Volume 06 · Issue 03 · 2020

肥胖是一种慢性、复发性、多因素的大流行，定义为由于遗传、生物、微生物和环境因素导致的身体脂肪的过度或异常积累，这些因素促进了主要与摄入增加和消耗减少相关的正能量平衡。^1,2,3肥胖是巨大的多系统疾病的结果，包括心血管疾病，⁴2型糖尿病、⁵肿瘤、⁶睡眠呼吸暂停、^7,8,9,10等，显著增加死亡率，^11,12,13并导致卫生支出大幅增加。¹⁴与西方国家相比，在体重指数（BMI）相同的情况下，中心性肥胖在腰臀比较高（男性腰围>102 cm或腰臀比>0.9，女性腰围>88 cm或腰臀比>0.85）的中国个体中更为典型。作为死亡率的独立危险因素，¹⁵中心性肥胖与给中国医疗保健系统带来沉重负担的相关医疗问题更为密切。大多数合并症，尤其是非酒精性脂肪性肝病和胃食管反流病（GERD），仅通过减肥就可以显著改善。如今，众所周知的方法主要包括生活方式干预、药物治疗或减肥手术，但仅导致轻微的体重减轻或不利的副作用。最近，我们发现与肥胖相关的胃肠道疾病往往比2型糖尿病和心血管疾病更常见，甚至更早出现。因此，胃肠病学家有机会充分参与肥胖管理，并通过更新当前的理论知识提前提供有效的治疗。

Defunctioning stoma is widely used to reduce anastomotic complications in rectal cancer surgery. However, the complications of stoma and stoma reversal surgery should not be underestimated. Furthermore, in some patients, stoma reversal failed. Here, we investigated the complications of defunctioning stoma surgery and subsequent reversal surgery and identify risk factors associated with the failure of getting stoma reversed.

In total, 154 patients who simultaneously underwent low anterior resection and defunctioning stoma were reviewed. Patients were divided into two groups according to whether their stoma got reversed or not. The reasons that patients received defunctioning stoma and experienced stoma-related complications and the risk factors for failing to get stoma reversed were analysed.

The mean follow-up time was 47.54 (range 4.0-164.0) months. During follow-up, 19.5% of the patients suffered stoma-related long-term complications. Only 79 (51.3%) patients had their stomas reversed. The morbidity of complications after reversal surgery was 45.6%, and these mainly consisted of incision-related complications. Multivariate analyses showed that pre-treatment comorbidity (HR =3.17, 95% CI 1.27-7.96, P =0.014), postoperative TNM stage (HR =2.55, 95% CI 1.05-6.18, P =0.038), neoadjuvant therapy (HR =2.75, 95% CI 1.07-7.05, P =0.036), anastomosis-related complications (HR =4.52, 95% CI 1.81-11.29, P =0.001), and disease recurrence (HR =24.83, 95% CI 2.90-213.06, P =0.003) were significant independent risk factors for a defunctioning stoma to be permanent.

Defunctioning stoma is an effective method to reduce symptomatic anastomotic leakage, but the stoma itself and its reversal procedure are associated with high morbidity of complications, and many defunctioning stomas eventually become permanent. Therefore, surgeons should carefully assess preoperatively and perform defunctioning stomas in very high risk patients. In addition, doctors should perform stoma reversal surgery more actively to prevent temporary stomas from becoming permanent.

To date, there is only scare evidence characterizing the temporal features and progression of metabolic dysfunction in high-fat diet (HFD)-fed obese mice. Hence, its specific pathogenesis remains unclear.

Sixty 6-week-old male C57BL/6J mice were randomly divided into HFD and control diet (CD) groups and sacrificed at 1, 5, 9, 13, 17, and 21 weeks, respectively. At weekly intervals, intraperitoneal glucose tolerance testing (IPGTT) and intraperitoneal insulin tolerance testing (IPITT) were performed in both groups. A detailed time course in HFD-fed mice was investigated by evaluating the initiation of glucose homeostasis impairment, dyslipidemia, systemic insulin sensitivity, monocyte chemoattractant protein-1 (MCP-1) levels, epididymal white adipose tissue (eWAT) expansion, macrophage content changes, proinflammatory (M1)/anti-inflammatory (M2) macrophage imbalance, lipid accumulation in the liver, and β-cell morphometry in the pancreas.

In the HFD group, progressive weight gain and impairments in glucose metabolism (elevated fasting blood glucose and area under the curve (AUC) of IPGTT) were observed from the 3rd week, and a significantly elevated AUC of IPITT was first detected after week 7 of HFD feeding. As for dyslipidemia, after 9 weeks of feeding, the low-density lipoprotein cholesterol level and total cholesterol level in HFD group were significantly higher than those in the CD group (all P < 0.05), whereas no significant differences were shown in triglyceride level. Adipocyte size increased significantly in the HFD group in the 1st week, a phenotypic switch in eWAT from anti-inflammatory (M2) to pro-inflammatory (M1) macrophages was observed in the 5th week, and the metabolic inflammation was distinct in eWAT in the 9th week. Additionally, liver steatosis was considerably obvious at the 17th week and pancreatic β-cell morphometry did not change during 21 weeks of HFD feeding.

The eWAT expansion was detected early in HFD-induced obese mice, which occurred prior to obvious insulin resistance.