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. Author manuscript; available in PMC: 2019 Aug 22.
Published in final edited form as: Clin Genet. 2005 Mar;67(3):230–239. doi: 10.1111/j.1399-0004.2004.00392.x

Table 3.

Laboratory variables analyzed in two obese groups [23 Prader–Willi syndrome (PWS) subjects and 18 controls] stratified by degree of visceral fat area (VFA)

Obese PWS Obese control
Variables VFA ≥ 130 cm2 VFA <130 cm2 p value VFA ≥ 130 cm2 VFA < 130 cm2 p value
Fasting leptin (ng/ml) 40.7 ± 16.2 (6) 44.8 ± 21.8 (7) 0.454 38.5 ± 27.0 (5) 44.3 ± 12.6 (6) 0.688
Fasting triglycerides (mg/dl) 226.3 ± 98.1 (7) 124.5 ± 66.3 (14) 0.006a 368.3 ± 228.2 (7) 162.2 ± 73.5 (9) 0.317
Fasting total cholesterol (mg/dl) 203.1 ± 30.1 (7) 172.3 ± 35.3 (14) 0.100 188.7 ± 39.4 (7) 192.4 ± 38.6 (9) 0.363
Fasting glucose (mg/dl) 113.7 ± 24.2 (7) 82.5 ± 9.3 (15) 0.000a 125.0 ± 58.1 (7) 91.0 ± 13.7 (9) 0.144
Fasting insulin (μU/ml) 24.9 ± 9.6 (6) 9.6 ± 5.0 (12) 0.000a 21.6 ± 8.8 (7) 26.9 ± 11.4 (10) 0.671
HOMA (insulin resistance): (mg/dl × μU/ml)/405 7.35 ± 3.49 (6) 2.04 ± 1.25 (11) 0.000a 7.47 ± 6.23 (7) 6.20 ± 2.58 (9) 0.165
QUICKI (insulin sensitivity): 1/[log(I0) + log(G0)] 0.30 ± 0.03 (6) 0.36 ± 0.05 (11) 0.007a 0.30 ± 0.03 (7) 0.30 ± 0.02 (9) 0.417

VFA stratification based on published study (27).

Obesity status determined by BMI.

a

Significant p values calculated using univariate anova and adjusting for age, gender, and BMI.