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  • 1
    ISSN: 1432-1041
    Keywords: deflazacort ; prednisone ; 3H-glucose infusion ; glucose metabolism ; insulin kinetics ; euglycaemic clamp ; glucose kinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Corticosteroid treatment produces glucose intolerance with insulin resistance. Recent reports have indicated that deflazacort (DF) is significantly less diabetogenic than prednisone (PN). A euglycaemic hyperinsulinaemic (100 µU/ml) glucose clamp (EHGC) and 3H-glucose infusion for 240 min were performed in 6 healthy volunteers (HV) after administration of 15 mg PN or 18 mg DF, 12 h and 2 h before test. The glucose metabolic clearance rate (MCR) was significantly (p=0.02) higher after DF (4.75±0.58 ml/min·kg) than after PN (3.31±0.27 ml/min·kg). Basal hepatic glucose production (HGP) was significantly (p=0.003) lower after DF (3.58±0.33 mg/kg·min) than after PN (4.44±0.23 mg/kg·min). A similar pattern was obtained for glucose volume (GV) and glucose pool (GP). The kinetic parameters of insulin were not significantly different after the two drugs. After 7 day of PN 30 mg/day or DF 36 mg/day, EHGC and 3H-glucose infusion for 240 min were performed in 10 HV. Glucose MCR values were significantly (p=0.03) higher after DF (5.03±0.91 ml/min·kg) than after PN (2.80±0.26 ml/min·kg). HGP values did not different significantly after the two drugs. GV (p=0.001) and GP (p=0.002) were significantly lower after DF than after PN. Insulin kinetics were not significantly different after the two drugs. It is concluded that on acute and 7-day administration to healthy subjects DF, in an anti-inflammatory dose equivalent to PN, shows significantly less influence on glucose metabolism.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-5233
    Keywords: Glucagon secretion ; Glucose tolerance ; Insulin secretion ; Obesity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the feedback inhibition of insulin and glucagon secretion during euglycemic-hyperinsulinemic clamp at about 350 pmol/l in 16 patients with abdominal obesity [8 with normal glucose tolerance (oNGT), 8 with impaired glucose tolerance (oIGT)] and 8 normal-weight subjects matched for age, sex and blood pressure. In oNGT and oIGT, fasting plasma C-peptide levels were twice those in the controls (962±51 and 915±85 vs 439±28 pmol/l,P〈0.001) and their suppression was lower than in the controls, both in absolute terms (155±19 and 185±17 vs 274±18 pmol/l,P〈0.001) and as a percentage decline from basal levels (16±2% and 21±2% vs 63±2%,P〈0.001). Fasting plasma glucagon levels were similar in the patients and in the controls, but were less suppressed during clamp in oNGT and oIGT, both in absolute terms (7.0±0.9 and 5.6±0.6 vs 13.2±1.2 pmol/l,P〈0.001) and as a percentage change from basal levels (23±3% and 19±2% vs 44±4%,P〈0.001). These results suggest that the insulin feedback on B and A cells is impaired in abdominal obesity, and that this defect is of similar degree in oNGT and oIGT. These alterations could be implicated in the pathogenesis of hyperinsulinemia in obesity.
    Type of Medium: Electronic Resource
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