Barber Thomas M, Casanueva Felipe F, Karpe Fredrik, Lage Mary, Franks Stephen, McCarthy Mark I, Wass John A H
Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Old Road, Headington, Oxford OX3 7LJ, UK.
Eur J Endocrinol. 2008 Apr;158(4):511-6. doi: 10.1530/EJE-07-0683.
Abnormal ghrelin regulation may influence the development of obesity-associated conditions including polycystic ovary syndrome (PCOS). Our aim was to compare ghrelin regulation between PCOS cases and controls.
We compared serum ghrelin (total) levels, fasting and 30-min post-oral (75 g) glucose load, between 50 PCOS cases and 28 female controls, including 22 body mass index (BMI)/fat mass-matched pairs. All subjects were of UK British/Irish origin.
Measurements included serum ghrelin (RIA technique (LINCO Research, St Charles MO, USA)), fat mass, serum testosterone, fasting serum insulin and plasma glucose levels. Insulin sensitivity was calculated as the homeostasis model assessment of insulin resistance (HOMA2 IR).
Fasting serum ghrelin levels were significantly lower in PCOS cases versus BMI/fat mass-matched controls (geometric mean (s.d. range), 1104 pg/ml (764-1595) vs 1756 pg/ml (1314-2347) respectively; P=2.3 x 10(-4)). Ghrelin suppression following oral glucose load was significantly blunted in PCOS cases versus BMI/fat mass-matched controls (geometric mean ghrelin suppression (s.d. range), 160 pg/ml (88-289) vs 424 pg/ml (220-818) respectively; P=2.0 x 10(-4)). Whole-group comparisons (50 PCOS cases versus 28 controls) adjusted for fat mass and age revealed similar results. In PCOS cases, there was a significant negative correlation between fasting serum ghrelin and HOMA2 IR (r(2)=-0.40, P=5.7 x 10(-3)). Following adjustment for HOMA2 IR, fat mass and age, comparisons between the whole groups of PCOS cases and controls revealed attenuated but significant differences in fasting serum ghrelin (P=1.3 x 10(-3)) and ghrelin suppression (P=1.8 x 10(-3)).
In women with PCOS, serum ghrelin levels are suppressed, showing a negative relationship with HOMA2 IR and a blunted response to oral glucose.
胃饥饿素调节异常可能会影响肥胖相关疾病的发展，包括多囊卵巢综合征（PCOS）。我们的目的是比较PCOS患者与对照组之间的胃饥饿素调节情况。
我们比较了50例PCOS患者和28名女性对照者（包括22对体重指数（BMI）/脂肪量匹配的配对）的血清胃饥饿素（总量）水平、空腹及口服（75g）葡萄糖负荷后30分钟的水平。所有受试者均为英国/爱尔兰裔。
测量指标包括血清胃饥饿素（放射免疫分析技术（美国密苏里州圣查尔斯的LINCO Research公司））、脂肪量、血清睾酮、空腹血清胰岛素和血浆葡萄糖水平。胰岛素敏感性通过胰岛素抵抗稳态模型评估（HOMA2 IR）计算得出。
与BMI/脂肪量匹配的对照组相比，PCOS患者的空腹血清胃饥饿素水平显著降低（几何平均数（标准差范围）分别为1104 pg/ml（764 - 1595）和1756 pg/ml（1314 - 2347）；P = 2.3×10⁻⁴）。与BMI/脂肪量匹配的对照组相比，PCOS患者口服葡萄糖负荷后胃饥饿素的抑制作用明显减弱（胃饥饿素抑制的几何平均数（标准差范围）分别为160 pg/ml（88 - 289）和424 pg/ml（220 - 818）；P = 2.0×10⁻⁴）。对脂肪量和年龄进行校正后的全组比较（50例PCOS患者与28例对照者）显示了相似的结果。在PCOS患者中，空腹血清胃饥饿素与HOMA2 IR之间存在显著的负相关（r² = -0.40，P = 5.7×10⁻³）。在对HOMA2 IR、脂肪量和年龄进行校正后，PCOS患者和对照组全组之间的比较显示，空腹血清胃饥饿素（P = 1.3×10⁻³）和胃饥饿素抑制（P = 1.8×10⁻³）的差异虽有所减弱但仍显著。
在PCOS女性中，血清胃饥饿素水平受到抑制，与HOMA2 IR呈负相关，且对口服葡萄糖的反应减弱。
