Improved Muscle Mitochondrial Capacity Following Gastric Bypass Surgery in Obese SubjectsShow others and affiliations
2016 (English)In: Obesity Surgery, ISSN 0960-8923, E-ISSN 1708-0428, Vol. 26, no 7, p. 1391-1397Article in journal (Refereed) Published
Abstract [en]
Background
Weight loss resulting from low-calorie diets is often less than expected. We hypothesized that energy restriction would influence proton leakage and improve mitochondrial efficiency, leading to reduced energy expenditure, partly explaining the difficulties in weight loss maintenance.
Methods
Eleven women with a median BMI of 38.5 kg/m2 (q-range 37–40), and referred to gastric bypass surgery participated. Before surgery, and at 6 months of follow-up, muscle biopsies were collected from the vastus lateralis muscle. Mitochondria were isolated and analyzed for coupled (state 3) and uncoupled (state 4) respiration and mitochondrial capacity (P/O ratio).
Results
At follow-up, the participants had a median BMI of 29.6 kg/m2 (28.3–32.0). State 3 increased from 20.6 (17.9–28.9) to 34.9 nmol O2/min/U citrate synthase (CS) (27.0–49.0), p = 0.01, while state 4 increased from 2.8 (1.8–4.2) to 4.2 nmol O2/min/U CS (3.1–6.1), although not statistically significant. The P/O ratio increased from 2.7 (2.5–2.8) to 3.2 (3.0–3.4), p = 0.02, indicating improved mitochondrial efficiency.
Conclusions
Six months after gastric bypass surgery, the mitochondrial capacity for coupled, i.e., ATP-generating, respiration increased, and the P/O ratio improved. Uncoupled respiration was not enhanced to the same extent. This could partly explain the decreased basal metabolism and the reduced inclination for weight loss during energy restriction. © Springer Science+Business Media New York 2015
Place, publisher, year, edition, pages
New York, NY: Springer, 2016. Vol. 26, no 7, p. 1391-1397
Keywords [en]
Energy metabolism, Mitochondria, Muscle, Obesity, Thermogenesis, Weight loss
National Category
Microbiology in the medical area
Identifiers
URN: urn:nbn:se:hh:diva-29648DOI: 10.1007/s11695-015-1932-zISI: 000377939200005PubMedID: 26471784Scopus ID: 2-s2.0-84944705891OAI: oai:DiVA.org:hh-29648DiVA, id: diva2:861957
Funder
Swedish Research Council, 14244
Note
Financial support was provided through grants from the Swedish Transport Administration, the Swedish Nutrition Foundation, the Swedish Research Council (no: 14244), Stiftelsen Serafimerlasarettet, and the regional agreement on medical training and clinical research between Stockholm County Council and Karolinska Institutet. The pedometers were generously provided by Abbott Scandinavia AB.
2015-10-192015-10-192018-01-11Bibliographically approved