Isidro Maria Luisa, Nemina Rosa, Garcia-Buela Jesus, Sangiao-Alvarellos Susana, Cordido Fernando
Department of Endocrinology, Hospital Juan Canalejo La Coruna, Spain.
Neuro Endocrinol Lett. 2007 Oct;28(5):596-603.
The pathophysiology of ghrelin secretion in acromegaly is unclear. Our aim was to study circulating fasting ghrelin levels and their response to oral glucose in acromegalic patients and normal control subjects.
9 acromegalic patients (4 male, 5 female; 59.4+/-3.6 years; 28.6+/-1.0 kg/m2) and 9 age and BMI matched healthy control subjects (4 male, 5 female; 59.1+/-1.4 years; 26.5+/-0.8 kg/m2) were included. We obtained blood samples for glucose, insulin, GH, total ghrelin and acylated ghrelin at times 0, 30, 60, 90 and 120 minutes after 75 g of oral glucose.
Fasting GH and IGF-I were statistically different between patients and controls: GH (microg/l): 6.7+/-1.4 vs. 0.8+/-0.4, p<0.01; IGF-I (ng/ml): 414+/-75 vs. 86+/-6, p<0.01. Fasting total ghrelin (pg/ml) were similar in the patient and in the control group, 916+/-132 vs. 844+/-169, p=ns. In both groups total ghrelin levels decreased during oral glucose, and nadir total ghrelin was lower than fasting ghrelin: patients: 916+/-132 vs. 747+/-95, p<0.05; controls: 844+/-169 vs. 625+/-90, p<0.05). The AUCs of total ghrelin (pg/mlmin) were not different between the two groups: 98953+/-13052 vs. 83773+/-13096, p=ns). Fasting acylated ghrelin (pg/ml) were similar in the patient and the control group 65+/-13 pg/ml vs.74+/-14 pg/ml, p=ns. In both groups acylated ghrelin levels decreased during oral glucose, and nadir acylated ghrelin levels were lower than basal acylated ghrelin levels: patients: 65+/-13 vs. 42+/-6, p<0.05; controls: 74+/-14 pg/ml vs. 37+/-4 pg/ml, p<0.05). The AUCs of acylated ghrelin (pg/mlmin) were not different between the two groups: patients: 6173+/-992 vs. controls 8648+/-2742, p=ns). In acromegalic patients there was a negative correlation between fasting, both total and acylated, ghrelin and both fasting and post oral glucose insulin levels.
These data suggest that circulating total and acylated ghrelin in acromegaly is regulated by insulin and not by GH hypersecretion.
肢端肥大症患者胃饥饿素分泌的病理生理学尚不清楚。我们的目的是研究肢端肥大症患者和正常对照者空腹循环胃饥饿素水平及其对口服葡萄糖的反应。
纳入9例肢端肥大症患者(4例男性,5例女性;年龄59.4±3.6岁;体重指数28.6±1.0kg/m²)和9例年龄及体重指数匹配的健康对照者(4例男性,5例女性;年龄59.1±1.4岁;体重指数26.5±0.8kg/m²)。口服75g葡萄糖后0、30、60、90和120分钟采集血样检测葡萄糖、胰岛素、生长激素、总胃饥饿素和酰化胃饥饿素。
患者与对照者的空腹生长激素和胰岛素样生长因子-I有统计学差异:生长激素(μg/L):6.7±1.4 vs. 0.8±0.4,p<0.01;胰岛素样生长因子-I(ng/ml):414±75 vs. 86±6,p<0.01。患者组和对照组的空腹总胃饥饿素(pg/ml)相似,分别为916±132和844±169,p=无统计学意义。两组口服葡萄糖期间总胃饥饿素水平均下降,且总胃饥饿素最低点低于空腹水平:患者组:916±132 vs. 747±95,p<0.05;对照组:844±169 vs. 625±90,p<0.05)。两组总胃饥饿素的曲线下面积(pg/ml*min)无差异:98953±13052 vs. 83773±13096,p=无统计学意义)。患者组和对照组的空腹酰化胃饥饿素(pg/ml)相似,分别为65±13 pg/ml和74±14 pg/ml,p=无统计学意义。两组口服葡萄糖期间酰化胃饥饿素水平均下降,且酰化胃饥饿素最低点低于基础水平:患者组:65±13 vs. 42±6,p<