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Departments of 1 Animal Physiology and 2 Pediatrics, University of Groningen, NL-9700AB Groningen, The Netherlands
We tested the hypothesis that
excessive portal venous supply of long-chain fatty acids to the liver
contributes to the development of insulin resistance via activation of
the hypothalamus-pituitary-adrenal axis (HPA axis) and sympathetic
system. Rats received an intraportal infusion of the long-chain fatty
acid oleate (150 nmol/min, 24 h), the medium-chain fatty acid
caprylate, or the solvent. Corticosterone (Cort) and norepinephrine
(NE) were measured as indexes for HPA axis and sympathetic
activity, respectively. Insulin sensitivity was assessed by means of an
intravenous glucose tolerance test (IVGTT). Oleate infusion induced
increases in plasma Cort (
= 13.5 ± 3.6 µg/dl;
P < 0.05) and NE ( = 235 ± 76 ng/l;
P < 0.05), whereas caprylate and solvent had no
effect. The area under the insulin response curve to the IVGTT was
larger in the oleate-treated group than in the caprylate and solvent
groups (area = 220 ± 35 vs. 112 ± 13 and 106 ± 8, respectively, P < 0.05). The area under the glucose
response curves was comparable [area = 121 ± 13 (oleate) vs. 135 ± 20 (caprylate) and 96 ± 11 (solvent)]. The
results are consistent with the concept that increased portal free
fatty acid is involved in the induction of visceral obesity-related
insulin resistance via activation of the HPA axis and sympathetic system.
insulin resistance; hypothalamus-pituitary-adrenal axis; sympathetic activity; visceral obesity
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