Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2026
Beyond Postprandial Symptoms: Fasting Hypoglycemia in Post-Bariatric Hypoglycemia.
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Lin Joanne, Shams Abtin, Lawler Helen M
Аннотация
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.
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.