Low myocardial glucose uptake in T urner syndrome is unaffected by growth hormone: a randomized, placebo‐controlled FDG ‐ PET study

Summary Background An unfavourable cardiovascular and metabolic phenotype causes threefold excess mortality in Turner syndrome ( TS ), and perturbed cardiac substrate metabolism is increasingly recognized as a common component of cardiovascular and metabolic diseases. We therefore hypothesized that myocardial glucose uptake ( MGU ) is reduced in TS and that growth hormone ( GH ) treatment improves MGU . To this end, this controlled trial elucidates MGU in TS and the impact of 6 months of growth hormone treatment on MGU . Methods and Results Women with TS ( n  = 9) were examined at baseline, sequentially treated with either Norditropin ® SimpleXx or placebo and re‐examined after 6 months. MGU and myocardial blood flow ( MBF ) were measured using 2‐deoxy‐2‐[18F]fluoro‐D‐glucose positron emission tomography ( FDG ‐ PET ) during a hyperinsulinaemic euglycaemic clamp (at baseline and 6 months). Blood pressure measurement, blood sampling, echocardiography and dual energy X‐ray absorptiometry scan were also performed. Age‐matched female controls ( n  = 9) were examined once. Baseline MGU was reduced in TS (0·24 ± 0·08 vs. 0·36 ± 0·13 μmol/g/min in controls; P  = 0·036) despite similar insulin sensitivity (whole body glucose uptake (M‐value): 9·69 ± 1·86 vs. 9·86 ± 2·58 mg/(min*kg) in controls; P  = 0·9). Six months of GH carried no impact on MGU (0·25 ± 0·08 vs. 0·26 ± 0·12 μmol/g/min in the placebo group; P  = 0·8). Plasma glucose, low‐density cholesterol and triglycerides increased, while M‐value and exercise capacity decreased during 6 months of GH treatment. Conclusion MGU is reduced in TS despite normal insulin sensitivity. GH treatment does not alter MGU despite decreased whole body insulin sensitivity. A perturbed cardiac glucose uptake appears to be a feature of TS .