Abstract

Hypopituitarism is associated with hyperlipidemia, the mechanisms of which are not fully known. One possible mechanism is an increased hepatic secretion of very—low-density lipoprotein (VLDL) apolipoprotein B100 (apo B100). To investigate this, 13 hypopituitary patients (seven women and six men; age, 46 ± 3 years [mean ± SEM]; body mass index [BMI], 29 ± 2 kg/m 2) and 13 matched controls (seven women and six men; age, 43 ± 3 years; BMI, 28 ± 2 kg/m 2) were investigated in a stable-isotope study. [1- 13C]leucine (1 mg/kg body weight) was administered, followed by a continuous 6-hour infusion of [1- 13C]leucine (at a rate of 1 mg/kg/h). Patients had a similar fractional secretion rate (FSR) of VLDL apo B100 versus controls (0.37 ± 0.05 v 0.38 ± 0.06 pools/h, respectively), but they had a significantly larger pool size (3.4 ± 0.3 v 1.9 ± 0.3 mg/kg) and higher absolute secretion rate ([ASR] 27.8 ± 2.9 v 16.0 ± 2.5 mg/kg/d). The increase in hepatic VLDL production may explain the lipid abnormalities found in hypopituitarism. Fasting circulating nonesterified fatty acids (NEFAs) were decreased in the patients (284 ± 26 v 664 ± 92 μmol/L, P < .001) despite the increase in VLDL secretion. An inverse relationship was observed between the NEFA level and VLDL apo B100 FSR in the patients ( r s = − .85, P < .005).

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