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Abstract
Growth hormone replacement therapy (GHRT) increases exercise capacity and insulin resistance while it decreases fat mass in growth hormone-deficient patients (GHD). Ectopic lipids (intramyocellular (IMCL) and intrahepatocellular lipids (IHCL) are related to insulin resistance. The effect of GHRT on ectopic lipids is unknown. It is hypothesized that exercise-induced utilization of ectopic lipids is significantly decreased in GHD patients and normalized by GHRT. GHD (4 females, 6 males) and age/gender/waist-matched control subjects (CS) were studied. VO2max was assessed on a treadmill and insulin sensitivity determined by a two-step hyperinsulinaemic-euglycaemic clamp. Visceral (VAT) and subcutaneous (SAT) fat were quantified by MR-imaging. IHCL and IMCL were measured before and after a 2 h exercise at 50–60% of VO2max using MR-spectroscopy (∆IMCL, ∆IHCL). Identical investigations were performed after 6 months of GHRT. VO2max was similar in GHD and CS and significantly increased after GHRT; GHRT significantly decreased SAT and VAT. 2 h-exercise resulted in a decrease in IMCL (significant in CS and GHRT) and a significant increase in IHCL in CS and GHD pre and post GHRT. GHRT didn’t significantly impact on ∆IMCL and ∆IHCL. We conclude that aerobic exercise affects ectopic lipids in patients and controls. GHRT increases exercise capacity without influencing ectopic lipids.
Highlights
Growth hormone replacement therapy (GHRT) increases exercise capacity and insulin resistance while it decreases fat mass in growth hormone-deficient patients (GHD)
As a measure of hepatic insulin sensitivity we show the percentage of suppression of endogenous glucose production (EGP) in the steady state of the first clamp step compared with the baseline value
insulin-like growth factor 1 (IGF-1) concentrations were significantly lower in growth hormone deficiency (GHD) patients compared to control subjects (CS)
Summary
Growth hormone replacement therapy (GHRT) increases exercise capacity and insulin resistance while it decreases fat mass in growth hormone-deficient patients (GHD). An acute aerobic 2 h physical exercise at 50% VO2max has been shown to decrease IMCL and intramyocardiocellular lipids (ICCL) and increase IHCL in healthy physically active subjects[3,4]. IMCL appear to be flexible energy stores in physically active healthy subjects[7,8] whereas sedentary (overweight) subjects tend to have high IMCL (like athletes, called the athletic paradox), but are less capable to deplete these stores during physical exercise[8] Based on these observations it is hypothesized that exercise-induced changes in ectopic fat depots are related to a) insulin sensitivity, b) fat mass (i.e. visceral and subcutaneous adipose tissue, VAT and SAT) and c) exercise capacity. An important confounding factor that influences insulin sensitivity[12] and potentially ectopic lipids, is avoided
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