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

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

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

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