Table 1.
HCR | LCR | 2-way ANOVA statistics | |||
---|---|---|---|---|---|
SED | EX | SED | EX | ||
Perigonadal fat depot mass (g) |
6.71 ± 1.22 |
9.72 ± 1.75 |
14.11 ± 1.33 |
8.61 ± 1.38 |
Line, P=0.042 Line × Treatment, P=0.008 |
Perirenal fat depot mass (g) |
3.38 ± 0.33 |
5.95 ± 1.19 |
9.70 ± 0.80 |
4.18 ± 0.81 |
Line, P=0.015 Line × Treatment, P<0.001 |
Omental fat depot mass (g) |
0.38 ± 0.04 |
0.79 ± 0.12 |
0.75 ± 0.12 |
0.48 ± 0.09 |
Line, P=0.002 Line × Treatment, P=0.003 |
BAT/WAT (g·g−1) |
0.030 ± 0.003 |
0.025 ± 0.004 |
0.015 ± 0.001 |
0.027 ± 0.006 |
NS |
Liver (g) | 6.67 ± 0.54 |
8.42 ± 0.53 |
6.71 ± 0.23 |
6.42 ± 0.14 |
Line, P=0.03 Line × Treatment, P=0.023 |
TG (mg·dl−1) |
32.71 ± 5.29 |
36.00 ± 6.33 |
52.00 ± 4.78 |
34.57 ± 1.90 |
Line × Treatment, P=0.037 |
NEFA (mmol·l−1) |
0.31 ± 0.05 |
0.42 ± 0.07 |
0.45 ± 0.05 |
0.27 ± 0.05 |
Line × Treatment, P=0.022 |
HDL (mg·dl−1) |
24.43 ± 1.34 |
29.00 ± 1.08 |
30.35 ± 1.31 |
29.85 ± 1.24 |
Line, P=0.026 Line × Treatment, P=0.046 |
LDL (mg·dl−1) |
2.28 ± 0.18 |
1.50 ± 0.18 |
3.21 ± 0.26 |
2.85 ± 0.24 |
Line, P<0.001 Treatment, P=0.029 |
Insulin (pg·ml−1) |
2.02 ± 0.49 |
2.95 ± 0.60 |
4.05 ± 0.76 |
2.87 ± 0.41 |
Line, P=0.067 (NS) |
Glucose (mg·dl−1) |
153.8 ± 4.9 |
166.12 ± 5.6 |
160.1 ± 7.7 |
149.0 ± 2.8 |
Line × Treatment, P=0.041 |
HOMA-IR index |
14.31 ± 4.07 |
22.40 ± 4.80 |
30.11 ± 6.13 |
19.18 ± 2.76 |
Line × Treatment, P=0.041 |
Adipocyte-IR index |
0.714 ± 0.27 |
1.185 ± 0.41 |
1.820 ± 0.46 |
0.727 ± 0.16 |
Line × Treatment, P=0.037 |
Body composition and metabolic markers were analyzed. Two-way ANOVA for line (i.e., HCR vs. LCR), treatment (i.e., SED vs. EX) and line × treatment interaction effects were determined; values are means ± SE (n=7–8 per group). BAT= brown adipose tissue; WAT = white adipose tissue; TG= triglycerides; NEFA = non-esterified fatty acids; HDL= high-density lipoprotein; LDL=low-density lipoprotein; HOMA-IR = homeostasis model assessment of insulin resistance.