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• W2010784488 abstract "Acute infections provoke insulin resistance. These experiments were designed to study the severity, duration, and mechanisms of insulin resistance caused by acute infections. First, we studied eight patients [mean age, 29 ± 11 (±SD) yr; body mass index, 23 ± 2 kg/m2] with acute viral or bacterial infections during the acute stage of their infection and 1–3 months after recovery. The rate of glucose infusion required to maintain normoglycemia during hyperinsulinemia (∼500 pmol/ L) was used as a measure of insulin action. During infection, the glucose requirements in the patients [21 ± 2 (±SE) μmol/kgmin] were 52% less than those in weight- and age-matched normal subjects (44 ± 2 μmol/kg.min; P < 0.001). Compared to data from a large group of normal subjects, the resistance to insulin during infection corresponded to that predicted for a weight-matched 84-yr-old normal person or an age-matched obese person with a body mass index of 37 kg/m2. One to 3 months after recovery, the patients' glucose requirements were still significantly lower (37 ± 3 μmol/kg.min; P < 0.02) than those in matched normal subjects. To assess the mechanism of insulin resistance, seven additional patients were studied during the acute stage of infection using a low dose insulin infusion (plasma insulin, 215 pmol/L) combined with a [3-3H]glucose infusion and indirect calorimetry. Again, the glucose requirements were 59% lower in the patients (14 ± 2 μmol/kg.min) than in matched normal subjects (34 ± 2 μmol/kg.min; P < 0.001). This decrease was due to a defect in glucose utilization (18 ± 2 vs. 37 ± 1 μmol/kg.min; P < 0.001, patients vs. normal subjects) rather than impaired suppression of glucose production (4 ± 1 vs. 3 ± 1 μmol/kg-min, respectively). Total carbohydrate oxidation rates were similar in both groups (16 ± 2 vs. 14 ± 1 μmol/kg.min, respectively), whereas the apparent glucose storage was neglible in the patients (2 ± 1 μmol/kg.min) compared to that in normal subjects (22 ± 2 μmol/kg.min; P < 0.001). We conclude that acute infections induce severe and longlasting insulin resistance, which is localized to glucose-utilizing pathways. The rate of carbohydrate oxidation is normal during infections, whereas the rate of nonoxidative glucose disposal, as determined by indirect calorimetry, is nearly zero. The apparent blockade in glucose storage could result from diminished glycogen synthesis, accelerated glycogenolysis, or both." @default.
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• W2010784488 date "1989-08-01" @default.
• W2010784488 modified "2023-10-16" @default.
• W2010784488 title "Severity, Duration, and Mechanisms of Insulin Resistance during Acute Infections*" @default.
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• W2010784488 doi "https://doi.org/10.1210/jcem-69-2-317" @default.
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