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Fat Calories May be Preferentially Stored in Reduced-Obese Women: A Permissive Pathway for Resumption of the Obese State^*

Division of Endocrinology, Department of Medicine, University of Colorado Health Sciences Center Denver, Colorado 80262

Address correspondence and requests for reprints to: Robert H. Eckel, M.D., Box B-151, Division of Endocrinology, University of Colorado Health Sciences Center, Denver, Colorado 80262.

We previously demonstrated in unpaired studies that corn oil ingestion at the beginning of a euglycemic insulin clamp study decreased the responsiveness of gluteal adipose tissue lipoprotein lipase (ATLPL) to glucose/insulin in lean subjects. In this investigation, we performed paired euglycemic insulin clamp studies with glucose/insulin with or without oral corn oil in each of six lean [mean, 64 ± 3 (±SE) kg] normal women and nine moderately obese (91 ± 3 kg) women before and after 12.4 ± 1.4-kg weight loss and 3 months of weight maintenance to determine if the inhibitory effect of fat calories existed in each of these states. In the obese women the fasting ATLPL activity [5.6 ± 1.1 (±SE) neq FFA/10⁶ cells-min] was greater than in the normal women (1.6 ± 0.2) and did not change after weight loss and maintenance (5.0 ± 0.7). As expected, in normal women corn oil ingestion diminished the responsiveness of ATLPL to glucose/insulin [change (), 0.2 ± 0.2 vs. 3.3 ± 0.8; P < 0.02] during a 6-h euglycemic insulin (40 mU/m²·min) clamp. In obese women ATLPL activity did not change under either experimental condition (glucose/insulin with or without corn oil). However, after weight reduction ATLPL activity increased not only in response to glucose/insulin alone (, 7.7 ± 2.4), but also in response to glucose/insulin when corn oil was ingested (, 7.9 ± 2.8). Moreover, the response of ATLPL activity to glucose/insulin and corn oil was greater than that in lean women (P < 0.05). Thus, in reduced-obese women not only did fasting ATLPL activity remain elevated and ATLPL responsiveness to glucose/insulin increase, but fat ingestion failed to blunt the ATLPL response. This inability of dietary fat to diminish the responsiveness of ATLPL to glucose/insulin and, therefore, the effect of the lipase on triglyceride deposition in adipose tissue could contribute to the resumption of the obese state that so commonly occurs after successful weight reduction.

^* This work was supported by NIH Grant AM-26356, a grant from the Mead-Johnson Nutritional Division, and Grant RR-00051 for the General Clinical Research Center (GCRC) at the University of Colorado Health Sciences Center. Computation assistance was provided by CLINFO computer system funded under the GCRC grant.

Received December 28, 1987.

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