Table 4. Univariate non-parametric regression of ∆IMCL and ∆IHCL with fat mass (subcutaneous adipose tissue and visceral adipose tissue), insulin sensitivity and exercise capacity (VO2max) in patients with GHD and CS subjects.
| Correlationcoefficient | p-values | Correlationcoefficient | p-values | |
|---|---|---|---|---|
| vs. ∆IMCL | vs. ∆IHCL | |||
| Fat mass | ||||
| Subcutaneous adipose tissue | 0.02 | 0.93(n = 17) | 0.18 | 0.27(n = 20) |
| Visceral adipose tissue | 0.15 | 0.41(n = 17) | 0.44 | 0.005(n = 20) |
| Insulin sensitivity | ||||
| Supp. EGP(low insulin dose) | 0.20 | 0.28(n = 16) | −0.24 | 0.15(n = 19) |
| M-value(high insulin dose) | 0.15 | 0.42(n = 16) | −0.37 | 0.03(n = 19) |
| Exercise parameters | ||||
| VO2max | 0.03 | 0.87(n = 17) | 0.20 | 0.22(n = 20) |
Correlation analysis (Kendall’s tau) was performed with data of patients with GHD and CS together.
Suppression EGP = suppression of endogenous glucose production = measure of hepatic insulin resistance; M-value = glucose infusion at high insulin dose = measure of peripheral insulin resistance; ∆IMCL/∆IHCL = 2 h-aerobic exercise induced changes of IMCL/IHCL.
The shaded boxes show positive correlations between fat availability and ΔIHCL, in particular for visceral fat; and negative correlations between insulin sensitivity and ΔIHCL. In contrast, the correlations with ΔIMCL are either very weak or positive.