Effects and mechanisms of neural and fluid regulation in bariatric surgery / 中华消化外科杂志

Currently, bariatric surgery, which includes restricted intake, malabsorptive and mixed surgeries, is known to be an effective measurement for the durable treatment of obesity and related comorbidities. By changing the anatomy of gastrointestinal tract, bariatric surgery achieves the principles of restricting food intake, reducing food absorption, increasing satiety and prolonging gastric emptying to help patients lose weight and regulate metabolic mechanism. Through the neuromodulation of brain-vagus-taste receptors, sensation-specific satiety can reduce the food intake. The brain-gut-microbe axis plays a central role in maintaining homeostasis through neuronal pathways in the brain, vagus, spinal nerves, enteric nervous system and signaling pathways. Bariatric surgery can inhibit the development of hypertension, diabetes, non-alcoholic fatty liver, cardio-vascular and cerebrovascular diseases in the regulation of body fluids through adipokines, bile acids, hormones and other signaling factors. Therefore, the improvement of metabolic-related diseases after bariatric surgery is the result of the interaction of multiple factors such as nerves, body fluids, and microorganisms. The authors summarize the literature reports to introduce the mechanism of neural and humoral factor regulation in weight loss and improvement of metabolic-related diseases after bariatric surgery.

Salt sensitivity and its implication in clinical practice

Hypertension (HTN) is a complex multi-factorial disease and is considered one of the foremost modifiable risk factors for stroke, heart failure, ischemic heart disease and renal dysfunction. Over the past century, salt and its linkage to HTN and cardiovascular (CV) mortality has been the subject of intense scientific scrutiny. There is now consensus that different individuals have different susceptibilities to blood pressure (BP)-raising effects of salt and this susceptiveness is called as salt sensitivity. Several renal and extra-renal mechanisms are believed to play a role. Blunted activity of the renin–angiotensin–aldosterone system (RAAS), adrenal Rac1-MR-Sgk1-NCC/ENaC pathway, renal SNS-GR-WNK4-NCC pathway, defect of membrane ion transportation, inflammation and abnormalities of Na+/Ca2+ exchange have all been implicated as pathophysiological basis for salt sensitive HTN. While salt restriction is definitely beneficial recent observation suggests that treatment with Azilsartan may improve salt sensitivity by selectively reducing renal proximal tubule Na+/H+ exchange. This encourages the future potential benefits of recognizing and therapeutically addressing the salt sensitive phenotype in humans.