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  • Title: Glucose turnover, fuel oxidation and forearm substrate exchange in patients with thyrotoxicosis before and after medical treatment.
    Author: Møller N, Nielsen S, Nyholm B, Pørksen N, Alberti KG, Weeke J.
    Journal: Clin Endocrinol (Oxf); 1996 Apr; 44(4):453-9. PubMed ID: 8706313.
    Abstract:
    OBJECTIVE: Accelerated metabolism is a hallmark of thyrotoxicosis, but the underlying biochemical mechanisms are incompletely understood and the majority of studies have investigated normal subjects rendered only modestly hyperthyroid for a brief period of time. We have therefore studied a group of thyrotoxic patients using several different techniques. DESIGN: Twelve patients with newly diagnosed diffuse (10 patients) or nodular (2 patients) toxic goitre (10 women, 2 men; age 42.8 +/- 3.2 years; BMI 21.6 +/- 0.7 kg/m2) before ('pretreatment') and after ('treated') 11.2 +/- 1.0 weeks treatment with methimazole and compared these patients to a control group ('control') of 11 subjects (9 women, 2 men; age 40.5 +/- 3.9 years; BMI 22.5 +/- 1.0 kg/m2). All were studied for 3 hours in the basal state, using indirect calorimetry, isotope dilution for the measurement of glucose turnover and the forearm technique for assessment of muscle metabolism. RESULTS: Prior to treatment patients with thyrotoxicosis were characterized by increased (P < 0.05) levels of T3 (3.75 +/- 0.23 nmol/l (pretreatment), 1.89 +/- 0.08 (treated) and 1.75 +/- 0.11 (control)), resting energy expenditure (130.5 +/- 3.5 (pretreatment), 107.7 +/- 2.7 (treated) and 106.3 +/- 3.1 (control), % of predicted), protein oxidation (0.67 +/- 0.03 (pretreatment), 0.54 +/- 0.06 (treated) and 0.46 +/- 0.05 (control), mg/kg/min), lipid oxidation (1.34 +/- 0.08 (pretreatment), 1.00 +/- 0.06 (treated) and 1.02 +/- 0.04 (control), mg/kg/min), endogenous glucose production (2.51 +/- 0.13 (pretreatment), 1.86 +/- 0.12 (treated) and 1.85 +/- 0.12 (control), mg/kg/min), non-oxidative glucose turnover (1.28 +/- 0.16 (pretreatment), 0.75 +/- 0.18 (treated) and 0.71 +/- 0.11 (control), mg/kg/min) and a 50% increase in total forearm blood flow. Glucose oxidation (1.23 +/- 0.09 (pretreatment), 1.13 +/- 0.10 (treated) and 1.21 +/- 0.11 (control) mg/kg/min), exchange of substrates in the muscles of the forearm and circulating levels of insulin, C-peptide, growth hormone or glucagon were not influenced by hyperthyroidism. Propranolol (20 mg thrice daily) given to 7 of the patients for 2 days did not affect circulating levels of thyroid hormones, energy expenditure or glucose turnover rates. CONCLUSIONS: These results suggest that all major fuel sources contribute to the hypermetabolism of thyrotoxicosis and that augmented non-oxidative glucose metabolism may further aggravate the condition. All abnormalities diminish with medical treatment of the disease.
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