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• W2022249257 abstract "Raised levels of free fatty acids (FFA) compete with glucose for utilization by insulin-sensitive tissues, and, therefore, they may induce insulin resistance in the normal subject. The influence of experimental elevations in FFA levels on glucose metabolism in native insulin-resistant states is not known. We studied seven women with moderate obesity (63% above their ideal body weight) but normal glucose tolerance with the use of the insulin clamp technique with or without an infusion of Intralipid + heparin. Upon raising plasma insulin levels to ∼60 μU/mL while maintaining euglycemia, whole body glucose utilization (3H-3-glucose) rose similarly without (from 66 ± 7 to 113 ± 11 mg/min m2, P < .02) or with (from 70 ± 7 to 137 ± 19 mg/min m2, P < .02) concomitant lipid infusion. In contrast, endogenous glucose production was considerably (73%) suppressed (from 66 ± 7 to 15 ± 8 mg/min m2, P < .001) during the clamp without lipid, but declined only marginally (from 70 ± 7 to 48 ± 7 mg/min m2, NS) with lipid administration. The difference between the control and the lipid study was highly significant (P < .02), and amounted to an average of 3.8 g of relative glucose overproduction during the second hour of the clamp. Blood levels of lactate rose by 34 ± 15% (.1 >P > .05) in the control study but only by 17 ± 10% (NS) during lipid infusion. Blood pyruvate concentrations fell in both sets of experiments (by ∼45% at the end of the study) with similar time courses. In contrast, blood alanine levels did not change from baseline during the control clamp (181 ± 18 v 185 ± 14 μmol/L) whereas they fell slightly (11 ± 3%) but consistently (175 ± 15 v 196 ± 14 μmol/L, P < .02) during lipid infusion. Furthermore, a positive correlation was found to exist in the pooled data between the decrease in blood alanine concentrations and the corresponding increase in endogenous glucose production (r = .59, P < .02). We conclude that in the obese subject an increased supply of fatty fuels fails to inhibit insulin-mediated glucose disposal but induces hepatic insulin resistance. The greater availability of exogenous glucose precursors (glycerol) and the lower circulating levels of endogenous precursors (lactate and alanine) suggest that the observed increase in endogenous glucose production is sustained by hepatic gluconeogenesis." @default.
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• W2022249257 date "1987-05-01" @default.
• W2022249257 modified "2023-10-17" @default.
• W2022249257 title "Acute elevation of free fatty acid levels leads to hepatic insulin resistance in obese subjects" @default.
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• W2022249257 doi "https://doi.org/10.1016/0026-0495(87)90051-5" @default.
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