Reversible hyperinsulinemic hypoglycemia after gastric bypass: a consequence of altered nutrient delivery

Tracey McLaughlin; Marcia Peck; Jens Holst; Carolyn Deacon

doi:10.1210/jc.2009-1628

Reversible hyperinsulinemic hypoglycemia after gastric bypass: a consequence of altered nutrient delivery

Tracey McLaughlin, Marcia Peck, Jens Holst, Carolyn Deacon

Endocrinology and Metabolism

128 Citationer (Scopus)

Abstract

Context: Severe hypoglycemia after Roux-en-Y gastric bypass surgery (RYGB) is an increasingly recognized condition, characterized by neuroglycopenia and inappropriately elevated insulin concentrations that occur primarily in the postprandial state. Both pathophysiology and treatment of this disorder remain elusive, but it has been postulated that hyperplasia and/or hypertrophy of β-cells due to morbid obesity and/or postsurgical nesidioblastosis may contribute. Objective: The objective of this study was to elucidate the pathophysiology of this condition; specifically, we hypothesized that metabolic abnormalities were a function of altered nutrient transit through the gastrointestinal tract rather than anatomical changes to pancreatic β-cells that would lead to consistently high insulin secretion irrespective of nutrient transit route. Design/Setting/Subject/Outcome Measures: We describe a unique case wherein gastrostomy tube (GT) insertion into the remnant stomach reversed neuroglycopenic symptoms. This subject was admitted to a university hospital research center for standardized measurement of glucose, insulin, and incretin hormones including glucagon-like peptide-1, gastric-inhibitory peptide, and glucagon. Results: Standardized liquid meal administration via GT vs. oral route demonstrated complete reversal of severe metabolic abnormalities that included hypersecretion of insulin and GLP-1. Conclusion: Post-RYGB hyperinsulinemia and hypoglycemia result entirely from altered nutrient delivery rather than generalized hyperfunction of β-cells due to presurgical hypertrophy/hyperfunction or postsurgical nesidioblastosis. These findings support the use of GT for treatment of severe cases and have implications for surgical manipulations that may reverse/prevent this condition.

Originalsprog	Engelsk
Tidsskrift	Journal of Clinical Endocrinology and Metabolism
Vol/bind	95
Udgave nummer	4
Sider (fra-til)	1851-5
Antal sider	5
ISSN	0021-972X
DOI	https://doi.org/10.1210/jc.2009-1628
Status	Udgivet - apr. 2010

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title = "Reversible hyperinsulinemic hypoglycemia after gastric bypass: a consequence of altered nutrient delivery",

abstract = "Context: Severe hypoglycemia after Roux-en-Y gastric bypass surgery (RYGB) is an increasingly recognized condition, characterized by neuroglycopenia and inappropriately elevated insulin concentrations that occur primarily in the postprandial state. Both pathophysiology and treatment of this disorder remain elusive, but it has been postulated that hyperplasia and/or hypertrophy of β-cells due to morbid obesity and/or postsurgical nesidioblastosis may contribute. Objective: The objective of this study was to elucidate the pathophysiology of this condition; specifically, we hypothesized that metabolic abnormalities were a function of altered nutrient transit through the gastrointestinal tract rather than anatomical changes to pancreatic β-cells that would lead to consistently high insulin secretion irrespective of nutrient transit route. Design/Setting/Subject/Outcome Measures: We describe a unique case wherein gastrostomy tube (GT) insertion into the remnant stomach reversed neuroglycopenic symptoms. This subject was admitted to a university hospital research center for standardized measurement of glucose, insulin, and incretin hormones including glucagon-like peptide-1, gastric-inhibitory peptide, and glucagon. Results: Standardized liquid meal administration via GT vs. oral route demonstrated complete reversal of severe metabolic abnormalities that included hypersecretion of insulin and GLP-1. Conclusion: Post-RYGB hyperinsulinemia and hypoglycemia result entirely from altered nutrient delivery rather than generalized hyperfunction of β-cells due to presurgical hypertrophy/hyperfunction or postsurgical nesidioblastosis. These findings support the use of GT for treatment of severe cases and have implications for surgical manipulations that may reverse/prevent this condition.",

keywords = "Adult, Blood Glucose, Body Mass Index, Female, Gastric Bypass, Gastric Inhibitory Polypeptide, Glucagon, Glucagon-Like Peptide 1, Humans, Hyperinsulinism, Hypoglycemia, Insulin, Nutritional Status, Obesity, Morbid, Postoperative Complications",

author = "Tracey McLaughlin and Marcia Peck and Jens Holst and Carolyn Deacon",

year = "2010",

month = apr,

doi = "10.1210/jc.2009-1628",

language = "English",

volume = "95",

pages = "1851--5",

journal = "Journal of Clinical Endocrinology and Metabolism",

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TY - JOUR

T1 - Reversible hyperinsulinemic hypoglycemia after gastric bypass: a consequence of altered nutrient delivery

AU - McLaughlin, Tracey

AU - Peck, Marcia

AU - Holst, Jens

AU - Deacon, Carolyn

PY - 2010/4

Y1 - 2010/4

N2 - Context: Severe hypoglycemia after Roux-en-Y gastric bypass surgery (RYGB) is an increasingly recognized condition, characterized by neuroglycopenia and inappropriately elevated insulin concentrations that occur primarily in the postprandial state. Both pathophysiology and treatment of this disorder remain elusive, but it has been postulated that hyperplasia and/or hypertrophy of β-cells due to morbid obesity and/or postsurgical nesidioblastosis may contribute. Objective: The objective of this study was to elucidate the pathophysiology of this condition; specifically, we hypothesized that metabolic abnormalities were a function of altered nutrient transit through the gastrointestinal tract rather than anatomical changes to pancreatic β-cells that would lead to consistently high insulin secretion irrespective of nutrient transit route. Design/Setting/Subject/Outcome Measures: We describe a unique case wherein gastrostomy tube (GT) insertion into the remnant stomach reversed neuroglycopenic symptoms. This subject was admitted to a university hospital research center for standardized measurement of glucose, insulin, and incretin hormones including glucagon-like peptide-1, gastric-inhibitory peptide, and glucagon. Results: Standardized liquid meal administration via GT vs. oral route demonstrated complete reversal of severe metabolic abnormalities that included hypersecretion of insulin and GLP-1. Conclusion: Post-RYGB hyperinsulinemia and hypoglycemia result entirely from altered nutrient delivery rather than generalized hyperfunction of β-cells due to presurgical hypertrophy/hyperfunction or postsurgical nesidioblastosis. These findings support the use of GT for treatment of severe cases and have implications for surgical manipulations that may reverse/prevent this condition.

AB - Context: Severe hypoglycemia after Roux-en-Y gastric bypass surgery (RYGB) is an increasingly recognized condition, characterized by neuroglycopenia and inappropriately elevated insulin concentrations that occur primarily in the postprandial state. Both pathophysiology and treatment of this disorder remain elusive, but it has been postulated that hyperplasia and/or hypertrophy of β-cells due to morbid obesity and/or postsurgical nesidioblastosis may contribute. Objective: The objective of this study was to elucidate the pathophysiology of this condition; specifically, we hypothesized that metabolic abnormalities were a function of altered nutrient transit through the gastrointestinal tract rather than anatomical changes to pancreatic β-cells that would lead to consistently high insulin secretion irrespective of nutrient transit route. Design/Setting/Subject/Outcome Measures: We describe a unique case wherein gastrostomy tube (GT) insertion into the remnant stomach reversed neuroglycopenic symptoms. This subject was admitted to a university hospital research center for standardized measurement of glucose, insulin, and incretin hormones including glucagon-like peptide-1, gastric-inhibitory peptide, and glucagon. Results: Standardized liquid meal administration via GT vs. oral route demonstrated complete reversal of severe metabolic abnormalities that included hypersecretion of insulin and GLP-1. Conclusion: Post-RYGB hyperinsulinemia and hypoglycemia result entirely from altered nutrient delivery rather than generalized hyperfunction of β-cells due to presurgical hypertrophy/hyperfunction or postsurgical nesidioblastosis. These findings support the use of GT for treatment of severe cases and have implications for surgical manipulations that may reverse/prevent this condition.

KW - Adult

KW - Blood Glucose

KW - Body Mass Index

KW - Female

KW - Gastric Bypass

KW - Gastric Inhibitory Polypeptide

KW - Glucagon

KW - Glucagon-Like Peptide 1

KW - Humans

KW - Hyperinsulinism

KW - Hypoglycemia

KW - Insulin

KW - Nutritional Status

KW - Obesity, Morbid

KW - Postoperative Complications

U2 - 10.1210/jc.2009-1628

DO - 10.1210/jc.2009-1628

M3 - Journal article

C2 - 20133462

SN - 0021-972X

VL - 95

SP - 1851

EP - 1855

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

IS - 4

ER -

Reversible hyperinsulinemic hypoglycemia after gastric bypass: a consequence of altered nutrient delivery

Abstract

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