孕前超重/肥胖的妊娠期糖尿病孕妇血糖管理：基于静息能量消耗计算每日总能量消耗

目的探讨基于静息能量消耗(REE)计算每日总能量消耗(TEE)，对孕前超重/肥胖的妊娠期糖尿病(GDM)孕妇血糖管理意义。 方法选择2018年6月至2019年6月，于首都医科大学附属北京潞河医院产科"糖尿病一日门诊"就诊时，被诊断为孕前超重/肥胖的67例GDM孕妇为研究对象。按照其首次就诊时间的奇、偶周，将其分为研究组(n＝34，首次就诊时间为奇数周者)和对照组(n＝33，首次就诊时间为偶数周者)。采用成组t检验对2组孕妇年龄、孕次、孕期体重增加值、新生儿出生体重、空腹血糖、餐后2 h血糖等进行统计学分析。采用Mann-Whitney U检验对2组孕妇分娩孕龄、产次等进行统计学分析。采用χ²检验、Fisher确切概率法、连续性校正χ²检验对2组孕妇尿酮体阳性率、巨大儿发生率等进行统计学分析。本研究经首都医科大学附属北京潞河医院医学伦理委员审核批准(审批文号：2018-LHKY-027-02)，并与所有受试者签署知情同意书。 结果①2组GDM孕妇年龄、孕次、产次、分娩孕龄及孕前人体质量指数(BMI)构成比比较，差异均无统计学意义(P>0.05)。②研究组孕妇TEE为(1 532.6±301.9)kcal/d，显著低于对照组的(1 824.1±313.2) kcal/d，并且差异有统计学意义(t＝3.311、P＝0.002)；2组孕妇血糖达标情况构成比比较，差异亦有统计学意义(P＝0.040)。③研究组孕妇孕期体重增加值、糖化血红蛋白(HbA1c)水平和新生儿出生体重分别为(13.4±6.2)kg、(5.6±0.3)%和(3 287.5±577.1)g，明显低于对照组的(18.2±4.8)kg、(6.2±0.2)%和(3 632.8±490.6)g，并且差异均有统计学意义(t＝2.235、P＝0.031，t＝2.882、P＝0.047，t＝2.121、P＝0.039)。 结论基于REE估算的TEE，较通用系数法估算的TEE，更接近于孕前超重/肥胖GDM孕妇的实际能量需求。因此，基于REE估算的TEE更有利于对孕前超重/肥胖的GDM进行孕期血糖管理。     

S100A6经RAGE介导影响肥胖儿童血管内皮损伤的机制研究

目的 探讨钙结合蛋白A6(S100A6)经终末糖基化产物受体(RAGE)介导影响肥胖儿童血管内皮损伤的机制,为进一步提出有针对性的治疗方案提供依据。方法 选取十堰市妇幼保健院2015年7月-2018年7月收治的肥胖患儿91例,根据患儿是否存在血管内皮损伤分成损伤组(n=43)、无损伤组(n=48)。选取同期于本院体检的健康体检儿童45例作为对照组。三组受检者均于入院当日采血检测血清S100A6与游离RAGE(sRAGE)水平,并测定三组血管内皮损伤标志物,包括血管内皮黏附分子-1(sVCAM-1)、可溶性细胞黏附分子-1(sICAN-1)、血管性血友病因子(vWF)水平,检测方法为酶联免疫吸附法。经Pearson线性相关分析S100A6、sRAGE与血管内皮损伤标志物间的相关性。结果 损伤组血清S100A6、sRAGE水平高于无损伤组、对照组,差异有统计学意义(P<0.05)。损伤组血清sVCAM-1、vWF、sICAN-1水平高于无损伤组、对照组,差异有统计学意义(P<0.05)。经Pearson线性相关分析提示S100A6、sRAGE与sVCAM-1、vWF、sICAN-1均呈正相关(P<0.05)。结论 与正常儿童及无血管内皮损伤的肥胖儿童相比,有血管内皮损伤的肥胖儿童血清S100A6、sRAGE明显上调,这可能与sRAGE增高导致S100A6上调,而进一步致sVCAM-1、vWF、sICAN-1水平增高有关。     

中药膳食辅助治疗肥胖性脂肪肝患儿的效果及对相关血清指标的调节作用

目的分析中药膳食辅助治疗肥胖性脂肪肝患儿的效果及对相关血清指标的调节作用。方法选择2018年3月至2020年3月收治的86例肥胖性脂肪肝患儿为研究对象,依据治疗方法将其分为对照组与研究组,各43例。对照组接受常规治疗,研究组在常规治疗基础上配合中药膳食治疗。比较两组的治疗效果。结果治疗后,两组的WC与BMI均降低,且研究组低于对照组(P<0.05)。治疗后,两组的TC、ALT、TG水平均降低,且研究组低于对照组(P<0.05)。研究组的治疗总有效率高于对照组(P<0.05)。结论中药膳食辅助治疗肥胖性脂肪肝患儿的效果理想,能够调节相关血清指标,值得临床应用推广。     

Omentin-1 attenuates adipose tissue inflammation via restoration of TXNIP/NLRP3 signaling in high-fat diet-induced obese mice

Omentin-1 is an adipokine expressed by the adipose tissue and is reduced in obesity. This study was designed to calculate the protective efficiency and mechanism of omentin-1 against inflammation of the adipose tissue in obese mice. A transgenic mouse model with omentin-1 protein overexpression was established by crossing omentin-1 transgenic mice with Fabp4-Cre mice. Obesity was induced in the mice by feeding them a high-fat diet for 10 weeks. Fabp4-Cre-mediated overexpression of omentin-1 significantly increased serum omentin-1 level, serum anti-inflammatory factor levels, and expression of M2-specific mRNAs; inhibited body weight and adipose tissue weight gain; improved glucose tolerance, insulin tolerance, and insulin sensitivity; decreased serum levels of insulin and proinflammatory factors, adipocyte size, and expression of M1-specific mRNAs; suppressed macrophage infiltration; downregulated expression of proinflammatory factors; upregulated expression of anti-inflammatory factors; and inhibited thioredoxin-interacting protein (TXNIP)/NOD-like receptor 3 (NLRP3) signaling in the adipose tissue of obese mice. An NLRP3 inhibitor (20 mg/kg MCC950) exhibited the same effects as overexpression of omentin-1. Pretreatment with omentin-1 inhibited lipopolysaccharide-induced inflammation via TXNIP/NLRP3 signaling in RAW 264.7 macrophages. These findings suggest that omentin-1 suppresses adipose tissue inflammation in obese mice, at least partly, via inhibiting the TXNIP/NLRP3 signaling pathway.     

Altered Fetal Skeletal Muscle Nutrient Metabolism Following an Adverse In Utero Environment and the Modulation of Later Life Insulin Sensitivity

The importance of the in utero environment as a contributor to later life metabolic disease has been demonstrated in both human and animal studies. In this review, we consider how disruption of normal fetal growth may impact skeletal muscle metabolic development, ultimately leading to insulin resistance and decreased insulin sensitivity, a key precursor to later life metabolic disease. In cases of intrauterine growth restriction (IUGR) associated with hypoxia, where the fetus fails to reach its full growth potential, low birth weight (LBW) is often the outcome, and early in postnatal life, LBW individuals display modifications in the insulin-signaling pathway, a critical precursor to insulin resistance. In this review, we will present literature detailing the classical development of insulin resistance in IUGR, but also discuss how this impaired development, when challenged with a postnatal Western diet, may potentially contribute to the development of later life insulin resistance. Considering the important role of the skeletal muscle in insulin resistance pathogenesis, understanding the in utero programmed origins of skeletal muscle deficiencies in insulin sensitivity and how they may interact with an adverse postnatal environment, is an important step in highlighting potential therapeutic options for LBW offspring born of pregnancies characterized by placental insufficiency.     

血清补体C5a及相关炎症因子在肥胖伴高血压儿童中的水平及临床意义

目的 分析肥胖患儿体内补体C5a及相关炎性因子对血压的影响及其在高血压中的作用,为临床干预提供科学依据。方法 以2016年7月－2017年8月就诊于西安交通大学第二附属医院小儿内分泌门诊的71例肥胖儿童为研究对象,测量儿童身高、体重、腰围、体重指数(BMI)及血压,根据血压测量结果,收缩压(SBP)和(或)舒张压(DBP)≥同年龄同性别P₉₅为高血压,进一步分为高血压组31例和非高血压组40例。用酶联免疫法检测血中胰岛素、白介素-6(IL-6)、C5a、超敏C反应蛋白(hsCRP)和肿瘤坏死因子-α(TNF-α),并计算胰岛素抵抗指数(HOMA-IR),并对检测结果进行分析。结果 高血压组儿童与非高血压组比较,HOMA-IR、甘油三酯(TG)、总胆固醇(TC)显著升高(P<0.05);此外,肥胖组高血压患儿血中TNF-α,IL-6以及补体C5a显著升高,与非高血压组比较差异均有统计学意义(P<0.05);SDS-DBP及SDS-SBP均与炎性因子TNF-α、hs-CRP、IL-6及补体C5a之间呈显著正相关(P<0.05);多元线性回归显示SDS-BMI、腰围、IL-6、C5a及hsCRP与SDS-SBP显著相关(P<0.05);IL-6、C5a及hsCRP均与SDS-DBP显著相关(P<0.05)。结论 炎性因子IL-6与hsCRP以及补体C5a与肥胖儿童高血压的发生密切相关,可能是引起血压升高的危险因素。