Ad libitum‐fed diets high in fat and carbohydrate (especially fructose) induce weight gain, obesity, and nonalcoholic fatty liver disease (NAFLD) in humans and animal models. However, interpretation is complicated since ad libitum feeding of such diets induces hyperphagia and upregulates expression of liver fatty acid binding protein (L‐FABP)—a protein intimately involved in fatty acid and glucose regulation of lipid metabolism. Wild‐type (WT) and L‐fabp gene ablated (LKO) mice were pair‐fed either high‐fat diet (HFD) or high‐fat/high‐glucose diet (HFGD) wherein total carbohydrate was maintained constant but the proportion of glucose was increased at the expense of fructose. In LKO mice, the pair‐fed HFD increased body weight and lean tissue mass (LTM) but had no effect on fat tissue mass (FTM) or hepatic fatty vacuolation as compared to pair‐fed WT counterparts. These LKO mice exhibited upregulation of hepatic proteins in fatty acid uptake and cytosolic transport (caveolin and sterol carrier protein‐2), but lower hepatic fatty acid oxidation (decreased serum β‐hydroxybutyrate). LKO mice pair‐fed HFGD also exhibited increased body weight; however, these mice had increased FTM, not LTM, and increased hepatic fatty vacuolation as compared to pair‐fed WT counterparts. These LKO mice also exhibited upregulation of hepatic proteins in fatty acid uptake and cytosolic transport (caveolin and acyl‐CoA binding protein, but not sterol carrier protein‐2), but there was no change in hepatic fatty acid oxidation (serum β‐hydroxybutyrate) as compared to pair‐fed WT counterparts.

中文翻译：

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高糖和肝脂肪酸结合蛋白基因消融对高脂对配对小鼠的全身和肝表型的影响不同。

随意摄入高脂肪和碳水化合物（特别是果糖）的饮食会在人和动物模型中导致体重增加，肥胖和非酒精性脂肪肝疾病（NAFLD）。但是，由于这种饮食的随意喂养会引起食欲亢进并上调肝脏脂肪酸结合蛋白（L-FABP）的表达，因此解释很复杂，后者是一种与脂肪酸和葡萄糖调节脂质代谢密切相关的蛋白。野生型（WT）和L-fabp将基因消融（LKO）小鼠与高脂饮食（HFD）或高脂/高糖饮食（HFGD）配对喂养，其中总碳水化合物保持恒定，但葡萄糖的比例却增加了以果糖为代价。在LKO小鼠中，与配对喂养的WT小鼠相比，配对喂养的HFD增加了体重和瘦肉组织质量（LTM），但对脂肪组织质量（FTM）或肝脂肪空泡没有影响。这些LKO小鼠在脂肪酸摄取和胞质运输中表现出肝蛋白上调（caveolin和固醇载体蛋白2），但肝脏脂肪酸氧化降低（血清β-羟基丁酸酯减少）。LKO小鼠配对喂养的HFGD也表现出体重增加。然而，与配对喂养的WT小鼠相比，这些小鼠的FTM升高，而非LTM升高，肝脂肪空泡增加。