Ym. Song et al., Methylprednisolone increases plasma leptin levels in Graves' hyperthyroidism patients with active Graves' ophthalmopathy, HORMONE MET, 32(7), 2000, pp. 277-282
Whether leptin, a product of the ob gene, can be stimulated by glucocortico
id administration has been an issue of controversy. We investigated the eff
ect of intravenous administration of methylprednisolone (500 mg/day x 3 day
s) on plasma levels of leptin in 16 patients (female/male = 11/5) with Grav
es' hyperthyroidism and active ophthalmopathy who received pulse therapy. S
ignificant elevation of plasma leptin levels started at the eighth hour (13
.9 +/- 1.8 ng/mL, p = 0.042) and lasted until the 72nd hour (21.2 +/- 5.0 n
g/mL, p = 0.009), as compared with basal levels (8.8 +/- 1.2 ng/mL). When m
ethylprednisolone was replaced with oral prednisolone (10 mg three times pe
r day x 2 weeks), no difference in plasma leptin levels was noted compared
with basal measurement. Under methylprednisolone administration, a signific
ant suppression of tumor necrosis factor-oc began at the 24th hour (8.1 +/-
1.3 pg/mL, p = 0.004) and lasted until the 48th hour (8.1 +/- 1.0 pg/mL, p
= 0.008), as compared with basal measurement (121.5 +/- 1.5 pg/mL). Compar
ed with basal levels (93 +/- 2 mg/dL), significant elevation in the plasma
glucose level started at the third hour (135 +/- 10 mg/dL, p = 0.000) and l
asted until the 72nd hour (110 +/- 4 mg/dL, p = 0.019). The timing of serum
insulin elevation approximated that of plasma glucose (3 hours: 14 +/- 3 m
u U/mL, p = 0.006) and lasted until the end of prednisolone administration
(2 weeks: 12 +/- 2 mu U/mL, p = 0.044), when compared with basal levels (14
+/- 3 mu U/mL). We concluded that the parental administration of pharmacol
ogical doses of methylprednisolone to patients with Graves' hyperthyroidism
could acutely raise their plasma level of leptin.