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Type 2 Diabetes Metabolic Improvement After Roux‐en‐Y Gastric Bypass May Include a Compensatory Mechanism That Balances Fatty Acid β and ω Oxidation
Author(s) -
Mendonça Machado Natasha,
Torrinhas Raquel Susana,
Sala Priscila,
Ishida Robson Kiyoshi,
Guarda Ismael Francisco Mota Siqueira,
Moura Eduardo Guimarães Hourneaux de,
Sakai Paulo,
Santo Marco Aurélio,
Linetzky Waitzberg Dan
Publication year - 2020
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1002/jpen.1960
Subject(s) - ketone bodies , medicine , ileum , endocrinology , jejunum , carnitine , chemistry , citric acid cycle , gluconeogenesis , biochemistry , biology , metabolism
Abstract Background More than half of patients who undergo Roux‐en‐Y gastric bypass (RYGB) can experience type 2 diabetes (T2D) remission, but the systemic and gastrointestinal (GI) metabolic mechanisms of this improvement are still elusive. Methods Paired samples collected before and 3 months after RYGB from 28 women with obesity and T2D were analyzed by metabolomics with gas chromatography coupled to mass spectrometry. Samples include plasma (n = 56) and biopsies of gastric pouch (n = 18), gastric remnant (n = 10), duodenum (n = 16), jejunum (n = 18), and ileum (n = 18), collected by double‐balloon enteroscopy. Results After RYGB, improvements in body composition and weight‐related and glucose homeostasis parameters were observed. Plasma‐enriched metabolic pathways included arginine and proline metabolism, urea and tricarboxylic acid (TCA) cycles, gluconeogenesis, malate‐aspartate shuttle, and carnitine synthesis. In GI tissue, we observed alterations of ammonia recycling and carnitine synthesis in gastric pouch, phenylacetate metabolism and trehalose degradation in duodenum and jejunum, ketone bodies in jejunum, and lactose degradation in ileum. Intermediates molecules of the TCA cycle were enriched, particularly in plasma, jejunum, and ileum. Fluctuations of dicarboxylic acids (DCAs) were relevant in several metabolomic tests, and metabolite alterations included aminomalonate and fumaric, malic, oxalic, and succinic acids. The product/substrate relationship between these molecules and its pathways may reflect a compensatory mechanism to balance metabolism. Conclusions RYGB was associated with systemic and GI metabolic reprogramming. DCA alterations link ω and β fatty acid oxidation to homeostatic mechanisms, including TCA cycle improvement.