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Objective: Weight regain after weight loss is a challenge in obesity management. The metabolic changes and underlying mechanisms in obese people with weight fluctuation remain to be elucidated. In the present study, we aimed to profile the features and clinical significance of liver transcriptome in obese mice with weight regain after weight loss. Methods: The male C57BL/6J mice were fed with standard chow diet or high-fat diet (HFD). After 9 weeks, the HFD-induced obese mice were randomly divided into weight gain (WG), weight loss (WL) and weight regain (WR) group. After 10 weeks of dietary intervention, body weight, fasting blood glucose (FBG), intraperitoneal glucose tolerance, triglycerides (TG), total cholesterol (T-CHO) and low-density lipoprotein cholesterol (LDL-C) were measured. Morphological structure and lipid droplet accumulation in the liver were observed by H&E staining and oil red O staining, respectively. The liver transcriptome was detected by RNA sequencing. Protein expressions of liver cytochrome P450 3a11 (Cyp3a11) and E4 promoter-binding protein 4 (E4bp4) were determined by Western blot. Results: After 10 weeks of dietary intervention, the body weight, FBG, glucose area under the curve, T-CHO and LDL-C in WL group were significantly lower than those in WG group (P < 0.05). At 4 weeks of HFD re-feeding, the mice in WR group presented body weight and T-CHO significantly lower than those in WG group, whereas higher than those in WL group (P < 0.05). Hepatic vacuolar degeneration and lipid droplet accumulation in the liver were significantly alleviated in WL group and WR group, compared to those in WG group. The liver transcriptome associated with lipid metabolism was significantly altered during weight fluctuation in obese mice. Compared with those in WG group, Cyp3a11 in the liver was significantly upregulated, and E4bp4 was significantly downregulated in WL and WR groups. Conclusion: Obese mice experience weight regain after weight loss by HFD re-feeding, but their glucose and lipid metabolism disorders are milder than those induced by the persistence of obesity. Downregulated E4bp4 and upregulated Cyp3a11 are detected in obese mice after weight loss, suggesting that the E4bp4-Cyp3a11 axis may involved in metabolic mechanisms underlying weight regulation. [ABSTRACT FROM AUTHOR]

Background: This study investigated the risk factors for severe weight loss (SWL) within one year after minimally invasive McKeown esophagectomy. Methods: Esophageal cancer patients who underwent McKeown esophagectomy between January and July 2017 were prospectively enrolled. Preoperative body weight (PBW) was chosen as the initial body weight. Results: Forty‐four patients were enrolled and successfully followed up for one year. Median weight loss was 7.4% (quartile: 5.3–8.1%) and 12.6% (quartile: 8.8–17.7%) four weeks and one year after surgery, respectively. Accelerated weight loss occurred during the first two weeks after discharge, with median weight loss of 5.6% (quartile: 4.2–7.1%). Multivariable analysis showed that age ≥ 70 years (odds ratio [OR] 7.65; P = 0.030), preoperative sarcopenia (OR 7.18; P = 0.030), the first surgery in the daily schedule (OR 6.87; P = 0.032) and vocal cord paralysis (OR 12.30; P = 0.046) were independent risk factors for short‐term (4 weeks) SWL (> 7.5% PBW), while an American Society of Anesthesiologists score of 3–4 (OR 6.58; P = 0.047), a high fat‐free mass (OR 21.91; P = 0.003), and vocal cord paralysis (OR 25.83; P = 0.017) were independent risk factors for long‐term (1 year) SWL (> 13.0% PBW) after esophagectomy. Postoperative symptoms of insomnia, appetite loss, dysphagia, eating difficulties, and taste issues were also related to SWL. Conclusions: In esophageal cancer patients who have undergone esophagectomy, the first two weeks after hospital discharge is a key period for nutrition intervention. Patients with associated factors for SWL require postoperative nutrition support. [ABSTRACT FROM AUTHOR]