Beyond Postprandial Symptoms: Fasting Hypoglycemia in Post-Bariatric Hypoglycemia
In brief
Five of 13 fasted patients with post-bariatric hypoglycemia had symptomatic fasting lows
In this selected group, five patients developed symptomatic fasting hypoglycemia during a supervised fast, with glucose averaging 49 mg/dL; the episodes were not driven by excess insulin. The retrospective findings suggest fasting lows can occur alongside the better-known post-meal episodes, but whether carbohydrate restriction contributes remains unclear.
- Journal
- Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists (Q1)
- Published
- 8 October 2026
- Study design
- Retrospective cohort
- Evidence level
- Level 4, Very Low (CEBM 4)
- Authors
- Joanne Lin, Abtin Shams, Helen M Lawler
- PMID
- 42849663
- DOI
- 10.1016/j.eprac.2026.09.119
Why clinicians should know about it
- Picked for Bariatric and Metabolic Surgery (paper of the day, 11 October 2026): Post‑bariatric hypoglycemia cohort, surgical relevance
Abstract
BACKGROUND: Post-bariatric hypoglycemia (PBH) is characterized by postprandial neuroglycopenia resulting from an exaggerated hyperinsulinemic response to nutrient intake in patients who have undergone Roux-en-Y gastric bypass, sleeve gastrectomy, or other upper gastrointestinal surgical procedures for weight loss. Fasting hypoglycemia is atypical. OBJECTIVE: We present a cohort of patients who developed symptomatic fasting hypoglycemia in the setting of established PBH and discuss the possible pathophysiological mechanisms. We also examine the role of β-cell hyperfunction in PBH. METHODS: A retrospective chart review was performed on 135 patients with PBH to identify patients with PBH undergoing a supervised 72-hour fast between 2013 and 2026. Inclusion criteria included a PBH diagnosis and an abnormal 72-hour fast. Exclusion criteria included asymptomatic fasting hypoglycemia, adrenal insufficiency, end-organ failure, hepatomegaly, alcohol or illicit drug use, or medications causing hypoglycemia. RESULTS: 13 patients underwent a 72-hour fast and 5 patients experienced symptomatic non-insulin mediated hypoglycemia with mean glucose of 49.2mg/dL occurring at 8-22 hours. Two patients underwent selective arterial calcium stimulation testing (SACST), one with a normal response and the other with β-cell hyperfunction. CONCLUSION: PBH is known to cause post-prandial hyperinsulinemic hypoglycemia, yet this PBH cohort also demonstrates atypical symptomatic fasting non-insulin-mediated hypoglycemia. This suggests a therapeutic paradox; carbohydrate restriction used to treat PBH may contribute to fasting hypoglycemia. In addition, discordant SACST results raise the question of whether β-cell hyperfunction is pre-existing, develops de novo as a consequence of altered gut anatomy, or reflects a combination of both.
Abstract as published, via PubMed.
For healthcare professionals. The summary is generated by AI from the published abstract, and the evidence level is assigned automatically from the study design on the Oxford CEBM hierarchy. Neither is medical advice. Read the full paper before changing practice.