Bariatric surgery is increasingly recognized as one of the most effective interventions to help patients achieve significant and sustained weight loss, as well as improved metabolic and overall health. Unfortunately, the cellular and physiological mechanisms by which bariatric surgery achieves weight loss have not been fully elucidated, yet are critical to understanding the central role of the intestinal tract in whole-body metabolism and to developing novel strategies for the treatment of obesity. In this review, we provide an overview of potential mechanisms contributing to weight loss, including effects on regulation of energy balance and both central and peripheral nervous system regulation of appetite and metabolism. Moreover, we highlight the importance of the gastrointestinal tract, including alterations in bile acid physiology, secretion of intestinally derived hormones, and the microbiome, as a potent mediator of improved metabolism in postbariatric patients.

Hypoglycemia is increasingly recognized as a complication of bariatric surgery. Although medications are often required, medical nutrition therapy remains the key cornerstone for successful prevention of hypoglycemia in patients with post-bariatric hypoglycemia (PBH). We provide suggested approaches to the dietary management of PBH, incorporating data from both the medical literature and extensive clinical experience in an academic referral center for PBH. The overall goal of medical nutrition therapy for PBH is to reduce postprandial surges in glucose, which often trigger surges in insulin secretion and promote subsequent hypoglycemia. Thus, strategies focus on controlled portions of low glycemic index carbohydrates, avoidance of rapidly-absorbed carbohydrates, adjustment of timing of meals and snacks, and attention to personal and cultural barriers to implementation.

Hypoglycemia is increasingly recognized as a complication of bariatric surgery. Typically hypoglycemia does not appear immediately postoperatively, but rather more than 1 year later, and usually occurs 1–3 hours after meals. While rare, insulinoma has been reported after bariatric surgery. Clinical factors which should raise suspicion for insulinoma and the need for comprehensive clinical and biochemical evaluation include hypoglycemia occurring in the fasting state, predating bariatric surgery and/or worsening immediately postoperatively, and lack of response to conservative therapy. Localization and successful resection of insulinoma can be achieved using novel endoscopic ultrasound and surgical approaches. In summary, hypoglycemia presenting shortly after gastric bypass or with a dominant fasting pattern should be fully evaluated to exclude insulinoma. Additionally, evaluation prior to gastric bypass should include screening for history of hypoglycemia symptoms.

Background: Hypoglycemia is an increasingly recognized complication of bariatric surgery. Mechanisms contributing to glucose lowering remain incompletely understood. We aimed to identify differentially abundant plasma proteins in patients with post-bariatric hypoglycemia (PBH) after roux-en-Y gastric bypass (RYGB), compared to asymptomatic post-RYGB. Methods: Proteomic analysis of blood samples collected after overnight fast and mixed meal challenge in individuals with PBH, asymptomatic RYGB, severe obesity, or overweight recruited from outpatient hypoglycemia or bariatric clinics.

Background Postbariatric hypoglycemia (PBH) can threaten safety and reduce quality of life. Current therapies are incompletely effective. Methods Patients with PBH were enrolled in a double-blind, placebo-controlled, crossover trial to evaluate a closed-loop glucose-responsive automated glucagon delivery system designed to reduce severe hypoglycemia. A hypoglycemia detection and mitigation algorithm was embedded in the artificial pancreas system connected to a continuous glucose monitor (CGM, Dexcom) driving a patch infusion pump (Insulet) filled with liquid investigational glucagon (Xeris) or placebo (vehicle). Sensor/plasma glucose responses to mixed meal were assessed during 2 study visits. The system delivered up to 2 doses of study drug (300/150 μg glucagon or equal-volume vehicle) if triggered by the algorithm. Rescue dextrose was given for plasma glucose <55 mg/dL or neuroglycopenia. Results Twelve participants (11 females/1 male, age 52 ± 2, 8 ± 1 years postsurgery, mean ± SEM) completed all visits. Predictive hypoglycemia alerts prompted automated drug delivery postmeal, when sensor glucose was 114 ± 7 vs 121 ± 5 mg/dL (P = .39). Seven participants required rescue glucose after vehicle but not glucagon (P = .008). Five participants had severe hypoglycemia (<55 mg/dL) after vehicle but not glucagon (P = .03). Nadir plasma glucose was higher with glucagon vs vehicle (67 ± 3 vs 59 ± 2 mg/dL, P = .004). Plasma glucagon rose after glucagon delivery (1231 ± 187 vs 16 ± 1 pg/mL at 30 minutes, P = .001). No rebound hyperglycemia occurred. Transient infusion site discomfort was reported with both glucagon (n = 11/12) and vehicle (n = 10/12). No other adverse events were observed. Conclusion A CGM-guided closed-loop rescue system can detect imminent hypoglycemia and deliver glucagon, reducing severe hypoglycemia in PBH. Clinical Trials Registration NCT03255629

Context Severe hypoglycemia with neuroglycopenia, termed post-bariatric hypoglycemia (PBH). typically occurs postprandially, but is also reported post-activity or mid-nocturnally. Objective To quantify glycemia, glycemic variability (GV), and magnitude/duration of low sensor glucose (SG) values in patients with PBH after Roux-en-Y gastric bypass (PBH-RYGB). Design Retrospective analysis Setting Academic medical center Participants Individuals with PBH-RYGB (n=40), reactive hypoglycemia without GI surgery (Non-Surg Hypo, n=20), pre-diabetes (Pre-DM, n=14), newly-diagnosed T2D (n=5), and healthy controls (HC, n=38). Interventions Masked CGM (Dexcom G4) was used to assess patterns over 24 hours, daytime (6 AM-midnight) and nighttime (midnight-6 AM). Outcome measures: Prespecified measures included mean and median SG, variability, and percent time at thresholds of sensor glucose. Results Mean and median SG were similar for PBH-RYGB and HC (mean: 99.8±18.6 vs. 96.9±10.2 mg/dL; median: 93.0±14.8 vs. 94.5±7.4 mg/dL). PBH-RYGB had a higher coefficient of variation (27.3±6.8 vs. 17.9±2.4%, p<0.0001) and range (154.5±50.4 vs. 112.0±26.7 mg/dL, p<0.0001). Nadir was lowest in PBH-RYGB (42.5±3.7 vs. HC 49.0±11.9 mg/dL, p=0.0046), with >2-fold greater time with SG<70 mg/dL vs. HC (7.7±8.4 vs. 3.2±4.1%, p=0.0013); these differences were greater at night (12.6±16.9 vs. 1.0±1.5%, p<0.0001). Non-Surg Hypo also had 4-fold greater time with SG<70 at night vs. HC (SG <70: 4.0 ± 5.9% vs 1.0 ± 1.5%), but glycemic variability was not increased. Conclusions Patients with PBH-RYGB experience higher glycemic variability and frequency of SG<70 compared to HC, especially at night. These data suggest that additional pathophysiologic mechanisms beyond prandial changes contribute to PBH.

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The management of inpatient hyperglycemia is a focus of quality improvement projects across many hospital systems while remaining a point of controversy among clinicians. The association of inpatient hyperglycemia with suboptimal hospital outcomes is accepted by clinical care teams; however, the clear benefits of targeting hyperglycemia as a mechanism to improve hospital outcomes remain contentious. Glycemic management is also frequently confused with efforts aimed at intensive glucose control, further adding to the confusion. Nonetheless, several regulatory agencies assign quality rankings based on attaining specified glycemic targets for selected groups of patients (Surgical Care Improvement Project (SCIP) measures). The current paper reviews the data supporting the benefits associated with inpatient glycemic control projects, the components of a successful glycemic control intervention, and utilization of the electronic medical record in implementing an inpatient glycemic control project.