Effect of Weight Loss after Bariatric Surgery on Thyroid-Stimulating Hormone Levels in Patients with Morbid Obesity and Normal Thyroid Function

Background: Several studies have reported that morbid obesity is associated with increased thyroid-stimulating hormone (TSH) levels. However, it is not clear what is the impact of bariatric surgery on postoperative thyroid function. The aim of this study was to evaluate the effect of weight loss after bariatric surgery on TSH levels in euthyroid patients with morbid obesity. Methods: We performed a retrospective observational study of 949 euthyroid patients (86.1% female; age 42.0 ± 10.3 years, BMI 44.3 ± 5.7 kg/m2) with morbid obesity submitted to bariatric surgery (laparoscopic adjustable gastric band, Roux-en-Y gastric bypass, or sleeve gastrectomy). Patients were subdivided in two groups: normal TSH group (TSH <2.5 mU/L) and high-normal TSH group (TSH ≥2.5 mU/L). The impact of anthropometric parameters, comorbidities, TSH, free thyroxine (FT4), free triiodothyronine (FT3), type of surgery, and excessive body weight loss (EBWL) on TSH variation 12 months after surgery was evaluated. Results: The high-normal TSH group (24.3% of patients) included more women, presented a higher BMI, higher systolic blood pressure, and higher FT3 levels. There was a significant decrease of TSH 12 months after surgery that was more marked in the high-normal TSH group (normal TSH group: 1.57 ± 0.49 to 1.53 ± 0.69 mIU/L, p = 0.063; high-normal TSH group: 3.23 ± 0.59 to 2.38 ± 0.86 mIU/L, p < 0.001). In a multivariate analysis, after adjusting for relevant covariates, EBWL, baseline BMI, and baseline FT3 were significantly associated with TSH decrease 12 months after bariatric surgery. Conclusion: Bariatric surgery promotes a decrease of TSH that is significantly greater in patients with high-normal TSH and is independently associated with EBWL after surgery

Pyrolysed almond shells used as electrodes in microbial electrolysis cell

9 p.The large cost of components used in microbial electrolysis cell (MEC) reactors represents an important limitation that is delaying the commercial implementation of this technology. In this work, we explore the feasibility of using pyrolysed almond shells (PAS) as a material for producing low-cost anodes for use in MEC systems. This was done by comparing the microbial populations that developed on the surface of PAS bioanodes with those present on the carbon felt (CF) bioanodes traditionally used in MECs. Raw almond shells were pyrolysed at three different temperatures, obtaining the best conductive material at the highest temperature (1000 °C). The behaviour of this material was then verified using a single-chamber cell. Subsequently, the main test was carried out using two-chamber cells and the microbial populations extant on each of the bioanodes were analysed. High-throughput sequencing of the 16S rRNA gene for eubacterial populations was carried out in order to compare the microbial communities attached to each type of electrode. The microbial populations on each electrode were also quantified by real-time polymerase chain reaction (realtime PCR) to determine the amount of bacteria capable of growing on the electrodes’surface. The results indicated that the newly developed PAS bioanodes possess a biofilm similar to those found on the surface of traditional CF electrodes. This research was possible thanks to the financial support of the Junta de Castilla y León, and was financed by European Regional Development Funds (LE320P18). C. B. thanks the Spanish Ministerio de Educación, Cultura y Deporte for support in the form of an FPI fellowship grant (Ref #: BES-2016-078329)

MCT1-mediated transport of a toxic molecule is an effective strategy for targeting glycolytic tumors

There is increasing evidence that oncogenic transformation modifies the metabolic program of cells. A common alteration is the upregulation of glycolysis, and efforts to target glycolytic enzymes for anticancer therapy are under way. Here, we performed a genome-wide haploid genetic screen to identify resistance mechanisms to 3-bromopyruvate (3-BrPA), a drug candidate that inhibits glycolysis in a poorly understood fashion. We identified the SLC16A1 gene product, MCT1, as the main determinant of 3-BrPA sensitivity. MCT1 is necessary and sufficient for 3-BrPA uptake by cancer cells. Additionally, SLC16A1 mRNA levels are the best predictor of 3-BrPA sensitivity and are most elevated in glycolytic cancer cells. Furthermore, forced MCT1 expression in 3-BrPA–resistant cancer cells sensitizes tumor xenografts to 3-BrPA treatment in vivo. Our results identify a potential biomarker for 3-BrPA sensitivity and provide proof of concept that the selectivity of cancer-expressed transporters can be exploited for delivering toxic molecules to tumors.National Institutes of Health (U.S.) (NIH CA103866)Jane Coffin Childs Memorial Fund for Medical Research (Fellowship)National Science Foundation (U.S.) (Fellowship)Howard Hughes Medical Institute (Investigator