缺氧缺血性脑病新生儿脂联素、胰岛素样生长因子-1的变化

目的探讨缺氧缺血性脑病(HIE)新生儿血清胰岛素样生长因子-1(IGF-1)、脂联素(APN)水平的变化。方法选择足月HIE新生儿52例(重度HIE组15例,中度HIE组20例,轻度HIE组17例),测定脐血及生后3~5 d(HIE急性期)、10~14 d(HIE恢复期)的血清IGF-1、APN水平;另选同期出生的20例足月健康新生儿作为对照组。结果轻、中、重度HIE组及对照组四组间脐血及生后3~5 d时APN、IGF-1水平的差异有统计学意义(P均0.01),均随HIE程度加重而下降,两两比较差异有统计学意义(P均0.05);HIE恢复期新生儿APN、IGF-1水平显著增加,但APN水平中度HIE组和重度HIE组仍低于对照组,差异有统计学意义(P均0.05);重度HIE组IGF-1仍低于对照组,差异有统计学意义(P0.05);HIE患儿脐血、急性期血清IGF-1、APN水平呈显著正相关(r=0.53、0.61,P均0.01)。结论 HIE患儿血清IGF-1、APN水平降低与HIE的病理生理过程密切相关,可作为病情程度的判断指标之一,对临床诊断及预后的判断具有指导意义。     

中药植物多糖对2型糖尿病胰岛素抵抗的作用机制研究进展

胰岛素抵抗(insulin resistance,IR)是2型糖尿病的重要病理生理机制,对胰岛素抵抗的治疗成为防治2型糖尿病的关键。目前,防治2型糖尿病,已经从降糖为主发展到利用胰岛素抵抗为靶点的综合治疗策略。中药多糖对改善2型糖尿病胰岛素抵抗具有良好的疗效,与西药治疗糖尿病胰岛素抵抗相比,中药多糖具有安全、疗效好、价格低的优势。但对其作用机制还缺乏科学系统的归纳。本文应用计算机中国知网数据库(CNKI),检索关键词"2型糖尿病,多糖,胰岛素抵抗",纳入全部有关中药植物多糖治疗糖尿病的文献,进行分析、归纳、总结。目的对中药多糖治疗2型糖尿病胰岛素抵抗的作用机制作一简要综述,希望为今后有关中药植物多糖种类、中药剂量以及服用时间等研究提供参考依据,开发出服用更便捷,疗效更好,更安全的新制剂。     

Liquiritigenin regulates insulin sensitivity and ameliorates inflammatory responses in the nonalcoholic fatty liver by activation PI3K/AKT pathway

Nonalcoholic fatty liver disease (NAFLD) is a prevalent long-term disease in the world. Liquiritigenin (LQ) is protective against a variety of hepatotoxins. Herein, we report the potential mechanism of LQ on a high-fat diet (HFD) induced NAFLD. NAFLD mice model was established by HFD for 12 weeks, and LQ treatment for 1 week. Commercially available assay kits measure liver triglycerides (TG) and total cholesterol (TC) levels. Plasm TC, TG, high-density-lipoprotein (HDL-C), and low-density-lipoprotein cholesterol (LDL-C) levels were also monitored by biochemistry. Enzyme linked immunosorbent assay (ELISA) kits were performed to analyze the pro-inflammatory factors, and intraperitoneal glucose tolerance test (IPGTT), insulin tolerance test (IPITT), and serum insulin were also determined. GO and KEGG pathway enrichment analysis was employed to analyze the overlapping genes of LQ targets and NAFLD development-related targets. Western blot was performed on key proteins of the enriched signaling pathway. HFD mice showed significant increases in hepatic TG and TC, and plasm TC, TG, and LDL-C in blood lipids, while HDL-C significantly decreased, and LQ treatment reversed their levels (p < 0.05). LQ also alleviated HFD-induced elevated levels of IPGTT, IPITT, and homeostasis model assessment of insulin resistance (HOMA-IR). And serum levels of the pro-inflammatory factor were also suppressed by LQ. PI3K/AKT pathway was enriched by KEGG pathway enrichment, and its key proteins p-PI3K and p-AKT were elevated after LQ treatment (p < 0.05). We found for the first time that LQ improves lipid accumulation, alleviates insulin resistance, and suppresses inflammatory responses in NAFLD mice, which might be associated with the activation of the PI3K/AKT pathway.     

胰岛素抵抗与2型糖尿病合并骨质疏松发生骨折风险的相关性研究

目的探讨2型糖尿病(type 2 diabetes mellitus,T2DM)合并骨质疏松患者发生骨折风险与胰岛素抵抗(insulin resistance,IR)之间的相关性。方法前瞻性纳入2015年6月至2017年6月在重庆市第九人民医院内分泌科就诊的T2DM患者,经骨密度测定诊断为骨质疏松症。根据随访结果,分为骨折组(A组)和无骨折对照组(B组)。收集患者一般信息,按照稳态模型评估公式计算胰岛素抵抗指数,根据IR指数进一步将IR患者分为高、中、低IR三个亚组。入院行骨代谢指标血清Ⅰ型前胶原N末端前肽(PINP)和Ⅰ型胶原羧基端β降解产物(β-CTX)检测,根据身高、体重计算体质量指数(bone mass index,BMI),同时记录随访期间再发骨折的不良事件。结果 A、B两组各纳入患者47例和110例,骨折发生率为29. 93%。A组患者血糖、IR的发病率和HOMA-IR值均显著高于B组(P0. 05),且两组骨代谢指标PINP和β-CTX值存在明显差异(P0. 05)。各IR亚组分析发现随着HOMA-IR值逐渐升高,血糖水平和骨折发生率也随之增高(P0. 05);高HOMA-IR值患者PINP值明显降低(P 0. 05),但β-CTX值在各IR组中差异并不明显(P 0. 05)。进一步相关性分析发现骨折发生率与HOMA-IR值呈正相关(r=0. 372,P=0. 009),与PINP值呈负相关(r=-0. 015,P0. 001)。结论 IR是T2DM合并骨质疏松患者发生骨折的危险因素,这一结果为此类患者的临床治疗提供了新思路。