Kristensen K, Pedersen S B, Fisker S, Nørrelund H, Rosenfalck A M, Jørgensen J O, Richelsen B
Department of Endocrinology and Metabolism, Aarhus University Hospital, Aarhus Amtssygehus, Denmark.
Metabolism. 1998 Dec;47(12):1514-9. doi: 10.1016/s0026-0495(98)90079-8.
Growth hormone (GH) treatment is associated with a reduction in fat mass in healthy and GH-deficient (GHD) subjects. This is mainly mediated via a direct GH action on adipose cells and stimulation of lipolysis. Leptin is secreted from adipose tissue and may be involved in signaling information about adipose tissue stores to the brain. Hormonal regulation of leptin is still not fully elucidated, and in the present study, we investigated both the long-term (4-month) and short-term (28-hour) GH effects on serum leptin and leptin gene expression in subcutaneous adipose tissue. In GHD adults (n = 24), leptin correlated with most estimates of adiposity (r = .62 to .86), as previously found in healthy subjects. However, no correlation was observed with intraabdominal fat determined by computed tomographic (CT) scan (INTRA-CT). GH treatment for 4 months had no independent effect on either serum leptin or leptin gene expression. In a short-term study, we found that fasting gradually reduced leptin levels in both healthy men and GHD adults, with a maximum reduction of 58% to 60% (P < .01) after 31 hours. No independent effect of GH suppression or GH substitution on serum leptin was found during fasting. Adipose tissue leptin mRNA correlated with serum leptin (r = .51, P < .01) and the body mass index ([BMI] r = .55, P < .05). Serum leptin levels and gene expression were significantly higher in women compared with men (26.6 +/- 5.8 v 10.0 +/- 1.30 ng/mL, P < .05). However, in regression analysis accounting for the gender differences in subcutaneous femoral adipose tissue (FEM-CT), the difference in serum leptin disappeared, indicating that subcutaneous femoral fat or factors closely related to femoral fat (eg, sex hormones) may be causal factors for the gender difference in leptin.
生长激素(GH)治疗与健康受试者及生长激素缺乏(GHD)受试者的脂肪量减少有关。这主要是通过生长激素对脂肪细胞的直接作用以及刺激脂肪分解来介导的。瘦素由脂肪组织分泌,可能参与将有关脂肪组织储存的信息传递至大脑。瘦素的激素调节仍未完全阐明,在本研究中,我们调查了生长激素对皮下脂肪组织中血清瘦素和瘦素基因表达的长期(4个月)和短期(28小时)影响。在GHD成年患者(n = 24)中,瘦素与大多数肥胖指标相关(r = 0.62至0.86),这与先前在健康受试者中发现的情况一致。然而,通过计算机断层扫描(CT)扫描测定的腹内脂肪(INTRA-CT)与瘦素无相关性。4个月的生长激素治疗对血清瘦素或瘦素基因表达均无独立影响。在一项短期研究中,我们发现禁食会使健康男性和GHD成年患者的瘦素水平逐渐降低,31小时后最大降幅为58%至60%(P < 0.01)。禁食期间未发现生长激素抑制或生长激素替代对血清瘦素有独立影响。脂肪组织瘦素mRNA与血清瘦素相关(r = 0.51,P < 0.01),与体重指数([BMI] r = 0.55,P < 0.05)相关。女性的血清瘦素水平和基因表达显著高于男性(26.6 ± 5.8对10.0 ± 1.30 ng/mL,P < 0.05)。然而,在考虑了股部皮下脂肪组织(FEM-CT)性别差异的回归分析中,血清瘦素的差异消失了,这表明股部皮下脂肪或与股部脂肪密切相关的因素(如性激素)可能是瘦素性别差异的因果因素。