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Endocrine Abstracts (2016) 41 GP122 | DOI: 10.1530/endoabs.41.GP122

1Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; 2Center of Excellence High-Field MR, Department of Radiodiagnostics, Medical University of Vienna, Vienna, Austria; 3Department of Neurosurgery, Medical University of Vienna, Vienna, Austria.

We have recently shown that patients with growth hormone (GH) excess (acromegaly) exhibit inadequately low intrahepatic lipid content (IHL) despite marked insulin resistance. GH might increase mitochondrial oxidation capacity thereby counteracting ectopic lipid accumulation; however, up-regulation of mitochondrial function has been reported in early stages of non-alcoholic fatty liver disease. Up to now, data on mitochondrial activity in patients with acromegaly are missing.

Patient population and methods: Magnetic resonance spectroscopy (MRS) for determination of ATP synthesis (k) by the saturation transfer technique and IHL by 1H-MRS was performed in four patients with active acromegaly (AKRO; two newly diagnosed, two uncontrolled after surgery, 43±3 years, BMI: 31±3 kg/m2, IGF1: 715±128 ng/ml) and five healthy controls matched for age and BMI (CON: 37±2 years, BMI: 31±2 kg/m2).

Results: As expected, IHL was markedly lower in AKRO compared to CON (0.7±0.3 vs 4.6±.3%, P=0.05). In contrast to our initial hypothesis, mitochondrial function was lower in AKRO (ATP synthesis (k): 0.21±0.02 vs 0.33±0.02 1/s, P=0.003). In the whole group, IHL was tightly correlated with K (R=0.78, P=0.014).

Discussion: Consistent with the suggestion that mitochondrial function of the liver adapts to the prevailing lipid load, ATP synthesis was lower in patients with active acromegaly and also low hepatic lipid content was observed in acromegaly compared to matched controls. In contrast to short-term animal studies, GH excess does not up-regulate hepatic energy metabolism in patients with GH-excess.

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