Plasma FGF-19 Levels are Increased in Patients with Post-Bariatric Hypoglycemia

Apr 13, 2019Obesity surgery

Higher Blood Levels of FGF-19 in People with Low Blood Sugar After Weight-Loss Surgery

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Abstract

Fibroblast growth factor 19 (FGF-19) levels were 2.4-fold higher in patients with post-bariatric hypoglycemia compared to asymptomatic individuals after a mixed meal.

FGF-19 levels in patients with post-bariatric hypoglycemia were significantly elevated at 120 minutes after a mixed meal.
The confirmed concentration of FGF-19 in patients with post-bariatric hypoglycemia was 360 ± 70, compared to 103 ± 18 in asymptomatic individuals.
Increased FGF-19 levels may be linked to insulin-independent mechanisms contributing to postprandial hypoglycemia.
Modulation of GLP-1 did not alter FGF-19 levels in overweight/obese individuals, suggesting distinct regulatory pathways.
The relationship between GLP-1 and FGF-19 appears to differ in individuals with post-bariatric hypoglycemia.

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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.

RESULTS: The top-ranking differentially abundant protein at 120 min after mixed meal was fibroblast growth factor 19 (FGF-19), an intestinally derived hormone regulated by bile acid-FXR signaling; levels were 2.4-fold higher in PBH vs. asymptomatic post-RYGB (mean + SEM, 1094 ± 141 vs. 428 ± 45, P < 0.001, FDR < 0.01). FGF-19 ELISA confirmed 3.5-fold higher concentrations in PBH versus asymptomatic (360 ± 70 vs. 103 ± 18, P = 0.025). To explore potential links between increased FGF-19 and GLP-1, residual samples from other human studies in which GLP-1 was modulated were assayed. FGF-19 levels did not change in response to infusion of GLP-1 and PYY in overweight/obese individuals. Infusion of the GLP-1 receptor antagonist exendin 9-39 in recently operated asymptomatic post-RYGB did not alter FGF-19 levels after mixed meal. By contrast, GLP-1 receptor antagonist infusion yielded a significant increase in FGF-19 levels after oral glucose in individuals with PBH. While plasma bile acids did not differ between PBH and asymptomatic post-RYGB, these data suggest unique interrelationships between GLP-1 and FGF-19 in PBH.

CONCLUSIONS: Taken together, these data support FGF-19 as a potential contributor to insulin-independent pathways driving postprandial hypoglycemia in PBH.

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Plasma FGF-19 Levels are Increased in Patients with Post-Bariatric Hypoglycemia

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