限制能量平衡膳食联合运动干预对肥胖儿童身体成分、脂质代谢及肠道菌群的影响

摘要 目的：观察限制能量平衡膳食联合运动干预对肥胖儿童身体成分、脂质代谢及肠道菌群的影响。方法：选取2020年4月至2022年10月期间浙江大学医学院附属儿童医院收治的肥胖儿童104例作为研究对象。按照随机数字表法将肥胖儿童分为对照组（n=52,限制能量平衡膳食）和观察组（n=52,限制能量平衡膳食联合运动干预）。对比两组身体成分、脂质代谢及肠道菌群变化情况。结果：观察组干预2个月后体重、体质量指数（BMI）、去脂体重、脂肪量、体脂率低于对照组（P<0.05）。观察组干预2个月后总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）低于对照组;高密度脂蛋白胆固醇（HDL-C）高于对照组（P<0.05）。观察组干预2个月后肠球菌、大肠杆菌低于对照组;乳杆菌、双歧杆菌高于对照组（P<0.05）。结论：限制能量平衡膳食联合运动干预可有效改善肥胖儿童身体成分,调节脂质代谢及肠道菌群平衡。     

肥胖合并高脂血症患者血清食欲素A、25-羟维生素D3、瘦素水平与胰岛素抵抗、脂代谢紊乱和肥胖评价指标的相关性分析

摘要 目的：探讨肥胖合并高脂血症患者血清食欲素A（orexin A）、25-羟维生素D3[25-(OH)D3]、瘦素（Leptin）水平与胰岛素抵抗、脂代谢紊乱和肥胖评价指标的相关性。方法：选择2019年2月至2021年12月中国医科大学附属第四医院收治的105例肥胖合并高脂血症患者为研究组,另取同期在中国医科大学附属第四医院健康体检的73例志愿者为对照组。检测并对比两组血清orexin A、25-(OH)D3、Leptin、胰岛素抵抗相关指标、脂代谢指标及肥胖评价指标水平的差异。采用Pearson相关性分析血清orexin A、25-(OH)D3、Leptin水平与胰岛素抵抗相关指标、脂代谢指标及肥胖评价指标的相关性。结果：研究组血清orexin A、25-(OH)D3水平低于对照组,而Leptin水平高于对照组（P＜0.05）。研究组空腹血糖（FPG）、空腹胰岛素（FINS）、胰岛素抵抗指数（HOMA-IR）水平均高于对照组（P＜0.05）。研究组总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）水平高于对照组,而高密度脂蛋白胆固醇（HDL-C）水平低于对照组（P＜0.05）。研究组体质量指数（BMI）、腰臀比、腰高比均高于对照组（P＜0.05）。肥胖合并高脂血症患者的血清orexin A、25-(OH)D3水平与FPG、FINS、HOMA-IR、TC、TG、LDL-C水平、BMI、腰臀比、腰高比均呈负相关,与HDL-C水平呈正相关（P＜0.05）;Leptin水平与FPG、FINS、HOMA-IR、TC、TG、LDL-C水平、BMI、腰臀比、腰高比均呈正相关,与HDL-C水平呈负相关（P＜0.05）。结论：肥胖合并高脂血症患者血清orexin A、25-(OH)D3水平降低,Leptin水平升高,且与胰岛素抵抗、脂代谢紊乱及肥胖指标升高有关。     

单纯性肥胖儿童血清Hcy、visfatin、E-FABP水平与糖脂代谢紊乱和炎症因子的相关性分析

摘要 目的：研究单纯性肥胖儿童血清同型半胱氨酸（Hcy）、内脂素（visfatin）、上皮型脂肪酸结合蛋白（E-FABP）水平与糖脂代谢紊乱和炎症因子的相关性。方法：将2019年4月～2020年10月于我院就诊的70例单纯性肥胖儿童纳入研究,记作肥胖组。另取同期于我院接受体检的健康儿童70例作为对照组。检测并比较两组血清Hcy、visfatin、E-FABP水平,糖脂代谢紊乱相关指标和炎症因子水平。以Pearson相关性分析明确单纯性肥胖儿童血清Hcy、visfatin、E-FABP水平与糖脂代谢紊乱和炎症因子的关系。结果：肥胖组血清Hcy、visfatin、E-FABP水平均高于对照组（均P＜0.05）。肥胖组空腹血糖（FPG）、空腹胰岛素（FINS）水平及胰岛素抵抗指数（HOMA-IR）均高于对照组（均P＜0.05）。肥胖组总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）水平均高于对照组,而高密度脂蛋白胆固醇（HDL-C）水平低于对照组（均P＜0.05）。肥胖组血清白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）及肿瘤坏死因子-α（TNF-α）水平均高于对照组（均P＜0.05）。经Pearson相关性分析可得：单纯性肥胖儿童血清Hcy、visfatin、E-FABP水平与FPG、FINS、HOMA-IR、TC、TG、LDL-C、IL-1β、IL-6、TNF-α水平均呈正相关,而与HDL-C水平呈负相关（均P＜0.05）。结论：单纯性肥胖儿童血清Hcy、visfatin、E-FABP水平均异常升高,且与其糖脂代谢紊乱及炎症反应密切相关,值得临床重点关注。     

中枢性性早熟对儿童生长发育的影响及其危险因素分析

摘要 目的：分析中枢性性早熟对儿童生长发育的影响及其危险因素。方法：选择我院自2020年1月至2023年1月收治的105例中枢性性早熟患儿作为观察组,另选同期的105例发育正常儿童作为对照组,比较两组生长发育指标、血清胰岛素样生长因子-1（IGF-1）、胰岛素样生长因子结合蛋白3（IGF-BP3）表达水平,对入组者膳食模式、生活情况、家庭状况进行问卷调查,使用单因素分析和多因素Logistic回归分析。结果：观察组身高、体重、身体质量指数、骨龄均大于对照组（P＜0.05）;观察组血清IGF-1、IGF-BP3表达水平均高于对照组（P＜0.05）;经单因素分析,午睡习惯、运动时间、亮灯睡觉、课业负担、经常使用塑料制品、成人洗漱护肤品、观看情感类电视、母亲学历、职业、初潮年龄,父母关系、陪伴、平衡膳食模式、高热量高脂膳食模式均与中枢性性早熟有关（P＜0.05）;经多因素Logistic回归分析,平衡膳食模式、有午睡习惯、运动时间长均是中枢性性早熟的保护因素（P＜0.05）,高热量高脂膳食模式、母亲初潮年龄小、父母关系不和睦、父母陪伴少均是中枢性性早熟的危险因素（P＜0.05）。结论：中枢性性早熟可影响儿童的生长发育进度,与高热量高脂膳食模式、母亲初潮年龄、父母关系和陪伴密切相关,应改善家庭关系,帮助儿童养成平衡膳食、午睡和运动的良好习惯,有益于儿童正常的生长发育。     

地中海饮食干预联合有氧运动训练对2型糖尿病患者脂糖代谢水平、肠道菌群及生活质量的影响

摘要 目的：探讨地中海饮食干预联合有氧运动训练对2型糖尿病（T2DM）患者脂糖代谢水平、肠道菌群及生活质量的影响。方法：选择2021年6月～2022年12月我院110例T2DM患者为研究对象,随机数字表法随机分组,各55例。对照组给予常规健康教育及饮食、运动干预,观察组给予地中海饮食干预及有氧运动训练。比较两组干预前后脂糖代谢指标[空腹血糖（FPG）、餐后2 h血糖（2hPG）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）]、肠道菌群、生活质量变化及并发症发生率。结果：干预后观察组HDL-C水平高于对照组,FPG、2hPG、TC、TG、LDL-C水平低于对照组（P＜0.05）;干预后观察组大肠埃希菌、肠球菌水平较对照组低,双歧杆菌水平较对照组高（P＜0.05）;干预后观察组治疗、心理精神、生理功能、社会关系评分较对照组高（P＜0.05）;两组并发症发生率差异无统计学意义（P＞0.05）。结论：地中海饮食干预联合有氧运动训练能有效纠正T2DM患者肠道菌群紊乱状态,改善脂糖代谢,减少并发症发生,提高生活质量。     

老年2型糖尿病患者人巨细胞病毒感染与脂糖代谢、胰岛素抵抗及免疫失衡的关系研究

摘要 目的：探讨老年2型糖尿病（T2DM）患者人巨细胞病毒（HCMV）感染与脂糖代谢、胰岛素抵抗及免疫失衡的关系。方法：选取2021年2月~2022年3月长沙市第三医院收治的老年T2DM患者100例为研究组,选取同期来体检健康的志愿者60例作为对照组。根据HCMV-脱氧核糖核酸（DNA）检测结果将研究组分为阳性组41例和阴性组59例。检测并比较对照组、研究组HCMV-DNA载量、T淋巴细胞亚群（CD4⁺、CD8⁺、CD4⁺/CD8⁺）、脂糖代谢[高密度脂蛋白胆固醇（HDL-C）、糖化血红蛋白（HbA1c）、总胆固醇（TC）、空腹血糖（FBG）、三酰甘油（TG）、低密度脂蛋白胆固醇（LDL-C）]、胰岛素抵抗[空腹胰岛素（FINS）、胰岛素抵抗指数（HOMA-IR）]。采用Pearson相关性分析老年T2DM患者HCMV感染与脂糖代谢、胰岛素抵抗及免疫失衡的关系。结果：研究组的HCMV-DNA阳性率、HCMV-DNA载量高于对照组,阴性率低于对照组（P<0.05）。阳性组、阴性组的CD4⁺、CD4⁺/CD8⁺低于对照组,且阳性组低于阴性组（P<0.05）。阳性组、阴性组的CD8⁺高于对照组,且阳性组高于阴性组（P<0.05）。阳性组、阴性组的HbA1c、FBG、TC、TG、LDL-C高于对照组,且阳性组高于阴性组（P<0.05）。阳性组、阴性组的HDL-C低于对照组,且阳性组低于阴性组（P<0.05）。阳性组、阴性组的HOMA-IR、FINS高于对照组,且阳性组高于阴性组（P<0.05）。Pearson相关性分析结果显示,HCMV-DNA载量与CD4⁺、CD4⁺/CD8⁺、HDL-C呈负相关（P<0.05）,而与CD8⁺、HbA1c、FBG、TC、TG、LDL-C、FINS、HOMA-IR呈正相关（P<0.05）。结论：HCMV病毒感染可导致老年T2DM患者脂糖代谢紊乱,促进胰岛素抵抗,加重免疫失衡,加速疾病进展。     

茵陈五苓散联合利拉鲁肽对肥胖型2型糖尿病患者糖脂代谢、胰岛素敏感性和氧化应激的影响

摘要 目的：探讨茵陈五苓散联合利拉鲁肽对肥胖型2型糖尿病（T2DM）患者糖脂代谢、胰岛素敏感性和氧化应激的影响。方法：选取2021年12月~2022年12月期间广州中医药大学附属佛山中医院收治的160例痰湿内蕴型肥胖T2DM患者。根据随机数字表法将患者分为对照组（利拉鲁肽治疗,80例）和研究组（茵陈五苓散联合利拉鲁肽治疗,80例）。对比两组疗效、糖脂代谢指标、肥胖相关指标、胰岛素敏感性、氧化应激和不良反应发生情况。结果：与对照组相比,研究组的临床总有效率更高（P<0.05）。研究组治疗后体质量指数（BMI）、空腹血糖（FBG）、腰臀比（WHR）、餐后2 h血糖（2hPG）、丙二醛（MDA）、糖化血红蛋白（HbAlc）、稳态模型胰岛素抵抗指数（HOMA-IR）、总胆固醇（TC）、黄嘌呤氧化酶（XO）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）较对照组低（P<0.05）。治疗后研究组稳态模型胰岛β细胞功能指数（HOMA-β）、高密度脂蛋白胆固醇（HDL-C）、超氧化物歧化酶（SOD）高于对照组（P<0.05）。两组不良反应发生率组间对比未见差异（P>0.05）。结论：茵陈五苓散联合利拉鲁肽治疗肥胖型T2DM患者疗效确切,可调节糖脂代谢水平,降低胰岛素敏感性,减轻氧化应激,且具有一定安全性,值得临床借鉴应用。     

益生菌联合膳食纤维的肠内营养对重型颅脑损伤患者术后营养状况、免疫功能和肠黏膜屏障功能的影响

摘要 目的：观察重型颅脑损伤患者术后经膳食纤维的肠内营养联合益生菌干预后,患者免疫功能、肠黏膜屏障功能以及营养状况的变化。方法：选取2016年6月~2020年5月期间我院收治的重型颅脑损伤患者136例。根据入院顺序奇偶法分为对照组68例和研究组68例,对照组给予膳食纤维的肠内营养干预,研究组在对照组的基础上联合益生菌干预,对比两组格拉斯哥昏迷量表（GCS）评分、营养状况、免疫功能、肠黏膜屏障功能及并发症发生情况。结果：两组干预14 d后白蛋白（ALB）、血红蛋白（Hb）、转铁蛋白（TR）均较干预前升高,且研究组较对照组高（P<0.05）。两组干预14 d后免疫球蛋白G（IgG） 、免疫球蛋白A（IgA）、免疫球蛋白M（IgM）均较干预前升高,且研究组较对照组高（P<0.05）。两组干预14 d后总超氧化物歧化酶（T-SOD）、谷胱甘肽过氧化物酶（GSH-PX）均较干预前升高,且研究组较对照组高（P<0.05）,丙二醛（MDA）较干预前降低,且研究组较对照组低（P<0.05）。两组干预14 d后GCS评分升高,且研究组较对照组高（P<0.05）。研究组的并发症发生率低于对照组（P<0.05）。结论：益生菌联合膳食纤维的肠内营养干预可有效改善重型颅脑损伤术后患者营养状况、免疫功能和肠黏膜屏障功能,同时还可减少并发症发生率,改善患者预后。     

HCMV-DNA定量检测和HCMV-IgG抗体AI检测在儿童HCMV感染诊断中的临床价值

摘要 目的：探讨人巨细胞病毒（HCMV）-DNA定量检测和HCMV-免疫球蛋白G（IgG）抗体亲和力指数（AI）检测在儿童HCMV感染诊断中的临床价值。方法：收集高度疑似HCMV活动性感染患儿血清样本103例作为研究组,健康体检儿童血清样本94例作为对照组。分析HCMV-DNA定量检测结果和HCMV-IgG抗体AI检测结果,并比较不同年龄、不同性别患儿HCMV-DNA阳性结果检出率和低HCMV-IgG抗体AI检出情况。结果：研究组血清HCMV-DNA阳性率为33.01%（34/103）,对照组血清HCMV-DNA均为阴性,研究组血清HCMV-DNA阳性率明显高于对照组,差异有统计学意义（P<0.05）。研究组血清低HCMV-IgG抗体AI检出率为13.59%（14/103）,对照组未检出低HCMV-IgG抗体AI,研究组血清低HCMV-IgG抗体AI检出率高于对照组,差异有统计学意义（P<0.05）。研究组不同性别之间患儿血清的HCMV-DNA阳性率、低HCMV-IgG抗体AI检测结果均无统计学差异（P>0.05）。研究组年龄1～5岁患儿血清HCMV-DNA阳性率明显低于年龄1 d～<6个月和年龄6个月～<1岁患儿（P<0.05）。三个年龄段患儿的血清低HCMV-IgG抗体AI检测结果均无统计学差异（P>0.05）。结论：1岁以下儿童更易受到HCMV感染,HCMV-DNA定量检测和HCMV-IgG抗体AI检测结果可以为临床早期诊断和治疗HCMV感染提供有效依据。     

运动对肥胖大鼠胰岛素抵抗的影响

目的：探讨急、慢性游泳运动对胰岛素抵抗大鼠半乳凝素-3（galectin-3）表达的影响。方法：100只大鼠随机分为：普通膳食对照组（CON组,n=10）;高脂膳食组（HFD组,n=90）。分别喂养8周后,从高脂膳食组筛选出肥胖（即体重位于上游）大鼠30只用于后续实验。将肥胖大鼠随机分为3组（n=10）：①HFD-SED组：高脂膳食安静组;②HFD-CE组：高脂膳食慢性运动组,进行慢性游泳运动;③HFD-AE组：高脂膳食急性运动组,进行急性游泳运动。肥胖大鼠继续高脂膳食喂养8周,并进行运动干预;CON组大鼠继续普通饲料喂养8周。运动干预结束后,各组进行口服糖耐量和胰岛素释放实验,计算葡萄糖-胰岛素指数;测定体重;以ELISA分析大鼠血液中Gal-3含量。结果：HFD-SED组葡萄糖-胰岛素指数明显大于CON组（P<0.01）,HFD-CE组和HFD-AE组葡萄糖-胰岛素指数明显小于HFD-SED组（P<0.01）;HFD-SED组血液Gal-3含量明显高于CON组（P<0.01）,HFD-CE和HFD-AE组血液Gal-3含量明显小于HFD-SED组（P<0.01）。运动干预结束后,HFD-SED组和HFD-AE组大鼠体重明显高于CON组（P<0.01）;HFD-CE组大鼠体重明显低于HFD-SED组（P<0.01）,而与CON组无统计学差异。结论：急、慢性游泳运动均能改善胰岛素抵抗状态、降低胰岛素抵抗大鼠的Gal-3表达,但慢性游泳运动能明显改善机体超重状态。建议临床上采用长期、规律的慢性有氧运动对肥胖、胰岛素抵抗等代谢疾病进行干预。     

4周有氧运动与饮食控制对肥胖女青少年血清IGF-1和IGF-1结合蛋白-3水平的影响

目的：研究4周中等强度有氧运动结合饮食控制对肥胖女青年、少年血清总胰岛素样生长因子1（IGF-1）、IGF-1结合蛋白3（IGFBP-3）水平和IGF-1活性的影响及其在体脂减少和糖脂代谢改善中的作用。方法：招募9名18~19岁肥胖女青年和30名14~16岁肥胖女少年,进行全封闭的4周中等强度有氧运动结合饮食控制干预。运动项目有游泳、跑步、健身操等,每周运动6 d,每天运动4 h,每运动30 min,休息5 min。运动强度从第1周的低强度（运动后即刻心率约100~120次/分）递增至第2~4周的中强度（运动后即刻心率约120~140次/分）。根据基础代谢率给予每日1 400或1 600 kcal的总能量。另招募正常体重女青年和女少年各9名作为对照组。检测肥胖女青年、少年在4周干预前、后和对照组女青年、少年的体重、身体质量指数（BMI）、腰围、空腹血糖、胰岛素和血脂水平以及血清总IGF-1和IGFBP-3的水平和IGF-1活性。结果：①与对照组相比,肥胖女青年、少年的血清总IGF-1和IGFBP-3水平均降低且肥胖女少年的IGF-1活性降低;②4周中等强度有氧运动结合饮食控制在显著降低肥胖女青年、少年的体脂、腰围和改善糖脂代谢的同时,降低血清IGFBP-3水平、增加IGF-1活性,但血清总IGF-1水平没有显著改变。且相关性分析显示IGF-1活性增加可能与肥胖女青年的腰围减少有关,但血清IGFBP-3水平的降低和IGF-1活性的增加与糖脂代谢的改善没有显著相关性。结论：4周中等强度有氧运动结合饮食控制降低肥胖女青年、少年的血清IGFBP-3水平、增加IGF-1活性;且IGF-1活性的增加可能与运动结合饮食控制降低肥胖女青年的腰围有关。     

Exercise and diet enhance fat oxidation and reduce insulin resistance in older obese adults.

Older, obese, and sedentary individuals are at high risk of developing diabetes and cardiovascular disease. Exercise training improves metabolic anomalies associated with such diseases, but the effects of caloric restriction in addition to exercise in such a high-risk group are not known. Changes in body composition and metabolism during a lifestyle intervention were investigated in 23 older, obese men and women (aged 66 +/- 1 yr, body mass index 33.2 +/- 1.4 kg/m(2)) with impaired glucose tolerance. All volunteers undertook 12 wk of aerobic exercise training [5 days/wk for 60 min at 75% maximal oxygen consumption (Vo(2max))] with either normal caloric intake (eucaloric group, 1,901 +/- 277 kcal/day, n = 12) or a reduced-calorie diet (hypocaloric group, 1,307 +/- 70 kcal/day, n = 11), as dictated by nutritional counseling. Body composition (decreased fat mass; maintained fat-free mass), aerobic fitness (Vo(2max)), leptinemia, insulin sensitivity, and intramyocellular lipid accumulation (IMCL) in skeletal muscle improved in both groups (P < 0.05). Improvements in body composition, leptin, and basal fat oxidation were greater in the hypocaloric group. Following the intervention, there was a correlation between the increase in basal fat oxidation and the decrease in IMCL (r = -0.53, P = 0.04). In addition, basal fat oxidation was associated with circulating leptin after (r = 0.65, P = 0.0007) but not before the intervention (r = 0.05, P = 0.84). In conclusion, these data show that exercise training improves resting substrate oxidation and creates a metabolic milieu that appears to promote lipid utilization in skeletal muscle, thus facilitating a reversal of insulin resistance. We also demonstrate that leptin sensitivity is improved but that such a trend may rely on reducing caloric intake in addition to exercise training.     

Beneficial effects of a long-term oral L-arginine treatment added to a hypocaloric diet and exercise training program in obese, insulin-resistant type 2 diabetic patients

Because chronic L-arginine supplementation improves insulin sensitivity and endothelial function in nonobese type 2 diabetic patients, the aim of this study was to evaluate the effects of a long-term oral L-arginine therapy on adipose fat mass (FM) and muscle free-fat mass (FFM) distribution, daily glucose levels, insulin sensitivity, endothelial function, oxidative stress, and adipokine release in obese type 2 diabetic patients with insulin resistance who were treated with a combined period of hypocaloric diet and exercise training. Thirty-three type 2 diabetic patients participated in a hypocaloric diet plus an exercise training program for 21 days. Furthermore, they were divided into two groups in randomized order: the first group was also treated with L-arginine (8.3 g/day), and the second group was treated with placebo. Although in the placebo group body weight, waist circumference, daily glucose profiles, fructosamine, insulin, and homeostasis model assessment index significantly decreased, L-arginine supplementation further decreased FM (P < 0.05) and waist circumference (P < 0.0001), preserving FFM (P < 0.03), and improved mean daily glucose profiles (P < 0.0001) and fructosamine (P < 0.03). Moreover, change in area under the curve of cGMP (second messenger of nitric oxide; P < 0.001), superoxide dismutase (index of antioxidant capacity; P < 0.01), and adiponectin levels (P < 0.02) increased, whereas basal endothelin-1 levels (P < 0.01) and leptin-to-adiponectin ratio (P < 0.05) decreased in the L-arginine group. Long-term oral L-arginine treatment resulted in an additive effect compared with a diet and exercise training program alone on glucose metabolism and insulin sensitivity. Furthermore, it improved endothelial function, oxidative stress, and adipokine release in obese type 2 diabetic patients with insulin resistance.     

Moderate exercise training is more effective than resveratrol supplementation for ameliorating lipid metabolic complication in skeletal muscle of high fat diet-induced obese mice

[Purpose]

The aim of this study was to compare the effectiveness of moderate exercise training or resveratrol supplementation with a low fat diet on lipid metabolism in the skeletal muscle of high fat diet-induced obese mice.

[Methods]

C57BL/6J mice (5 weeks old, n = 30) were fed a high fat diet (45% fat) for 8 weeks first to make them obese. Afterward, all the mice were fed a low fat diet during 8 weeks of intervention with moderate exercise training and resveratrol supplementation. Before the intervention, the mice were separated into 3 groups: low-fat diet control (HLC; n = 10), low fat diet with resveratrol (HLR; n = 10) or low fat diet with exercise (HLE n = 10). The exercise group (HLE) performed treadmill running for 30-60 min/day at 10-22 m/min, 0% grade, 5 times/week for 8 weeks, while the resveratrol group (HLR) received a daily dose of resveratrol (10 mg/kg of body weight), 5 days/week for 8 weeks.

[Results]

Body weight was significantly reduced in HLE. Further, the lipogenesis marker SREBP and the inflammatory cytokine TNF-α were significant reduced in HLE. However, there was no significant effect from resveratrol supplementation with a low fat diet. Taken together, exercise training with a low fat diet has the positive effect of ameliorating lipid disturbance in the skeletal muscle of high fat diet-induced obese mice.

[Conclusion]

These findings suggest that exercise training with a low fat diet is most effective to improve lipid metabolism by reducing lipogenesis and inflammation in the skeletal muscle of high fat diet-induced obese mice.     

The Effect of Low‐Intensity Exercise Training on Fat Metabolism of Obese Women

Objective: Previous studies have shown that fat metabolism is different in upper body (UB) and lower body (LB) obese women. The present study investigated whether the effect of low‐intensity exercise training on fat metabolism is different in UB and LB obese premenopausal women. Research Methods and Procedures: Twenty‐one healthy, premenopausal women with either LB obesity (waist‐to‐hip ratio of ≤0.79; n = 8) or UB obesity (waist‐to‐hip ratio of ≥0.85; n = 13) participated in the present study. The UB obese women were matched and randomly divided in an exercise training group (UB) and a nonexercising control group (UB‐C). Subjects in the UB and LB groups participated in a low‐intensity exercise training program (40% Vo ₂max) three times per week for 12 weeks. Before and after the intervention, measurements of fat metabolism at rest and during exercise, body composition, and maximal aerobic capacity were performed. Results: Exercise training did not change the respiratory exchange ratio at rest in the UB and LB groups. During exercise, relative fat oxidation increased in the UB group by 19% (p < 0.05), whereas no change in the LB and UB‐C groups was found. Plasma free fatty acid oxidation did not change by exercise training, and nonplasma fatty acid oxidation tended to increase in the UB group compared with the UB‐C group (p = 0.08). Discussion: Low‐intensity exercise training increased the contribution of fat oxidation to total energy expenditure during exercise but not at rest in UB obese women. Exercise training had no significant effect on fat metabolism in the LB obese women.     

Exercise-induced reversal of insulin resistance in obese elderly is associated with reduced visceral fat.

Exercise improves glucose metabolism and delays the onset and/or reverses insulin resistance in the elderly by an unknown mechanism. In the present study, we examined the effects of exercise training on glucose metabolism, abdominal adiposity, and adipocytokines in obese elderly. Sixteen obese men and women (age = 63 +/- 1 yr, body mass index = 33.2 +/- 1.4 kg/m2) participated in a 12-wk supervised exercise program (5 days/wk, 60 min/day, treadmill/cycle ergometry at 85% of heart rate maximum). Visceral fat (VF), subcutaneous fat, and total abdominal fat were measured by computed tomography. Fat mass and fat-free mass were assessed by hydrostatic weighing. An oral glucose tolerance test was used to determine changes in insulin resistance. Exercise training increased maximal oxygen consumption (21.3 +/- 0.8 vs. 24.3 +/- 1.0 ml.kg(-1).min(-1), P < 0.0001), decreased body weight (P < 0.0001) and fat mass (P < 0.001), while fat-free mass was not altered (P > 0.05). VF (176 +/- 20 vs. 136 +/- 17 cm2, P < 0.0001), subcutaneous fat (351 +/- 34 vs. 305 +/- 28 cm2, P < 0.03), and total abdominal fat (525 +/- 40 vs. 443 +/- 34 cm2, P < 0.003) were reduced through training. Circulating leptin was lower (P < 0.003) after training, but total adiponectin and tumor necrosis factor-alpha remained unchanged. Insulin resistance was reversed by exercise (40.1 +/- 7.7 vs. 27.6 +/- 5.6 units, P < 0.01) and correlated with changes in VF (r = 0.66, P < 0.01) and maximal oxygen consumption (r = -0.48, P < 0.05) but not adipocytokines. VF loss after aerobic exercise training improves glucose metabolism and is associated with the reversal of insulin resistance in older obese men and women.     

Effects of excess dietary iron and fat on glucose and lipid metabolism

PurposeDiets rich in fat and energy are associated with metabolic syndrome (MS). Increased body iron stores have been recognized as a feature of MS. High-fat diets (HFs), excess iron loading and MS are closely associated, but the mechanism linking them has not been clearly defined. We investigated the interaction between dietary fat and dietary Fe in the context of glucose and lipid metabolism in the body.MethodsC57BL6/J mice were divided into four groups and fed the modified AIN-93G low-fat diet (LF) and HF with adequate or excess Fe for 7 weeks. The Fe contents were increased by adding carbonyl iron (2% of diet weight) (LF+Fe and HF+Fe).ResultsHigh iron levels increased blood glucose levels but decreased high-density lipoprotein cholesterol levels. The HF group showed increases in plasma levels of glucose and insulin and insulin resistance. HF+Fe mice showed greater changes. Representative indices of iron status, such hepatic and plasma Fe levels, were not altered further by the HF. However, both the HF and excess iron loading changed the hepatic expression of hepcidin and ferroportin. The LF+Fe, HF and HF+Fe groups showed greater hepatic fat accumulation compared with the LF group. These changes were paralleled by alterations in the levels of enzymes related to hepatic gluconeogenesis and lipid synthesis, which could be due to increases in mitochondrial dysfunction and oxidative stress.ConclusionsHigh-fat diets and iron overload are associated with insulin resistance, modified hepatic lipid and iron metabolism and increased mitochondrial dysfunction and oxidative stress.     

A 12‐Week Aerobic Exercise Program Reduces Hepatic Fat Accumulation and Insulin Resistance in Obese,Hispanic Adolescents

The rise in obesity‐related morbidity in children and adolescents requires urgent prevention and treatment strategies. Currently, only limited data are available on the effects of exercise programs on insulin resistance, and visceral, hepatic, and intramyocellular fat accumulation. We hypothesized that a 12‐week controlled aerobic exercise program without weight loss reduces visceral, hepatic, and intramyocellular fat content and decreases insulin resistance in sedentary Hispanic adolescents. Twenty‐nine postpubertal (Tanner stage IV and V), Hispanic adolescents, 15 obese (7 boys, 8 girls; 15.6 ± 0.4 years; 33.7 ± 1.1 kg/m²; 38.3 ± 1.5% body fat) and 14 lean (10 boys, 4 girls; 15.1 ± 0.3 years; 20.6 ± 0.8 kg/m²; 18.9 ± 1.5% body fat), completed a 12‐week aerobic exercise program (4 × 30 min/week at ≥70% of peak oxygen consumption (VO₂peak)). Measurements of cardiovascular fitness, visceral, hepatic, and intramyocellular fat content (magnetic resonance imaging (MRI)/magnetic resonance spectroscopy (MRS)), and insulin resistance were obtained at baseline and postexercise. In both groups, fitness increased (obese: 13 ± 2%, lean: 16 ± 4%; both P < 0.01). In obese participants, intramyocellular fat remained unchanged, whereas hepatic fat content decreased from 8.9 ± 3.2 to 5.6 ± 1.8%; P < 0.05 and visceral fat content from 54.7 ± 6.0 to 49.6 ± 5.5 cm²; P < 0.05. Insulin resistance decreased indicated by decreased fasting insulin (21.8 ± 2.7 to 18.2 ± 2.4 µU/ml; P < 0.01) and homeostasis model assessment of insulin resistance (HOMA_IR) (4.9 ± 0.7 to 4.1 ± 0.6; P < 0.01). The decrease in visceral fat correlated with the decrease in fasting insulin (R² = 0.40; P < 0.05). No significant changes were observed in any parameter in lean participants except a small increase in lean body mass (LBM). Thus, a controlled aerobic exercise program, without weight loss, reduced hepatic and visceral fat accumulation, and decreased insulin resistance in obese adolescents.     

mTOR/S6K1信号通路与胰岛素抵抗的关系及有氧运动对其影响的研究

目的:通过研究高脂饮食和有氧运动对胰岛素抵抗(IR)小鼠骨骼肌雷帕霉素靶蛋白/核糖体S6激酶1(mTOR/S6K1)通路的影响,试图为运动防治IR提供理论依据。方法:8周C57BL/6小鼠随机分为正常饮食组和高脂饮食组,每组各20只,高脂饮食组喂养8周后建立IR模型。随后将正常饮食组再次随机分为正常饮食安静组(NC)和正常饮食运动组(NE);高脂饮食组也随机分为高脂饮食安静组(HC)和高脂饮食运动组(HE)。各运动组进行为期6周、75%VO2max强度跑台训练,每天1次,每次60min,每周5次。实验结束后采用OGTT检测葡萄糖耐量,组织学检测胰岛形态变化,ELISA法检测血清空腹胰岛素水平,Northern blot、Western blot检测骨骼肌中mTOR和S6K1 mRNA和蛋白及其磷酸化蛋白pS6K1-Thr389的表达。结果:与NC组相比,HC组小鼠体重、空腹血清胰岛素值和胰岛β细胞团面积百分比均呈显著增加,且OGTT曲线显示糖耐量明显受损,然而6周有氧运动后以上各指标呈显著性降低,葡萄糖耐量也得到明显改善;且骨骼肌中mTOR、S6K1、pS6K1-Thr389 mRNA和蛋白表达均明显降低。结论:mTOR/S6K1信号通路与高脂饮食诱导IR的发生密切相关,有氧运动明显增加了机体组织对胰岛素的敏感性,推测有氧运动可能通过抑制mTOR/S6K1信号通路,增加IR小鼠骨骼肌的能量代谢从而改善IR。