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The association between bariatric surgery (BS) and the prevention of type 2 diabetes (T2D) and its complications in patients with obesity has been rarely addressed in large, nationwide database studies.To estimate the preventive effect of BS against T2D and its vascular complications in patients with obesity without co-morbidity at baseline.All French public and private hospitals.Data were extracted from the French National Health Service database between 2008 and 2016. All patients with obesity aged 18- to 60-years old, free of T2D and major co-morbidities, and with at least 1 year of follow-up were analyzed. Patients who had undergone gastric bypass (GB), sleeve gastrectomy (SG), or adjustable gastric banding (AGB) were included in the BS group, and patients with obesity with no history of BS were considered as controls.Of 328,509 patients with obesity, 102,627 had BS. Between 2009 and 2016, 9.7% (31,946/328,509) of patients had a diagnosis of T2D associated with morbid obesity, 13.2% of the control group versus 2.0% of the BS group (P.001). BS was associated with favorable 8-year T2D event-free survival estimates of 92.3% in the BS group against 58.2% in the control group. The hazard ratio for the diagnosis of T2D was .18 (95% confidence interval, .17-.19) for the BS group versus controls, after adjustment on age, sex, body mass index, and baseline differences. A significant difference was found between the type of bariatric procedure (P.001) with more T2D after AGB (4.5%) than after GB (1.2%) or SG (0.9%). T2D complications were more common in controls (P.001) with multiple T2D complications occurring in 1% of patients in the control group and .1% in the BS group (P0.001). GB and SG were more effective than AGB.This nationwide study shows that BS reduces the new onset of T2D in patients with obesity by 82%. SG and GB give comparable results and both are more effective than AGB.

Aims: Long-term clinical trials evaluating the effects of metabolic-bariatric surgery (MBS) on type 2 diabetes (T2D) demonstrate that a significant proportion of patients either fail to achieve remission or experience T2D recurrence over time. Furthermore, patients with recurrent T2D might require reinstitution of pharmacotherapy to control comorbidities (hypertension, dyslipidemia). This paper reviews therapeutic options in patients with T2D relapse. Data synthesis: Although presently there is no recommended pharmacological strategy, the available data support GLP-1 analogues (GLP-1a) as the most suitable option to control hyperglycemia post-MBS. Beside their efficacy in lowering glycemia and body weight while preserving lean mass, GLP-1a exert cardiovascular/renal-protection and are also safe and well tolerated in surgical patients. In addition, the s.c. route of administration of these medications circumvents the problem of changes in oral drugs bioavailability following MBS. Of note, the available data refers to liraglutide and needs to be confirmed with weekly GLP-1a agents. Information regarding the impact of MBS on the pharmacokinetics of lipid lowering and anti-hypertensive drugs is scarce and inconclusive. The findings indicate that timing from intervention is particularly important because of adaptive intestinal mechanisms. Conclusions: The recurrence of T2D following MBS is a clinically relevant issue. GLP-1a therapy represents the best option to improve glycemic and weight control with good tolerability. Long-term clinical trials will clarify the impact of these drugs on cardiovascular outcomes. A close monitoring of MBS patients is advised to guide drug dosage adjustments and ensure the control of cardiovascular risk factors.

In the central nervous system, the active form of thyroid hormone, T3, derives from the cellular uptake and intracellular 5'-monodeiodination of T4 by type II 5'-monodeiodinase (DII). Here, we report that using an antiserum raised against the C-terminus of the full-length SeDII, immunolabeled cells were found in the rat hypothalamus in agreement with the DII mRNA distribution. Light and electron microscopy shows that DII is localized in astrocytes and tanycytes, supporting the hypothesis that these cells play an important role in the mediation peripheral signals, such as thyroid hormones, on hypothalamic functions.