Long-term high-protein diet intake reverts weight gain and attenuates metabolic dysfunction on high-sucrose-fed adult rats.
Long-term high-protein diet intake reverts weight gain and attenuates metabolic dysfunction on high-sucrose-fed adult rats.
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DOI：
10.1186/s12986-018-0290-y
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发表时间：
2018
影响因子：
4.5
通讯作者：
Paes AMA
中科院分区：
文献类型：
--
作者：
Sousa RML;Ribeiro NLX;Pinto BAS;Sanches JR;da Silva MU;Coêlho CFF;França LM;de Figueiredo Neto JA;Paes AMA
添加糖的摄入与代谢综合征及其合并症有关，已被认为是一个世界性的公共卫生问题。同时，目前的研究表明，高蛋白饮食可以促进减肥和改善代谢结果。因此，本研究旨在探讨长期摄入高蛋白饮食（HPD， 34.3%蛋白）对高糖喂养大鼠的影响。断奶雄性Wistar大鼠随机分为两组，分别饲喂标准饲料（CT/CT， 10%蔗糖）和高蔗糖饲料（HSD， 25%蔗糖），观察20周。随后，HS/HS动物随机分为3个新组：维持HSD饮食的大鼠（HS/HS）；用标准饲料替代HSD的大鼠（HS/CT）；HSD替换为HPD （HS/HP）。所有组均随访12周，在此期间，我们研究了HPD对体重、能量摄入、肥胖发展、血糖/脂质谱、葡萄糖耐量、胰岛素抵抗、组织重量（脂肪组织、肝脏和骨骼肌）、脂溶活性、肝脏脂过氧化和组织学以及肝功能血清标志物的影响。断奶后暴露于HSD导致成年期代谢综合征表型，其特征为中枢性肥胖、葡萄糖耐受不良、血脂异常和胰岛素抵抗。只有HPD喂养能够恢复体重增加和脂肪组织积累，并恢复脂肪组织对交感刺激的脂溶反应。另一方面，在12周的营养干预后，无论是HPD还是退出HSD，都促进了非常相似的代谢结果。HS/HP和HS/CT大鼠空腹血清葡萄糖、甘油三酯和总胆固醇水平降低，从kITT和TyG指数值推断，这与外周胰岛素敏感性的改善相关。两种营养干预都恢复了肝脏形态功能模式，但只有HPD恢复了脂质过氧化。我们的数据显示，12周的等热量中等高蛋白饮食持续恢复高蔗糖诱导的中枢性肥胖和肥胖，以及其他重要的代谢结果的衰减，如改善与胰岛素敏感性增加和肝脂肪变性逆转相关的糖脂稳态。另一方面，单纯停止高糖摄入也促进了上述代谢结果，但对体重没有影响。本文的在线版本（10.1186/s12986-018-0290-y）包含补充材料，授权用户可使用。
Consumption of added sugars has been considered a worldwide public health concern by its association with metabolic syndrome and its comorbidities. Meanwhile, current studies have suggested high-protein diets to promote weight loss and improved metabolic outcomes. Thus, this study aimed to investigate the effects of long-term high-protein diet (HPD, 34.3% protein) intake on high-sucrose-fed rats. Weaned male Wistar rats were randomized into two groups: rats fed a standard chow (CT/CT, 10% sucrose) or rats fed a high-sucrose diet (HSD, 25% sucrose) for a 20-week observational period. Subsequently, HS/HS animals were randomized into 3 new groups: rats maintained on HSD diet (HS/HS); rats submitted to HSD replacement by standard chow (HS/CT); and those with HSD replaced by HPD (HS/HP). All groups were followed up for 12 weeks during which we investigated the effects of HPD on body weight, energy intake, obesity development, glicemic/lipid profile, glucose tolerance, insulin resistance, tissue weight (adipose tissue, liver and skeletal muscles), lipolytic activity, liver lipoperoxidation and histology, as well as serum markers of hepatic function. Post-weaning exposure to HSD led to metabolic syndrome phenotype at adulthood, herein characterized by central obesity, glucose intolerance, dyslipidaemia and insulin resistance. Only HPD feeding was able to revert weight gain and adipose tissue accumulation, as well as restore adipose tissue lipolytic response to sympathetic stimulus. On the other hand, either HPD or withdrawal from HSD promoted very similar metabolic outcomes upon 12-week nutritional intervention. HS/HP and HS/CT rats showed reduced fasting serum levels of glucose, triacylglycerol and total cholesterol, which were correlated with the improvement of peripheral insulin sensitivity, as inferred from kITT and TyG Index values. Both nutritional interventions restored liver morphofunctional patterns, but only HPD restored lipid peroxidation. Our data showed that 12-week intake of an isocaloric moderately high-protein diet consistently restored high-sucrose-induced central adiposity and obesity in addition to the attenuation of other important metabolic outcomes, such as improvement of glucolipid homeostasis associated to increased insulin sensitivity and reversal of hepatic steatosis. On the other hand, simple withdrawal from high-sucrose consumption also promoted the abovementioned metabolic outcomes with no impact on body weight. The online version of this article (10.1186/s12986-018-0290-y) contains supplementary material, which is available to authorized users.
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影响因子：
3.6
作者：
Campos-Nonato, Ismael;Hernandez, Lucia;Barquera, Simon
通讯作者：
Barquera, Simon
影响因子：
5.6
作者：
Diaz-Rua, Ruben;Keijer, Jaap;Oliver, Paula
通讯作者：
Oliver, Paula
DOI：
10.1080/07315724.2009.10719767
发表时间：
2009-04-01
影响因子：
3.5
作者：
Greenberg, Ilana;Stampfer, Meir J.;Shai, Iris
通讯作者：
Shai, Iris
影响因子：
16.2
作者：
Kahn, Richard;Sievenpiper, John L.
通讯作者：
Sievenpiper, John L.
影响因子：
3.6
作者：
Gaysinskaya, V. A.;Karatayev, O.;Leibowitz, S. F.
通讯作者：
Leibowitz, S. F.