Sherif Awad1, Francis Stephens, Chris Shannon, Dileep N Lobo. 1. Division of Gastrointestinal Surgery, Nottingham Digestive Diseases Centre NIHR Biomedical Research Unit, Nottingham University Hospitals, Queen's Medical Centre, Nottingham NG7 2UH, UK.
Abstract
BACKGROUND & AIMS: Fasting increases lipid flux into mitochondria causing excessive β-oxidation, carnitine acylation and impaired cellular glucose uptake. Preoperative carbohydrate treatment (PCT) attenuates postoperative insulin resistance, but mechanisms underlying this and the effects on carnitine metabolism remain largely unknown. METHODS: Pre-, intra- and-postoperative (day 1) plasma, and intraoperative rectus muscle mitochondrial free (FC), acyl (AC) and total (TC) carnitine concentrations were determined radioenzymatically in non-diabetic patients undergoinglaparoscopic cholecystectomy in a post hoc analysis of a randomised double-blind study (NCT00662376). Patients received 600 ml of a carbohydrate-based drink (ONS, Fresenuis Kabi, N = 15, 50 g carbohydrate, 15 g glutamine and antioxidants/300 ml) or placebo (N = 15, 0 g carbohydrate) the evening before surgery, and 300 ml 3-4 h pre-anaesthesia. RESULTS: No intra- or intergroup differences occurred in pre- or intraoperative plasma FC, TC or AC concentrations. Postoperatively, plasma TC and FC concentrations increased in the placebo group (p = 0.005 and p = 0.013). In the ONS group, postoperative increases occurred in plasma TC (p = 0.048). Increases in postoperative plasma TC and FC concentrations were attenuated in the ONS group (p = 0.013 and p = 0.044, respectively). No intergroup differences occurred in intraoperative mitochondrial carnitine concentrations. CONCLUSIONS: Preventing excessive/incomplete mitochondrial β-oxidation, characterised by perturbed carnitine metabolism, may be a mechanism by which PCT attenuates the reduction in postoperative insulin sensitivity.
RCT Entities:
BACKGROUND & AIMS: Fasting increases lipid flux into mitochondria causing excessive β-oxidation, carnitine acylation and impaired cellular glucose uptake. Preoperative carbohydrate treatment (PCT) attenuates postoperative insulin resistance, but mechanisms underlying this and the effects on carnitine metabolism remain largely unknown. METHODS: Pre-, intra- and-postoperative (day 1) plasma, and intraoperative rectus muscle mitochondrial free (FC), acyl (AC) and total (TC) carnitine concentrations were determined radioenzymatically in non-diabeticpatients undergoing laparoscopic cholecystectomy in a post hoc analysis of a randomised double-blind study (NCT00662376). Patients received 600 ml of a carbohydrate-based drink (ONS, Fresenuis Kabi, N = 15, 50 g carbohydrate, 15 g glutamine and antioxidants/300 ml) or placebo (N = 15, 0 g carbohydrate) the evening before surgery, and 300 ml 3-4 h pre-anaesthesia. RESULTS: No intra- or intergroup differences occurred in pre- or intraoperative plasma FC, TC or AC concentrations. Postoperatively, plasma TC and FC concentrations increased in the placebo group (p = 0.005 and p = 0.013). In the ONS group, postoperative increases occurred in plasma TC (p = 0.048). Increases in postoperative plasma TC and FC concentrations were attenuated in the ONS group (p = 0.013 and p = 0.044, respectively). No intergroup differences occurred in intraoperative mitochondrial carnitine concentrations. CONCLUSIONS: Preventing excessive/incomplete mitochondrial β-oxidation, characterised by perturbed carnitine metabolism, may be a mechanism by which PCT attenuates the reduction in postoperative insulin sensitivity.