Introduction: The biggest risk factor for obesity and its associated comorbidities is a Western diet. This Western diet induces adipose tissue (AT) inflammation, which causes an AT dysfunction. Since AT is a vital endocrine organ, its dysfunction damages other organs, thus inducing a state of chronic inflammation and causing various comorbidities. Even though it is evident a Western diet, high in fat and carbohydrates, induces obesity and its complications, it is not known yet which macronutrient plays the most important role. Therefore, the aim of this study was to investigate the effect of macronutrient composition on obesity and to reverse the Western diet-induced metabolic risk via caloric restriction (CR) or a change of diet composition. Materials and Methods: Male, C57BL/6JRj mice were fed with a diet high in fat, sucrose, fructose, sucrose and fructose, starch, a Western diet, or a control diet for 15 weeks. To assess reversibility of the metabolic risk, mice were first made obese via 15 weeks of WD and then put on either a CR or switched to a sucrose-rich diet. Results: A sucrose-rich and high-starch diet induced less obesity and a better metabolic profile than a Western diet, evidenced by less hepatic steatosis, lower plasma cholesterol, and less insulin resistance. Furthermore, these diets induced less intra-abdominal AT inflammation than a Western diet, since mRNA levels of pro-inflammatory markers were lower and there was less macrophage infiltration. Expression of tight junction markers in colon tissue was higher in the sucrose-rich and high-starch group than the Western group, indicating a better intestinal integrity upon sucrose-rich and high-starch feeding. Additionally, CR induced weight loss and decreased both metabolic abnormalities and AT inflammation, regardless of macronutrient composition. However, effects were more pronounced upon CR with sucrose-rich or high-starch diet. Even without CR, switching obese mice to a sucrose-rich diet induced weight loss and decreased AT inflammation and metabolic aberrations. Discussion: A diet high in sucrose or starch induces less obesity and obesity-associated complications. Moreover, switching obese mice to a sucrose-rich diet elicits weight loss and decreases obesity-induced metabolic complications, highlighting the potential of carbohydrates to treat obesity.
Obes Facts

中文翻译：

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碳水化合物在饮食诱导的肥胖小鼠模型中预防和治疗肥胖

简介：肥胖及其相关合并症的最大风险因素是西方饮食。这种西方饮食会诱发脂肪组织 (AT) 炎症，从而导致 AT 功能障碍。由于AT是重要的内分泌器官，其功能障碍会损害其他器官，从而诱发慢性炎症状态并引起各种合并症。尽管很明显，高脂肪和碳水化合物的西方饮食会导致肥胖及其并发症，但尚不清楚哪种常量营养素起最重要的作用。因此，本研究的目的是研究常量营养素成分对肥胖的影响，并通过热量限制 (CR) 或改变饮食成分来逆转西方饮食诱导的代谢风险。材料和方法：用高脂肪、蔗糖、果糖、蔗糖和果糖、淀粉、西方饮食或对照饮食喂养雄性 C57BL/6JRj 小鼠 15 周。为了评估代谢风险的可逆性，首先通过 15 周的 WD 使小鼠变得肥胖，然后进行 CR 或切换到富含蔗糖的饮食。结果：与西方饮食相比，富含蔗糖和高淀粉的饮食可减少肥胖并改善代谢状况，这可以通过减少肝脏脂肪变性、降低血浆胆固醇和减少胰岛素抵抗来证明。此外，与西方饮食相比，这些饮食诱导的腹内 AT 炎症较少，因为促炎标志物的 mRNA 水平较低，巨噬细胞浸润较少。富含蔗糖和高淀粉组结肠组织中紧密连接标志物的表达高于西方组，表明富含蔗糖和高淀粉喂养的肠道完整性更好。此外，CR 诱导体重减轻并减少代谢异常和 AT 炎症，无论宏量营养素成分如何。然而，富含蔗糖或高淀粉饮食对 CR 的影响更为明显。即使没有 CR，讨论：高蔗糖或淀粉饮食可减少肥胖和肥胖相关并发症。此外，将肥胖小鼠改为富含蔗糖的饮食可以减轻体重并减少肥胖引起的代谢并发症，突出碳水化合物治疗肥胖的潜力。
肥胖事实