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  • 1
    ISSN: 1432-1440
    Keywords: L-Carnitine ; Respiratory quotient ; Fat oxidation ; Total parenteral nutrition ; Nitrogen balance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary During episodes of trauma carnitine-free total parenteral nutrition (TPN) may result in a reduction of the total body carnitine pool, leading to a diminished rate of fat oxidation. Sixteen patients undergoing esophagectomy were equally and randomly divided and received isonitrogenous (0.2 gN/kg·day) and isocaloric (35 kcal/kg·day TPN over 11 days without and with L-carnitine supplementation (12 mg/kg·day). Compared with healthy controls, the total body carnitine pool was significantly reduced in both groups prior to the operation. Without supplementation carnitine concentrations were maintained, while daily provision of carnitine resulted in an elevation of total carnitine mainly due to an increase of the free fraction. Without supplementation the cumulative urinary carnitine losses were 11.5±6.3 mmol corresponding to 15.5%±8.5% of the estimated total body carnitine pool. Patients receiving carnitine revealed a positive carnitine balance in the immediate postoperative phase, 11.1%±19.0% of the infused carnitine being retained. After 11 days of treatment comparable values for respiratory quotient, plasma triglycerides, free fatty acids, ketone bodies, and cumulative nitrogen balance were observed. It is concluded that in the patient population studied here carnitine supplementation during postoperative TPN did not improve fat oxidation or nitrogen balance.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of applied physiology 63 (1991), S. 242-249 
    ISSN: 1439-6327
    Keywords: Atropine ; Glucose ; Fructose ; Dietary thermogenesis ; Insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Muscarinic blockade by atropine has been shown to decrease the thermic effect of a mixed meal, but not of intravenous glucose. To further delineate the mechanisms involved in the atropine-induced inhibition of thermogenesis after a meal, plasma substrate and hormone concentrations, energy expenditure (EE) and substrate oxidation rates were measured before and during a continuous glucose infusion (44.4 μmol·kg−1·min−1) with or without atropine. After 2 h of glucose infusion, a 20-g oral fructose load was administered while the glucose infusion was continued. Plasma insulin concentrations attained a plateau at 596 (SEM 100) pmol·l−1 after 120 min of glucose infusion and were not affected by muscarinic blockade; plasma glucose concentrations peaked at 13.3 (SEM 0.5) mmol·l−1 at 90 min and decreased progressively thereafter; no difference was observed with or without atropine. Plasma free fatty acid and glucagon concentrations, with or without atropine, were both decreased to 201 (SEM 18) μmol·l−1 and 74 (SEM 4) ng·l−1, respectively, after 2 h of glucose infusion, and were not further suppressed after oral fructose. Carbohydrate oxidation rates (CHOox) increased to 20.8 (SEM 1.4) μmol·kg−1·min−1 and lipid oxidation rates (Lox) decreased to 1.5 (SEM 0.3) μmol·kg−1·min−1 between 90 and 120 min after the beginning of glucose infusion and were not affected by atropine. Glucose-induced thermogenesis was similar with [6.5% (SEM 1.4%) of basal EE] or without [6.0% (SEM 1.0%), NS) muscarinic blockade during the 30 min preceding fructose ingestion. During the second half-hour after fructose ingestion, atropine infusion inhibited markedly the stimulation of CHOox [+2.8 (SEM 1.0) μmol·kg−1·min−1 vs +6.9 (SEM 1.0) μmol·kg−1·min−1, saline, P〈0.02] and the suppression of Lox [−0.8 (SEM 0.2) μmol·kg−1·min−1 vs −1.4 (SEM 0.2) μmol·kg−1·min−1, saline, P〈0.05]. Carbohydrate-induced thermogenesis during the second half-hour after fructose ingestion, increased to 13.0% (SEM 2.0%) without atropine and was suppressed to 7.7% (SEM 1.9%) (P〈 0.05, vs saline) with atropine. It was concluded that muscarinic blockade suppressed the increase of thermogenesis observed after oral fructose, but not during intravenous glucose infusion and that this suppression occurred independently of alterations of plasma insulin concentrations.
    Type of Medium: Electronic Resource
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