Alicja Pakiet1, Maciej Wilczynski2, Olga Rostkowska2, Justyna Korczynska3, Patrycja Jabłonska4, Lukasz Kaska2, Monika Proczko-Stepaniak2, Ewa Sobczak5,6, Piotr Stepnowski1, Faidon Magkos7, Tomasz Sledzinski8, Adriana Mika1,3. 1. Department of Environmental Analytics, Faculty of Chemistry, University of Gdansk, Wita Stwosza 63, 80-308, Gdansk, Poland. 2. Department of General, Endocrine and Transplant Surgery, Faculty of Medicine, Medical University of Gdansk, 17 Smoluchowskiego, 80-214, Gdansk, Poland. 3. Department of Pharmaceutical Biochemistry, Faculty of Pharmacy, Medical University of Gdansk, 1 Debinki Str., 80-211, Gdansk, Poland. 4. Department of Biochemistry, Faculty of Medicine, Medical University of Gdansk, Debinki 1, 80-211, Gdansk, Poland. 5. Department of Clinical Nutrition, Faculty of Health Sciences, Medical University of Gdansk, Debinki 7, 80-211, Gdansk, Poland. 6. Western Sussex Hospitals NHS Foundation Trust, Worthing Hospital, Worthing, Lyndhurst Rd, Worthing, West Sussex, BN11 2DH, UK. 7. Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Bülowsvej 17, 1870, Frederiksberg C, Denmark. 8. Department of Pharmaceutical Biochemistry, Faculty of Pharmacy, Medical University of Gdansk, 1 Debinki Str., 80-211, Gdansk, Poland. tsledz@gumed.edu.pl.
Abstract
BACKGROUND: Subjects with morbid obesity have low levels of serum branched-chain fatty acids (BCFAs), which correlate inversely with insulin resistance, hypertriglyceridemia, and inflammation. Recent evidence suggests BCFAs are produced during branched-chain amino acid (BCAA) catabolism in human adipose tissue. Elevated concentrations of BCAAs are associated with insulin resistance. OBJECTIVES: In this single-center study, we evaluated the effect of one anastomosis gastric bypass (OAGB) on circulating BCFA and BCAA. Moreover, we determined the expression of genes involved in BCAA catabolism in adipose tissue of patients with obesity and lean controls. METHODS: Fasting levels of BCFAs and BCAAs were determined by gas and liquid chromatography, respectively, coupled with mass spectrometry, in 50 patients with morbid obesity before and 6-9 months after surgery, and in 32 lean controls. Visceral and subcutaneous adipose tissue (VAT and SAT, respectively) biopsies were collected at baseline to determine mRNA levels for enzymes involved in BCAA catabolism. RESULTS: Before surgery, patients with obesity had lower BCFAs and greater BCAAs than control subjects. OAGB increased BCFA and decreased BCAA levels. Insulin resistance (assessed by HOMA) correlated inversely with BCFAs and positively with BCAAs. Expression of genes involved in BCAA catabolism in VAT (but not SAT) was lower in patients with obesity than in lean controls. CONCLUSIONS: OAGB-induced weight loss increases circulating BCFAs and decreases circulating BCAAs in patients with morbid obesity, perhaps by altering BCAA catabolism in VAT. We speculate that this shift may be related to the improvement in insulin sensitivity after surgery.
BACKGROUND: Subjects with morbid obesity have low levels of serum branched-chain fatty acids (BCFAs), which correlate inversely with insulin resistance, hypertriglyceridemia, and inflammation. Recent evidence suggests BCFAs are produced during branched-chain amino acid (BCAA) catabolism in human adipose tissue. Elevated concentrations of BCAAs are associated with insulin resistance. OBJECTIVES: In this single-center study, we evaluated the effect of one anastomosis gastric bypass (OAGB) on circulating BCFA and BCAA. Moreover, we determined the expression of genes involved in BCAA catabolism in adipose tissue of patients with obesity and lean controls. METHODS: Fasting levels of BCFAs and BCAAs were determined by gas and liquid chromatography, respectively, coupled with mass spectrometry, in 50 patients with morbid obesity before and 6-9 months after surgery, and in 32 lean controls. Visceral and subcutaneous adipose tissue (VAT and SAT, respectively) biopsies were collected at baseline to determine mRNA levels for enzymes involved in BCAA catabolism. RESULTS: Before surgery, patients with obesity had lower BCFAs and greater BCAAs than control subjects. OAGB increased BCFA and decreased BCAA levels. Insulin resistance (assessed by HOMA) correlated inversely with BCFAs and positively with BCAAs. Expression of genes involved in BCAA catabolism in VAT (but not SAT) was lower in patients with obesity than in lean controls. CONCLUSIONS:OAGB-induced weight loss increases circulating BCFAs and decreases circulating BCAAs in patients with morbid obesity, perhaps by altering BCAA catabolism in VAT. We speculate that this shift may be related to the improvement in insulin sensitivity after surgery.
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