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肥胖患者生长激素对生长激素释放因子的反应受损。垂体缺陷可通过减轻体重得到逆转。

Impaired growth hormone responses to growth hormone-releasing factor in obesity. A pituitary defect reversed with weight reduction.

作者信息

Williams T, Berelowitz M, Joffe S N, Thorner M O, Rivier J, Vale W, Frohman L A

出版信息

N Engl J Med. 1984 Nov 29;311(22):1403-7. doi: 10.1056/NEJM198411293112203.

DOI:10.1056/NEJM198411293112203
PMID:6436706
Abstract

To investigate whether the impaired growth hormone secretion associated with obesity is a result of a hypothalamic or a pituitary disorder and whether it is a cause or a consequence of obesity, we studied plasma growth hormone responses to growth hormone-releasing factor in morbidly obese patients before gastrointestinal surgical therapy, in formerly obese subjects who had lost considerable weight postoperatively, and in non-obese controls. Growth hormone secretion was also assessed in response to insulin-induced hypoglycemia (in seven patients preoperatively and four postoperatively). In patients studied preoperatively, growth hormone responses to growth hormone-releasing factor were markedly impaired (P less than 0.001 as compared with controls), whereas in patients studied postoperatively they were partially restored to normal (P less than 0.05 as compared with those studied preoperatively). Growth hormone responses to insulin-induced hypoglycemia were similarly diminished in obese patients studied before operation (P less than 0.02). The growth hormone response to growth hormone-releasing factor was inversely correlated with the percentage of ideal body weight (P less than 0.01) and directly correlated with the growth hormone response to insulin (P less than 0.01). The impaired responsiveness to growth hormone-releasing factor suggests that the diminished response to insulin hypoglycemia is mediated by an impaired pituitary response to endogenous growth hormone-releasing factor. The reversibility of the defect after weight reduction suggests that it is a consequence rather than a cause of obesity.

摘要

为了研究与肥胖相关的生长激素分泌受损是下丘脑还是垂体疾病的结果,以及它是肥胖的原因还是后果,我们研究了病态肥胖患者在胃肠道手术治疗前、术后体重显著减轻的既往肥胖受试者以及非肥胖对照者对生长激素释放因子的血浆生长激素反应。还评估了对胰岛素诱导的低血糖的生长激素分泌情况(术前7例患者和术后4例患者)。术前研究的患者对生长激素释放因子的生长激素反应明显受损(与对照组相比,P<0.001),而术后研究的患者其反应部分恢复正常(与术前研究的患者相比,P<0.05)。术前研究的肥胖患者对胰岛素诱导的低血糖的生长激素反应同样减弱(P<0.02)。对生长激素释放因子的生长激素反应与理想体重百分比呈负相关(P<0.01),与对胰岛素的生长激素反应呈正相关(P<0.01)。对生长激素释放因子反应性受损表明,对胰岛素低血糖反应减弱是由垂体对内源性生长激素释放因子反应受损介导的。体重减轻后缺陷的可逆性表明它是肥胖的后果而非原因。

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