Background: Endoscopic techniques have become the first-line therapy in bariatric surgery-related complications such as leaks and fistulas. We performed a systematic review and meta-analysis on the effectiveness of self-expandable stents, clipping, and tissue sealants in closing of post-bariatric surgery leak/fistula. Methods: A systematic literature search of the Medline/Scopus databases was performed to identify full-text articles published up to February 2019 on the use of self-expandable stents, clipping, or tissue sealants as primary endoscopic strategies used for leak/fistula closure. Meta-analysis of studies reporting stents was performed with the PRISMA guidelines. Results: Data concerning the efficacy of self-expanding stents in the treatment of leaks/fistulas after bariatric surgery were extracted from 40 studies (493 patients). The overall proportion of successful leak/fistula closure was 92% (95% CI, 90–95%). The overall proportion of stent migration was 23% (95% CI, 19–28%). Seventeen papers (98 patients) reported the use of clipping: the over-the-scope clips (OTSC) system was used in 85 patients with a successful closure rate of 67.1% and a few complications (migration, stenosis, tear). The successful fistula/leak closure using other than OTSC types was achieved in 69.2% of patients. In 10 case series (63 patients), fibrin glue alone was used with a 92.8–100% success rate of fistula closure that usually required repeated sessions at scheduled intervals. The complications of fibrin glue applications were reported in only one study and included pain and fever in 12.5% of patients. Conclusions: Endoscopic techniques are effective for management of post-bariatric leaks and fistulas in properly selected patients.

Gastrointestinal perforations, leaks and fistulas may be serious and life-threatening. The increasing number of endoscopic procedures with a high risk of perforation and the increasing incidence of leakage associated with bariatric operations call for a minimally invasive treatment for these complications. The therapeutic approach can vary greatly depending on the size, location, and timing of gastrointestinal wall defect recognition. Some asymptomatic patients can be treated conservatively, while patients with septic symptoms or cardio-pulmonary insufficiency may require intensive care and urgent surgical treatment. However, most gastrointestinal wall defects can be satisfactorily treated by endoscopy. Although the initial endoscopic closure rates of chronic fistulas is very high, the long-term results of these treatments remain a clinical problem. The efficacy of endoscopic therapy depends on several factors and the best mode of treatment will depend on a precise localization of the site, the extent of the leak and the endoscopic appearance of the lesion. Many endoscopic tools for effective closure of gastrointestinal wall defects are currently available. In this review, we summarized the basic principles of the management of acute iatrogenic perforations, as well as of postoperative leaks and chronic fistulas of the gastrointestinal tract. We also described the effectiveness of various endoscopic methods based on current research and our experience.

Skeletal muscle is perceived as a major tissue in glucose and lipid metabolism. High fat diet (HFD) lead to the accumulation of intramuscular lipids, including: long chain acyl-CoA, diacylglycerols, and ceramides. Ceramides are considered to be one of the most important lipid groups in the generation of skeletal muscle insulin resistance. So far, it has not been clearly established whether all ceramides adversely affect the functioning of the insulin pathway, or whether there are certain ceramide species that play a pivotal role in the induction of insulin resistance. Therefore, we designed a study in which the expression of CerS1 and CerS5 genes responsible for the synthesis of C18:0-Cer and C16:0-Cer, respectively, was locally silenced in the gastrocnemius muscle of HFD-fed mice through in vivo electroporation-mediated shRNA plasmids. Our study indicates that HFD feeding induced both, the systemic and skeletal muscle insulin resistance, which was accompanied by an increase in the intramuscular lipid levels, decreased activation of the insulin pathway and, consequently, a decrease in the skeletal muscle glucose uptake. CerS1 silencing leads to a reduction in C18:0-Cer content, with a subsequent increase in the activity of the insulin pathway, and an improvement in skeletal muscle glucose uptake. Such effects were not visible in case of CerS5 silencing, which indicates that the accumulation of C18:0-Cer plays a decisive role in the induction of skeletal muscle insulin resistance.

Background: Metabolic syndrome (MS) is usually diagnosed based on the presence of abdominal obesity, elevated blood pres­sure (BP), elevated fasting plasma glucose, high serum triglycerides (TG), and low high-density lipoprotein (HDL) cholesterol levels. Whether HIV is associated with a higher prevalence of MS than in the general population remains unclear. Aim: The aim of the study was to determine the incidence of MS in the population of HIV-infected adults and its association with clinical, virological, and biochemical features. Methods: Two hundred and seventy HIV-infected Caucasian adult patients were enrolled in the study and evaluated based on clinical records in the years 2013–2015. Results: Metabolic syndrome was diagnosed in 60 of 270 (22%) patients, 47 (24%) males and 13 (17%) females, mostly (72%) aged above 40 years. The percentage of patients with diagnosed MS in specific age groups in comparison to the general Polish population for females aged < 40 years was 7% vs. 4%, and males in the same age — 18% vs. 9%, for females aged 40–59 years — 47% vs. 24.4%, and males — 33% vs. 28.3%. Particular components of MS in the MS population were found as follows: body mass index > 30 kg/m2 in 29%, waist circumference exceeding 94 cm in men and 80 cm in woman — 87.5%, TG ≥ 150 mg/dL — 82%, HDL cholesterol < 40/50 mg/dL (males/females) — 42%, systolic/diastolic BP ≥ 130 mmHg/≥ 85 mmHg — 83%, and fasting glucose > 100 mg/dL — 42%. In stepwise multivariate logistic regression analysis, age (odds ratio [OR] 1.052, 95% con­fidence interval [CI] 1.018–1.088, p = 0.003) and nadir CD4 < 350 cells/mm3 (OR 3.576, 95% CI 1.035–12.355, p = 0.04) were associated with MS. Patients with MS compared with those without this disorder had low, intermediate, high, and very high cardiovascular risk in 10% vs. 23%, 73% vs. 70%, 7% vs. 5%, and 10% vs. 2%, respectively (p = 0.006). Conclusions: Prevalence of MS in the HIV-infected population is higher than in the general Polish population. Age and low nadir CD4 were found to be associated with MS. Background: Metabolic syndrome (MS) is usually diagnosed based on the presence of abdominal obesity, elevated blood pres­sure (BP), elevated fasting plasma glucose, high serum triglycerides (TG), and low high-density lipoprotein (HDL) cholesterol levels. Whether HIV is associated with a higher prevalence of MS than in the general population remains unclear. Aim: The aim of the study was to determine the incidence of MS in the population of HIV-infected adults and its association with clinical, virological, and biochemical features. Methods: Two hundred and seventy HIV-infected Caucasian adult patients were enrolled in the study and evaluated based on clinical records in the years 2013–2015. Results: Metabolic syndrome was diagnosed in 60 of 270 (22%) patients, 47 (24%) males and 13 (17%) females, mostly (72%) aged above 40 years. The percentage of patients with diagnosed MS in specific age groups in comparison to the general Polish population for females aged < 40 years was 7% vs. 4%, and males in the same age — 18% vs. 9%, for females aged 40–59 years — 47% vs. 24.4%, and males — 33% vs. 28.3%. Particular components of MS in the MS population were found as follows: body mass index > 30 kg/m2 in 29%, waist circumference exceeding 94 cm in men and 80 cm in woman — 87.5%, TG ≥ 150 mg/dL — 82%, HDL cholesterol < 40/50 mg/dL (males/females) — 42%, systolic/diastolic BP ≥ 130 mmHg/≥ 85 mmHg — 83%, and fasting glucose > 100 mg/dL — 42%. In stepwise multivariate logistic regression analysis, age (odds ratio [OR] 1.052, 95% con­fidence interval [CI] 1.018–1.088, p = 0.003) and nadir CD4 < 350 cells/mm3 (OR 3.576, 95% CI 1.035–12.355, p = 0.04) were associated with MS. Patients with MS compared with those without this disorder had low, intermediate, high, and very high cardiovascular risk in 10% vs. 23%, 73% vs. 70%, 7% vs. 5%, and 10% vs. 2%, respectively (p = 0.006). Conclusions: Prevalence of MS in the HIV-infected population is higher than in the general Polish population. Age and low nadir CD4 were found to be associated with MS.

Incidence of colorectal cancer (CRC) is growing worldwide. Pathogenetic mechanisms responsible for its onset and progression need further clarification. Colorectal adenomatous polyps are precancerous lesions with malignant potential dependent on histological architecture and grade of nuclear dysplasia. One of the factors conditioning CRC development are abnormalities in sphingolipid metabolism. The aim of this study was to assess the levels of sphingolipids in human colorectal adenomas. The control group (C, n = 12) consisted of patients with no colonic polyps. The examined group consisted of patients with prior diagnosed colonic polyps, qualified to endoscopic polypectomy. This group was further divided due to histological architecture into tubular adenomas group (TA, n = 10), tubulovillous adenomas with low‐grade dysplasia (LGD‐TVA, n = 10), and tubulovillous adenomas group with high‐grade dysplasia (HGD‐TVA, n = 11). In tissue samples, sphingolipd metabolite contents were measured using high performance liquid chromatography (HPLC). In cases of polypoid lesions with low malignancy potential (tubular adenomas), concentration of ceramide, which is characterized by proapoptotic and anti‐proliferative properties, increases compared with control group (p < 0.05), whereas content of sphingosine‐1‐phosphate with anti‐apoptotic and stimulating cellular proliferation properties is reduced in comparison with control group (p < 0.05). On the contrary, in cases of more advanced form of adenomatous polyps (tubulovillous adenomas with high‐grade dysplasia), the ceramide level decreases compared with control group (p < 0.05) while sphingosine‐1‐phosphate concentration is elevated (p < 0.05). We found that concentrations of pro‐apoptotic ceramide are decreased and pro‐proliferative S1P levels are increased in polypoid lesions with high malignancy potential, and it was the opposite in those with low malignancy potential.

The liver plays a crucial role in glucose metabolism. Obesity and a diet rich in fats (HFD) contribute to the accumulation of intracellular lipids. The aim of the study was to explore the involvement of acyl-CoA synthetase 1 (ACSL1) in bioactive lipid accumulation and the induction of liver insulin resistance (InsR) in animals fed an HFD. The experiments were performed on male C57BL/6 mice divided into the following experimental groups: 1. Animals fed a control diet; 2. animals fed HFD; and 3. HFD-fed animals with the hepatic ACSL1 gene silenced through a hydrodynamic gene delivery technique. Long-chain acyl-CoAs, sphingolipids, and diacylglycerols were measured by LC/MS/MS. Glycogen was measured by means of a commercially available kit. The protein expression and phosphorylation state of the insulin pathway was estimated by Western blot. HFD-fed mice developed InsR, manifested as an increase in fasting blood glucose levels (202.5 mg/dL vs. 130.5 mg/dL in the control group) and inhibition of the insulin pathway, which resulted in an increase in the rate of gluconeogenesis (0.420 vs. 0.208 in the control group) and a decrease in the hepatic glycogen content (1.17 μg/mg vs. 2.32 μg/mg in the control group). Hepatic ACSL1 silencing resulted in decreased lipid content and improved insulin sensitivity, accounting for the decreased rate of gluconeogenesis (0.348 vs. 0.420 in HFD_(+/+)) and the increased glycogen content (4.3 μg/mg vs. 1.17 μg/mg in HFD_(+/+)). The elevation of gluconeogenesis and the decrease in glycogenesis in the hepatic tissue of HFD-fed mice resulted from cellular lipid accumulation. Inhibition of lipid synthesis through silencing ACSL1 alleviated HFD-induced hepatic InsR.