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ABSTRACT Objective Method Results Discussion Renourishment and weight restoration are critical first steps in anorexia nervosa (AN) treatment. The ability of the gastrointestinal tract to harvest and utilize energy from food is essential for successful weight restoration, but the functional capacity of the intestine after prolonged caloric restriction remains unknown. In an exploratory study, we quantified the stool energy content of individuals with AN before and after renourishment.We used archived stool samples from a multisite cohort (NCT03119272) of 103 individuals with AN at admission and discharge from inpatient renourishment and 122 sex‐matched non‐eating disorder controls (non‐ED). To determine whether bomb calorimetry may have utility in AN, we measured stool calorie loss as the number of kilocalories per gram of stool. Analyses included ANOVA, paired/unpaired t‐tests, and Spearman rank correlations for associations between stool energy and clinical variables.Following 25.10 ± 19.73 days of renourishment, patients gained an average of 5.67 ± 4.27 kg. Raw stool energy at discharge (AN‐DIS: 5.72 ± 0.86 kcal/g) was significantly higher than admission (AN‐AD: 5.41 ± 0.86 kcal/g; p < 0.01). Weight and BMI at admission and discharge were negatively correlated with raw stool energy at discharge.Energy content in stool increases after inpatient refeeding, likely due to increased calorie consumption. Findings should be interpreted cautiously due to methodological limitations in this post hoc study design. Future studies should use a priori, gold‐standard protocols to investigate stool calorie loss in AN, as prolonged restriction in AN may disrupt the gut and impede energy harvest.Trial Registration: clinicaltrials.gov: NCT03119272 [ABSTRACT FROM AUTHOR]

Introduction Cystic fibrosis (CF) is a life-limiting genetic disease affecting approximately 70,000 people worldwide (1). Severe pathology develops in the lungs, where absent or dysfunctional CF transmembrane regulator (CFTR) protein [...], The vast majority of people with cystic fibrosis (CF) are now eligible for CF transmembrane regulator (CFTR) modulator therapy. The remaining individuals with CF harbor premature termination codons (PTCs) or rare CFTR variants with limited treatment options. Although the clinical modulator response can be reliably predicted using primary airway epithelial cells, primary cells carrying rare CFTR variants are scarce. To overcome this obstacle, cell lines can be created by overexpression of mouse Bmi-1 and human TERT (hTERT). Using this approach, we developed 2 non-CF and 6 CF airway epithelial cell lines, 3 of which were homozygous for the W1282X PTC variant. The Bmi-1/hTERT cell lines recapitulated primary cell morphology and ion transport function. The 2 F508del-CFTR cell lines responded robustly to CFTR modulators, which was mirrored in the parent primary cells and in the cell donors&apos; clinical response. Cereblon E3 ligase modulators targeting eukaryotic release factor 3a (eRF3a) rescued W1282X-CFTR function to approximately 20% of WT levels and, when paired with G418, rescued G542XCFTR function to approximately 50% of WT levels. Intriguingly, eRF3a degraders also diminished epithelial sodium channel (ENaC) function. These studies demonstrate that Bmi-1/hTERT cell lines faithfully mirrored primary cell responses to CFTR modulators and illustrate a therapeutic approach to rescue CFTR nonsense mutations.