following IP CNO or saline (n=5). c , Cumulative food intake following IP ghrelin with CNO or saline pre-treatment at 0, 1, 2, 4, 6, and 8 hours (n=4). d, Effect of leptin (dark teal) versus saline (light teal) pre-treatment on ghrelin-induced 24-hour food intake in <t>lean</t> <t>Lepr</t> Glp1r KO (KO) and control (WT) mice. Lines connect within-subject measurements (crossover design). e, Cumulative post-fast food intake following leptin (dark teal) or saline (light teal) administration in WT (left) and KO (right) mice. f, g , Body weight (f) and daily food intake (g) before and 7 days after HFD exposure in Lepr Glp1r KO (n=9) and Control (n=10) mice. h , Food intake from (g) separated by dark (top) and light (bottom) cycle. The excess intake in Lepr Glp1r KO mice was concentrated in the dark cycle (genotype × time: χ²(9)=38.33, P =1.52×10⁻⁵). Dashed line indicates HFD switch. All panels: * P <0.05, **P<0.01, ***P<0.001. A-c, e-h: Plotted points represent mean values. Error bars (a-c) and shaded regions (e-h) denote SEM.
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    Mice containing activating DREADDs in Glp1r/Trh neurons were treated with saline or CNO at the onset of the dark cycle (a), during refeeding following an overnight fast (b), or prior to <t>ghrelin</t> treatment (c). a , Cumulative dark-cycle food intake at 0, 1, 2, and 3 hours following IP CNO or saline in a within-subject crossover design (n=5).. b , Cumulative post-fast food intake at 0, 1, 2, 4, 6, and 8 hours following IP CNO or saline (n=5). c , Cumulative food intake following IP ghrelin with CNO or saline pre-treatment at 0, 1, 2, 4, 6, and 8 hours (n=4). d, Effect of leptin (dark teal) versus saline (light teal) pre-treatment on ghrelin-induced 24-hour food intake in <t>lean</t> <t>Lepr</t> Glp1r KO (KO) and control (WT) mice. Lines connect within-subject measurements (crossover design). e, Cumulative post-fast food intake following leptin (dark teal) or saline (light teal) administration in WT (left) and KO (right) mice. f, g , Body weight (f) and daily food intake (g) before and 7 days after HFD exposure in Lepr Glp1r KO (n=9) and Control (n=10) mice. h , Food intake from (g) separated by dark (top) and light (bottom) cycle. The excess intake in Lepr Glp1r KO mice was concentrated in the dark cycle (genotype × time: χ²(9)=38.33, P =1.52×10⁻⁵). Dashed line indicates HFD switch. All panels: * P <0.05, **P<0.01, ***P<0.001. A-c, e-h: Plotted points represent mean values. Error bars (a-c) and shaded regions (e-h) denote SEM.
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    Mice containing activating DREADDs in Glp1r/Trh neurons were treated with saline or CNO at the onset of the dark cycle (a), during refeeding following an overnight fast (b), or prior to <t>ghrelin</t> treatment (c). a , Cumulative dark-cycle food intake at 0, 1, 2, and 3 hours following IP CNO or saline in a within-subject crossover design (n=5).. b , Cumulative post-fast food intake at 0, 1, 2, 4, 6, and 8 hours following IP CNO or saline (n=5). c , Cumulative food intake following IP ghrelin with CNO or saline pre-treatment at 0, 1, 2, 4, 6, and 8 hours (n=4). d, Effect of leptin (dark teal) versus saline (light teal) pre-treatment on ghrelin-induced 24-hour food intake in <t>lean</t> <t>Lepr</t> Glp1r KO (KO) and control (WT) mice. Lines connect within-subject measurements (crossover design). e, Cumulative post-fast food intake following leptin (dark teal) or saline (light teal) administration in WT (left) and KO (right) mice. f, g , Body weight (f) and daily food intake (g) before and 7 days after HFD exposure in Lepr Glp1r KO (n=9) and Control (n=10) mice. h , Food intake from (g) separated by dark (top) and light (bottom) cycle. The excess intake in Lepr Glp1r KO mice was concentrated in the dark cycle (genotype × time: χ²(9)=38.33, P =1.52×10⁻⁵). Dashed line indicates HFD switch. All panels: * P <0.05, **P<0.01, ***P<0.001. A-c, e-h: Plotted points represent mean values. Error bars (a-c) and shaded regions (e-h) denote SEM.
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    Cusabio ghrelin levels
    Mice containing activating DREADDs in Glp1r/Trh neurons were treated with saline or CNO at the onset of the dark cycle (a), during refeeding following an overnight fast (b), or prior to <t>ghrelin</t> treatment (c). a , Cumulative dark-cycle food intake at 0, 1, 2, and 3 hours following IP CNO or saline in a within-subject crossover design (n=5).. b , Cumulative post-fast food intake at 0, 1, 2, 4, 6, and 8 hours following IP CNO or saline (n=5). c , Cumulative food intake following IP ghrelin with CNO or saline pre-treatment at 0, 1, 2, 4, 6, and 8 hours (n=4). d, Effect of leptin (dark teal) versus saline (light teal) pre-treatment on ghrelin-induced 24-hour food intake in <t>lean</t> <t>Lepr</t> Glp1r KO (KO) and control (WT) mice. Lines connect within-subject measurements (crossover design). e, Cumulative post-fast food intake following leptin (dark teal) or saline (light teal) administration in WT (left) and KO (right) mice. f, g , Body weight (f) and daily food intake (g) before and 7 days after HFD exposure in Lepr Glp1r KO (n=9) and Control (n=10) mice. h , Food intake from (g) separated by dark (top) and light (bottom) cycle. The excess intake in Lepr Glp1r KO mice was concentrated in the dark cycle (genotype × time: χ²(9)=38.33, P =1.52×10⁻⁵). Dashed line indicates HFD switch. All panels: * P <0.05, **P<0.01, ***P<0.001. A-c, e-h: Plotted points represent mean values. Error bars (a-c) and shaded regions (e-h) denote SEM.
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    Phoenix Pharmaceuticals ghrelin
    A-C Simple linear regressions between the devaluation coefficient (k DD ) on DDT3 and plasma levels of <t>ghrelin</t> ( A <t>),</t> <t>LEAP2</t> ( B ), and the ghrelin/LEAP2 molar ratio ( C ) in refed animals. D Simple linear regression between plasma levels of LEAP2 and the percentage decrease in preference for the LL reward on DDT3. Data are expressed as the coefficient of determination (r 2 ) and p-value. Dotted lines represent the 95% confidence band of the best fit line. CT control, DDT delay discounting task, LL Large Late, FR food restriction, FR + R food restriction + refeeding, LEAP2 Liver Expressed Antimicrobial Peptide 2, k DD Coefficient of devaluation. Correlations were performed using simple ( A – C ) or multiple ( D ) linear regression.
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    Image Search Results


    Changes in adipokine and gut hormone levels after 24 weeks of dulaglutide treatment. Values are presented as mean±standard error (SE). (A) Leptin, (B) adiponectin, (C) obestatin, (D) ghrelin, and (E) resistin. Statistical significance is indicated as follows: a P <0.01, b P <0.001 vs. baseline (week 0).

    Journal: Diabetes & Metabolism Journal

    Article Title: Glycemic Improvement with Low-Dose Dulaglutide Is Associated with Leptin and Obestatin Modulation in Type 2 Diabetes Mellitus

    doi: 10.4093/dmj.2025.0681

    Figure Lengend Snippet: Changes in adipokine and gut hormone levels after 24 weeks of dulaglutide treatment. Values are presented as mean±standard error (SE). (A) Leptin, (B) adiponectin, (C) obestatin, (D) ghrelin, and (E) resistin. Statistical significance is indicated as follows: a P <0.01, b P <0.001 vs. baseline (week 0).

    Article Snippet: Ghrelin levels were determined using the Ghrelin Human ELISA kit (Invitrogen, Thermo Fisher Scientific; Cat No. BMS2192).

    Techniques:

    Metabolic, food craving, and adipokine changes in glycemic responders vs. non-responders to dulaglutide. Glycemic responders are shown as black circles with solid lines and non-responders as white circles with dashed lines. Values are presented as mean±standard error. (A) Glycosylated hemoglobin (HbA1c), (B) General Food Cravings Questionnaire (FCQ)-Trait score, (C) homeostatic model assessment of β-cell function (HOMA-β), (D) waist circumference, (E) body mass index (BMI), (F) leptin, (G) adiponectin, and (H) obestatin. Statistical significance is indicated as follows: a P <0.05, b P <0.01, c P <0.001 vs. baseline (week 0).

    Journal: Diabetes & Metabolism Journal

    Article Title: Glycemic Improvement with Low-Dose Dulaglutide Is Associated with Leptin and Obestatin Modulation in Type 2 Diabetes Mellitus

    doi: 10.4093/dmj.2025.0681

    Figure Lengend Snippet: Metabolic, food craving, and adipokine changes in glycemic responders vs. non-responders to dulaglutide. Glycemic responders are shown as black circles with solid lines and non-responders as white circles with dashed lines. Values are presented as mean±standard error. (A) Glycosylated hemoglobin (HbA1c), (B) General Food Cravings Questionnaire (FCQ)-Trait score, (C) homeostatic model assessment of β-cell function (HOMA-β), (D) waist circumference, (E) body mass index (BMI), (F) leptin, (G) adiponectin, and (H) obestatin. Statistical significance is indicated as follows: a P <0.05, b P <0.01, c P <0.001 vs. baseline (week 0).

    Article Snippet: Ghrelin levels were determined using the Ghrelin Human ELISA kit (Invitrogen, Thermo Fisher Scientific; Cat No. BMS2192).

    Techniques: Cell Function Assay

    Mice containing activating DREADDs in Glp1r/Trh neurons were treated with saline or CNO at the onset of the dark cycle (a), during refeeding following an overnight fast (b), or prior to ghrelin treatment (c). a , Cumulative dark-cycle food intake at 0, 1, 2, and 3 hours following IP CNO or saline in a within-subject crossover design (n=5).. b , Cumulative post-fast food intake at 0, 1, 2, 4, 6, and 8 hours following IP CNO or saline (n=5). c , Cumulative food intake following IP ghrelin with CNO or saline pre-treatment at 0, 1, 2, 4, 6, and 8 hours (n=4). d, Effect of leptin (dark teal) versus saline (light teal) pre-treatment on ghrelin-induced 24-hour food intake in lean Lepr Glp1r KO (KO) and control (WT) mice. Lines connect within-subject measurements (crossover design). e, Cumulative post-fast food intake following leptin (dark teal) or saline (light teal) administration in WT (left) and KO (right) mice. f, g , Body weight (f) and daily food intake (g) before and 7 days after HFD exposure in Lepr Glp1r KO (n=9) and Control (n=10) mice. h , Food intake from (g) separated by dark (top) and light (bottom) cycle. The excess intake in Lepr Glp1r KO mice was concentrated in the dark cycle (genotype × time: χ²(9)=38.33, P =1.52×10⁻⁵). Dashed line indicates HFD switch. All panels: * P <0.05, **P<0.01, ***P<0.001. A-c, e-h: Plotted points represent mean values. Error bars (a-c) and shaded regions (e-h) denote SEM.

    Journal: bioRxiv

    Article Title: A uniquely leptin sensitive hypothalamic neuron population limits hyperphagia and weight gain in diet-induced obesity

    doi: 10.64898/2026.03.26.714161

    Figure Lengend Snippet: Mice containing activating DREADDs in Glp1r/Trh neurons were treated with saline or CNO at the onset of the dark cycle (a), during refeeding following an overnight fast (b), or prior to ghrelin treatment (c). a , Cumulative dark-cycle food intake at 0, 1, 2, and 3 hours following IP CNO or saline in a within-subject crossover design (n=5).. b , Cumulative post-fast food intake at 0, 1, 2, 4, 6, and 8 hours following IP CNO or saline (n=5). c , Cumulative food intake following IP ghrelin with CNO or saline pre-treatment at 0, 1, 2, 4, 6, and 8 hours (n=4). d, Effect of leptin (dark teal) versus saline (light teal) pre-treatment on ghrelin-induced 24-hour food intake in lean Lepr Glp1r KO (KO) and control (WT) mice. Lines connect within-subject measurements (crossover design). e, Cumulative post-fast food intake following leptin (dark teal) or saline (light teal) administration in WT (left) and KO (right) mice. f, g , Body weight (f) and daily food intake (g) before and 7 days after HFD exposure in Lepr Glp1r KO (n=9) and Control (n=10) mice. h , Food intake from (g) separated by dark (top) and light (bottom) cycle. The excess intake in Lepr Glp1r KO mice was concentrated in the dark cycle (genotype × time: χ²(9)=38.33, P =1.52×10⁻⁵). Dashed line indicates HFD switch. All panels: * P <0.05, **P<0.01, ***P<0.001. A-c, e-h: Plotted points represent mean values. Error bars (a-c) and shaded regions (e-h) denote SEM.

    Article Snippet: For immunohistochemical analysis of neuronal activation after stimulation with ghrelin, ad libitum fed DIO male and female Lepr Glp1r KO and DIO control mice were injected i.p. with 1mg/kg ghrelin (Hello Bio, HB2942) or 0.9% saline (0.5 U/g).

    Techniques: Saline, Control

    a,b, Baseline characteristics of Glp1r Lepr KO and control mice used in the chow vs DIO fasting-refeeding experiment (main text ). Chow-fed and DIO cohorts are independent groups of animals. c-e, Baseline characteristics of DIO Glp1r Lepr KO (n=12) and control (n=11) mice used in the ghrelin feeding experiment. c , Summary table including plasma leptin for a subset of mice (KO n=4, WT n=3). d , Individual body weights and ( e ) plasma leptin by genotype, confirming hyperleptinemia in both genotypes. Data are mean ± SD (tables) or mean ± SEM (dot plots) with individual animals shown.

    Journal: bioRxiv

    Article Title: A uniquely leptin sensitive hypothalamic neuron population limits hyperphagia and weight gain in diet-induced obesity

    doi: 10.64898/2026.03.26.714161

    Figure Lengend Snippet: a,b, Baseline characteristics of Glp1r Lepr KO and control mice used in the chow vs DIO fasting-refeeding experiment (main text ). Chow-fed and DIO cohorts are independent groups of animals. c-e, Baseline characteristics of DIO Glp1r Lepr KO (n=12) and control (n=11) mice used in the ghrelin feeding experiment. c , Summary table including plasma leptin for a subset of mice (KO n=4, WT n=3). d , Individual body weights and ( e ) plasma leptin by genotype, confirming hyperleptinemia in both genotypes. Data are mean ± SD (tables) or mean ± SEM (dot plots) with individual animals shown.

    Article Snippet: For immunohistochemical analysis of neuronal activation after stimulation with ghrelin, ad libitum fed DIO male and female Lepr Glp1r KO and DIO control mice were injected i.p. with 1mg/kg ghrelin (Hello Bio, HB2942) or 0.9% saline (0.5 U/g).

    Techniques: Control, Clinical Proteomics

    a , Cumulative post-fast food intake (kcal) at 0, 1, 2, 4, and 8 hours in Control (WT, left) and Lepr Glp1r KO (right) mice on chow (light) or HFD (dark). * P <0.05, *** P <0.001. Shaded regions denote SEM. b , Five-hour food intake following IP ghrelin (dark) or saline (light) in DIO WT (n=11) and Lepr Glp1r KO (n=12) mice. Lines connect within-subject measurements (crossover design). ** P <0.01, error bars denote SEM. c , Representative FOS immunofluorescence in the mbARC of DIO Control and Lepr Glp1r KO mice following saline (top) or ghrelin (bottom) injection. 3V, third ventricle; ME, median eminence. d , Quantification of FOS-positive ARC neurons after saline (top; P=0.15) or ghrelin (bottom; P =0.013). Shown are mean-/+ SEM, along with individual data points. e , Left: schematic indicating the mbARC region sampled. Right: representative IBA1 immunofluorescence in DIO WT and Lepr Glp1r KO (KO) mice. f , Quantification of IBA1-positive microglia in the ARC of control (ctrl) and KO mice. Shown are mean-/+ SEM, along with individual data points.

    Journal: bioRxiv

    Article Title: A uniquely leptin sensitive hypothalamic neuron population limits hyperphagia and weight gain in diet-induced obesity

    doi: 10.64898/2026.03.26.714161

    Figure Lengend Snippet: a , Cumulative post-fast food intake (kcal) at 0, 1, 2, 4, and 8 hours in Control (WT, left) and Lepr Glp1r KO (right) mice on chow (light) or HFD (dark). * P <0.05, *** P <0.001. Shaded regions denote SEM. b , Five-hour food intake following IP ghrelin (dark) or saline (light) in DIO WT (n=11) and Lepr Glp1r KO (n=12) mice. Lines connect within-subject measurements (crossover design). ** P <0.01, error bars denote SEM. c , Representative FOS immunofluorescence in the mbARC of DIO Control and Lepr Glp1r KO mice following saline (top) or ghrelin (bottom) injection. 3V, third ventricle; ME, median eminence. d , Quantification of FOS-positive ARC neurons after saline (top; P=0.15) or ghrelin (bottom; P =0.013). Shown are mean-/+ SEM, along with individual data points. e , Left: schematic indicating the mbARC region sampled. Right: representative IBA1 immunofluorescence in DIO WT and Lepr Glp1r KO (KO) mice. f , Quantification of IBA1-positive microglia in the ARC of control (ctrl) and KO mice. Shown are mean-/+ SEM, along with individual data points.

    Article Snippet: For immunohistochemical analysis of neuronal activation after stimulation with ghrelin, ad libitum fed DIO male and female Lepr Glp1r KO and DIO control mice were injected i.p. with 1mg/kg ghrelin (Hello Bio, HB2942) or 0.9% saline (0.5 U/g).

    Techniques: Control, Saline, Immunofluorescence, Injection

    A-C Simple linear regressions between the devaluation coefficient (k DD ) on DDT3 and plasma levels of ghrelin ( A ), LEAP2 ( B ), and the ghrelin/LEAP2 molar ratio ( C ) in refed animals. D Simple linear regression between plasma levels of LEAP2 and the percentage decrease in preference for the LL reward on DDT3. Data are expressed as the coefficient of determination (r 2 ) and p-value. Dotted lines represent the 95% confidence band of the best fit line. CT control, DDT delay discounting task, LL Large Late, FR food restriction, FR + R food restriction + refeeding, LEAP2 Liver Expressed Antimicrobial Peptide 2, k DD Coefficient of devaluation. Correlations were performed using simple ( A – C ) or multiple ( D ) linear regression.

    Journal: Translational Psychiatry

    Article Title: The role of LEAP2 on cognitive impulsivity after refeeding: evidence from a preclinical study in female mice and from patients with anorexia nervosa

    doi: 10.1038/s41398-026-03912-y

    Figure Lengend Snippet: A-C Simple linear regressions between the devaluation coefficient (k DD ) on DDT3 and plasma levels of ghrelin ( A ), LEAP2 ( B ), and the ghrelin/LEAP2 molar ratio ( C ) in refed animals. D Simple linear regression between plasma levels of LEAP2 and the percentage decrease in preference for the LL reward on DDT3. Data are expressed as the coefficient of determination (r 2 ) and p-value. Dotted lines represent the 95% confidence band of the best fit line. CT control, DDT delay discounting task, LL Large Late, FR food restriction, FR + R food restriction + refeeding, LEAP2 Liver Expressed Antimicrobial Peptide 2, k DD Coefficient of devaluation. Correlations were performed using simple ( A – C ) or multiple ( D ) linear regression.

    Article Snippet: Plasma concentrations of ghrelin and LEAP2 were evaluated with commercial EIA kits (Ref. A05117 for mouse/rat ghrelin, Bertin Bioreagents, Montigny le Bretonneux, France and Ref. EK-075-40 for LEAP2, Phoenix Pharmaceuticals, Burlingame, USA) as previously performed (See ).

    Techniques: Clinical Proteomics, Control