D. S. Hardin, A. Leblanc, G. Marshall, and D. K. Seilheimer
Mechanisms of insulin resistance in cystic fibrosis
Am J Physiol Endocrinol Metab, November 1, 2001; 281(5): E1022 - 1028.
[Abstract] [Full Text] [PDF]
Journal of Clinical Endocrinology & Metabolism, Vol 69, 317-323, Copyright © 1989 by Endocrine Society
H Yki-Jarvinen, K Sammalkorpi, VA Koivisto and EA
Nikkila
Second Department of Medicine, Helsinki
University, Finland.
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 (approximately 500
pmol/L) was used as a measure of insulin action. During
infection, the glucose requirements in the patients
[21 +/- 2 (+/- SE) mumol/kg.min] were 52% less than
those in weight- and age- matched normal subjects (44 +/- 2 mumol/kg.min;
P less than 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 mumol/kg.min; P less than 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 mumol/kg.min) than in matched normal
subjects (34 +/- 2 mumol/kg.min; P less than 0.001). This decrease
was due to a defect in glucose utilization (18 +/- 2 vs. 37 +/- 1
mumol/kg.min; P less than 0.001, patients vs. normal
subjects) rather than impaired suppression of glucose
production (4 +/- 1 vs. 3 +/- 1 mumol/kg.min,
respectively). Total carbohydrate oxidation rates were similar
in both groups (16 +/- 2 vs. 14 +/- 1 mumol/kg.min,
respectively), whereas the apparent glucose storage
was neglible in the patients (2 +/- 1 mumol/kg.min)
compared to that in normal subjects (22 +/- 2 mumol/kg.min; P
less than 0.001). We conclude that acute infections induce
severe and long-lasting 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.
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