Overfeeding of a hypercaloric diet leads to obesity, diabetes, chronic inflammation, and fatty liver disease. Although limiting fat or carbohydrate intake is the cornerstone for obesity management, whether lowering fat or reducing carbohydrate intake is more effective for health management remains controversial. This study used murine models to determine how dietary fat and carbohydrates may influence metabolic disease manifestation. Age-matched C57BL/6J mice were fed 2 hypercaloric diets with similar caloric content, one with very high fat and low carbohydrate content (VHF) and the other with moderately high fat levels with high sucrose content (HFHS) for 12 weeks. Both groups gained more weight and displayed hypercholesterolemia, hyperglycemia, hyperinsulinemia, and liver steatosis compared to mice fed a normal low-fat (LF) diet. Interestingly, the VHF-fed mice showed a more robust adipose tissue inflammation compared to HFHS-fed mice, whereas HFHS-fed mice showed liver fibrosis and inflammation that was not observed in VHF-fed mice. Taken together, these results indicate macronutrient-specific tissue inflammation with excess dietary fat provoking adipose tissue inflammation, whereas moderately high dietary fat with extra sucrose is necessary and sufficient for hepatosteatosis advancement to steatohepatitis. Hence, liver and adipose tissues respond to dietary fat and sucrose in opposite manners, yet both macronutrients are contributing factors to metabolic diseases.

中文翻译：

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以脂肪或脂肪和蔗糖为主的高热量饮食对小鼠脂肪组织和肝脏炎症的明显影响

过度喂养高热量饮食会导致肥胖、糖尿病、慢性炎症和脂肪肝。虽然限制脂肪或碳水化合物的摄入量是肥胖管理的基石，但降低脂肪或减少碳水化合物摄入量对健康管理是否更有效仍存在争议。本研究使用小鼠模型来确定膳食脂肪和碳水化合物如何影响代谢疾病的表现。年龄匹配的 C57BL/6J 小鼠被喂食 2 种热量含量相似的高热量饮食，一种具有非常高的脂肪和低碳水化合物含量 (VHF)，另一种具有中等高脂肪含量和高蔗糖含量 (HFHS)，持续 12 周。与喂食正常低脂 (LF) 饮食的小鼠相比，两组均增加了更多的体重，并表现出高胆固醇血症、高血糖症、高胰岛素血症和肝脂肪变性。有趣的是，与 HFHS 喂养的小鼠相比，VHF 喂养的小鼠表现出更强烈的脂肪组织炎症，而 HFHS 喂养的小鼠表现出在 VHF 喂养的小鼠中未观察到的肝纤维化和炎症。综上所述，这些结果表明宏量营养素特异性组织炎症与过量膳食脂肪引起脂肪组织炎症，而适度高膳食脂肪和额外的蔗糖对于肝脂肪变性进展为脂肪性肝炎是必要且足够的。因此，肝脏和脂肪组织以相反的方式对膳食脂肪和蔗糖做出反应，但这两种常量营养素都是导致代谢疾病的因素。这些结果表明宏量营养素特异性组织炎症与过量膳食脂肪引起脂肪组织炎症，而适度高膳食脂肪和额外的蔗糖对于肝脂肪变性进展为脂肪性肝炎是必要且足够的。因此，肝脏和脂肪组织以相反的方式对膳食脂肪和蔗糖做出反应，但这两种常量营养素都是导致代谢疾病的因素。这些结果表明宏量营养素特异性组织炎症与过量膳食脂肪引起脂肪组织炎症，而适度高膳食脂肪和额外的蔗糖对于肝脂肪变性进展为脂肪性肝炎是必要且足够的。因此，肝脏和脂肪组织以相反的方式对膳食脂肪和蔗糖做出反应，但这两种常量营养素都是导致代谢疾病的因素。