Gastrostomy tube: an effective treatment for refractory post-bariatric hyperinsulinemic hypoglycemia

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 695-707-Obesity Treatment
Clinical
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-695
Colleen M Craig*1, Cindy A Lamendola1, Carolyn F Deacon2, Jens J Holst2 and Tracey L McLaughlin1
1Stanford Univ. School of Medicine, Stanford, CA, 2Panum Institute, Univ. Of Copenhagen, Copenhagen N, Denmark
Introduction:  Roux-en-Y Gastric Bypass (RYGB) performed for medically complicated obesity typically results in weight loss with enhanced insulin sensitivity and improved glucose homeostasis.  An increasingly reported complication of RYGB is hyperinsulinemic hypoglycemia, with a subset of patients exhibiting neuroglycopenia.  Consensus as to the etiology of this disorder has not yet been reached, with postulations diverging around the source of hyperinsulinemia: beta-cell hypertrophy with nesidioblastosis vs. an exaggerated incretin effect due to altered nutrient transit.

Previously, we reported a case wherein post-RYGB metabolic derangements were reversed through enteral feeding to the remnant stomach via gastrostomy tube (GT).(1)  This study pointed to rapid nutrient transit to the distal bowel and the consequent elicitation of a GLP-1 surge as the cause of postprandial hyperinsulinemic hypoglycemia.  To our knowledge, no replication studies have been conducted.

Objective: In the present study, we repeated our methodology on a second subject with the goals of confirming our interpretation and establishing GT as a safe and effective treatment. 

Clinical Case: A 40 year-old woman with post-RYGB hyperinsulinemic hypoglycemia had severe neuroglycopenia, with marked cognitive and psychomotor impairment.  The subject had failed treatment with dietary discretion, diazoxide, verapamil, acarbose, and calcium channel blockers.  GT was placed to the remnant stomach, with resultant amelioration of her postprandial symptoms.

Design: Standardized liquid meal was administered via GT vs. oral route over 15 minutes.  Plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), gastric-inhibitory peptide (GIP), and glucagon were assayed at timepoints 0-180 minutes postprandially.

Results: Hypersecretion of insulin, GLP-1, and glucagon seen with oral administration were reversed via GT route.  GIP was not secreted in excess of normal via oral vs. GT route.

Conclusion:  These results support our view that hyperinsulinemia is mediated through an exaggerated incretin response due to rapid nutrient transit to the “hindgut.” The lack of GIP stimulation via oral vs. GT feeding implicates GLP-1 over GIP as the primary stimulus to insulin secretion.  While it is possible that an unmeasured “foregut” factor could be secreting a putative signal post-GT feeding, thereby suppressing hyperinsulinemia and averting hypoglycemia, the dramatic GLP-1 secretion post-oral feeding corroborates the “hindgut” hypothesis, and promotes GT as an effective treatment for refractory disease.  Notably, hyperglucagonemia seen with oral vs. GT despite elevated GLP-1 was unexpected, but confirms our prior observation.

(1) McLaughlin TL, Peck M, Holst J, Deacon C 2010 Reversible hyperinsulinemic hypoglycemia after gastric bypass: a consequence of altered nutrient delivery. J Clin Endocrinol Metab 95(4):1851-1855.

Nothing to Disclose: CMC, CAL, CFD, JJH, TLM

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

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