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Departments of 1 Medicine and 2 Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642
To determine the
effect of physiological hyperinsulinemia on renal and hepatic substrate
metabolism, we assessed systemic and renal glucose release and uptake,
systemic and renal gluconeogenesis from glutamine, and certain aspects
of systemic and renal glutamine and free fatty acid (FFA) metabolism.
These were assessed under basal postabsorptive conditions and during
4-h hyperinsulinemic euglycemic clamp experiments in nine normal
volunteers using a combination of isotopic techniques and renal balance
measurements. Hepatic glucose release (HGR) and glutamine
gluconeogenesis were calculated as the difference between systemic and
renal measurements. Infusion of insulin suppressed systemic glucose
release and glutamine gluconeogenesis by ~50% during the last hour
of the insulin infusion (P < 0.001).
Renal glucose release and glutamine gluconeogenesis decreased from 2.3 ± 0.4 to 0.9 ± 0.2 (P < 0.002) and from 0.52 ± 0.07 to 0.14 ± 0.03 µmol · kg
1 · min1
(P < 0.001), respectively. HGR and
glutamine gluconeogenesis decreased from 8.7 ± 0.4 to 4.5 ± 0.5 (P < 0.001) and from 0.35 ± 0.02 to 0.27 ± 0.03 µmol · kg1 · min1
(P < 0.002), respectively. Renal
glucose uptake (RGU) increased from 1.61 ± 0.19 to 2.18 ± 0.25 µmol · kg1 · min1
(P = 0.029) but accounted
for only ~5% of systemic glucose disposal (40.6 ± 4.3 µmol · kg1 · min1).
Both systemic and renal FFA clearance increased approximately fourfold
(P < 0.001 for both). Nevertheless,
renal FFA uptake decreased (P = 0.024)
and was inversely correlated with RGU
(r = 
0.582,
P = 0.011). Finally, insulin increased
systemic glutamine release (P = 0.007), uptake (P < 0.005), and
clearance (P < 0.001) but left renal
glutamine uptake and release unaffected
(P > 0.4 for both).
liver; gluconeogenesis; free fatty acids
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