目的 觀測(cè)長(zhǎng)效生長(zhǎng)激素聚乙二醇化重組人生長(zhǎng)激素（PEG-rhGH）是否引起胰島素抵抗及其與短效生長(zhǎng)激素注射用重組人生長(zhǎng)激素（rhGH）的差異。方法 3周齡SD雄性幼鼠106只，隨機(jī)取88只進(jìn)行去垂體手術(shù)造模，取成模的幼鼠54只分為模型組、rhGH組、PEG-rhGH組，另18只假手術(shù)組為對(duì)照組。分別給予生理鹽水（0.25 mg·kg^-1·d^-1）、rhGH（0.25 mg·kg^-1·d^-1）、PEG-rhGH（1.4 mg·kg^-1·周^-1）處理。4周后進(jìn)行糖耐量實(shí)驗(yàn)和胰島素釋放試驗(yàn)，計(jì)算胰島素曲線面積與葡萄糖曲線面積比值，胰島素穩(wěn)態(tài)模型（HOMA-IR）；檢測(cè)血清生長(zhǎng)抑素水平；免疫組織化學(xué)法檢測(cè)胰島胰島素（INS）、胰高血糖素（GLU）、生長(zhǎng)抑素（SS）、胰多肽（PP）。結(jié)果 PEG-rhGH組HOMA-IR較對(duì)照組、模型組低（P<0.05），與rhGH組比較無(wú)差異。AUCI/AUCG值組間比較顯示PEG-rhGH組高于rhGH組，但無(wú)統(tǒng)計(jì)學(xué)差異。PEG-rhGH組GLU蛋白表達(dá)與模型組表達(dá)無(wú)差異。PEG-rhGH組INS表達(dá)較模型組表達(dá)上升（P<0.05）。PEG-rhGH組SS、PP表達(dá)與rhGH無(wú)差異。血清SS各組間均無(wú)明顯差異。結(jié)論 未觀察到PEG-rhGH引起去垂體大鼠胰島素抵抗和胰島β細(xì)胞分泌能力下降，對(duì)胰島分泌蛋白的表達(dá)無(wú)明顯影響。

Objective To observe whether the long-acting growth hormone polyethylene glycol recombinant human growth hormone (PEG-rhGH) causing insulin resistance or not, and the differences with the short-acting growth hormone recombinant human growth hormone (rhGH). Methods Sprague-Dawley young rats (106 rats) weighing 60 — 80 g were underwent hypophysectomy via parapharyngeal approach, and 18 rats with Sham operation were selected into the control group. Fifty-four qualified rats were randomly divided into the model, rhGH, and PEG-rhGH groups after two weeks, which were administered with saline (0.25 mg·kg^-1·d^-1), rhGH (0.25 mg·kg^-1·d^-1), and PEG-rhGH (1.4 mg·kg^-1·week^-1), respectively. After treatment for 4 weeks, glucose tolerance test and insulin release test were performed to calculate area under the curve insulin (AUCI), area under the curve glucose (AUCG), and homeostasis model assessment (HOMA-IR). Serum somatostatin (SS) levels were determined. Immunohistochemistry displayed the insulin (INS), glucagon (GLU), SS, and pancreatic polypeptide (PP). Results Glucose tolerance test and insulin release test indicated that HOMA-IR in PEG-rhGH group declined compared with those in the control and model groups (P< 0.05), and there were no difference between rhGH and PEG-rhGH groups. The value of AUCI/AUCG in PEG-rhGH group was higher than that of rhGH group without significant difference. Protein expression of GLU indicated no difference among PEG-rhGH, control, and model groups. The INS expression in PEG-rhGH group increased compared with the control group (P<0.05). SS and PP expression in PEG-rhGH group had no difference compared with that in rhGH group, and there was no significant difference of SS in serum among each group. Conclusion Insulin resistance and decreased islet β cell secretory capacity are not observed, and no significant effects of PEG-rhGH on secretion function of pancreas islet in hypophysectomized rats are observed.