Insulin Responsiveness of Adipose Tissue Lipoprotein Lipase Is Delayed but Preserved in Obesity*

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Abstract
Because increases in adipose tissue lipoprotein lipase (ATLPL) may be important in the pathogenesis of obesity, the response of ATLPL to insulin during maintenance of euglycemia was examined in 22 obese and 8 normal weight subjects. Basal levels of ATLPL per g fat tissue for the obese and control groups were 18.7 ± 2.0 (±SEM) and 9.6 ± 2.7 neq/g · min, respectively. Insulin and glucose infusion rapidly produced antilipolysis in both groups, as evidenced by large falls in FFA by 20 min. When the responses of ATLPL in absolute change from basal were compared between the obese and control groups, no significant differences were found. However, because of the higher baseline ATLPL values in the obese subjects, the percent change in ATLPL from basal was significantly blunted at the 80 (P = 0.02), 180 (P < 0.05), and 360 (P = 0.005) min timepoints compared to those in the normal subjects. By 3 h into the infusion, the control group had a significant rise in ATLPL above the basal level (4.2 ± 1.3 neq/g · min; P = 0.01), whereas the obese group did not (2.3 ± 1.9 neq/g · min; P = NS). However, by 6 h, the ATLPL per g response above baseline was significantly increased in both normal (19.2 ± 6.5 neq/g · min; P = 0.01) and obese subjects (9.8 ± 2.3; P < 0.001). Because adipose cell size was greater in obese subjects, data were also expressed per 106 cells. Basal ATLPL per 106 cells [11.8 ± 1.7 neq/106 cells min (obese); 3.4 ± 0.9 neq/106 cells min (normal)] was a function of cell size (r8 = 0.713; P < 0.001), body mass index (r8, = 0.565; P < 0.005), and basal insulin levels (r8 = 0.434; P < 0.05). As with the ATLPL per g response, the increases in ATLPL per 106 cells above basal were significant at both the 3 and 6 h marks for the noraml subjects, but only at the 6 h timepoint for the obese group. Both steady state insulin levels [342 ± 24 μ/ml (obese); 251 ± 27 μ/ml (normal)] and the glucose infusion rates needed to maintain euglycemia [319 ± 23 mg/m2 · min (obese); 312 ± 33 mg/m2 · min (normal)] did not correlate with changes in ATLPL. Thus, insulin responsiveness of ATLPL in obese subjects was delayed but preserved. This phenomenon may be important in maintenance of the obese state.

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