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-cell function contributes to impaired glucose
tolerance in dogs made obese by high-fat feeding
1 Department of Psychology and 2 Department of Medicine, University of Washington School of Medicine, Seattle 98195; and Veterans Affairs Puget Sound Health Care System, Seattle, Washington 98108, and 3 Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio 45267
The ability to
increase 
-cell function in the face of reduced insulin sensitivity
is essential for normal glucose tolerance. Because high-fat feeding
reduces both insulin sensitivity and glucose tolerance, we hypothesized
that it also reduces -cell compensation. To test this hypothesis, we
used intravenous glucose tolerance testing with minimal model analysis
to measure glucose tolerance
(Kg), insulin
sensitivity (SI), and the acute
insulin response to glucose
(AIRg) in nine dogs fed a chow
diet and again after 7 wk of high-fat feeding. Additionally, we
measured the effect of consuming each diet on 24-h profiles of insulin
and glucose. After high-fat feeding,
SI decreased by 57%
(P = 0.003) but
AIRg was unchanged. This absence
of -cell compensation to insulin resistance contributed to a 41%
reduction of Kg
(P = 0.003) and abolished the normal
hyperbolic relationship between
AIRg and
SI observed at baseline. High-fat
feeding also elicited a 44% lower 24-h insulin level
(P = 0.004) in association with an 8%
reduction of glucose (P = 0.0003). We
conclude that high-fat feeding causes insulin resistance that is not
compensated for by increased insulin secretion and that this
contributes to the development of glucose intolerance. These effects of
high-fat feeding may be especially deleterious to individuals
predisposed to type 2 diabetes mellitus.
glucose tolerance; glucose effectiveness; insulin secretion; diabetes; obesity
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