Endocrine Abstracts

Background: Insulin resistance as part of the metabolic syndrome is associated with ectopic lipid deposition. Growth hormone (GH) status also modulates ectopic lipid accumulation but how this associates with insulin resistance in patients with GH disorders is not well established.

Aim: To study body composition, ectopic lipid deposition and insulin sensitivity in acromegaly and adult GH-deficiency before and after treatment.

Subjects and Methods: Twenty-one patients newly diagnosed with acromegaly and twelve patients with adult GH deficiency (GHD) were studied at diagnosis and after treatment. A reference group of twelve subjects was studied on a single occasion. Each study day comprised assessment of body composition with dual-energy X-ray absorptiometry, ectopic lipid deposition in the liver and skeletal muscle by MR spectroscopy, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR).

Results: Disease control of acromegaly decreased lean body mass (LBM) (P< 0.000) and increased the percentage of total body fat (TBF) (P< 0.000). GH replacement increased LBM in the GHD patients (P=0.007) and decreased the percentage of TBF (P=0.010). The intrahepatic lipid content (IHL) increased after disease control in acromegaly (P=0.004) to levels resembling a reference group (P=0.28), whereas IHL did not change significantly after GH replacement in GHD (P=0.34). Insulin resistance (HOMA-IR) improved after disease control of acromegaly (P<0.000) and remained unaltered after GH replacement in the GHD patients (P=0.829). IHL and HOMA-IR correlated positively in the reference group (r=0.75, P=0.005) and in GHD patients before (r=061, P=0.038) and after (r=0.66, P=0.020) GH replacement, whereas in acromegaly the correlation only manifested after disease control (r=0.52, P=0.038).

Conclsions: 1) GH status is a significant modulator of body composition and insulin sensitivity.

2) GH excess reduces total fat mass and intrahepatic lipid content together with induction of insulin resistance.

The data support the notion that GH-induced insulin resistance is unassociated with hepatic lipid accumulation.