Department of Production Animal Health, Faculty of Veterinary Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada.
Gastrointestinal Research Group, Snyder Institute for Chronic Diseases, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada.
Mol Nutr Food Res. 2019 Nov;63(21):e1900088. doi: 10.1002/mnfr.201900088. Epub 2019 Aug 7.
Dietary protein restriction elicits hyperphagia and increases energy expenditure; however, less is known of whether these responses are a consequence of increasing carbohydrate content. The effects of protein-diluted diets with fixed carbohydrate content on energy balance, hormones, and key markers of protein sensing and thermogenesis in tissues are determined.
Obesity-prone rats (n = 13-16 per group) are randomized to diets containing fixed carbohydrate (52% calories) and varying protein concentrations: 15% (control), 10% (mild protein restriction), 5% (moderate protein restriction) or 1% (severe protein restriction) protein calories, or protein-matched to 5% protein, for 21 days. Propranolol and ondansetron are administered to interrogate the roles of sympathetic and serotonergic systems, respectively, in diet-induced changes in energy expenditure. It is found that mild-to-moderate protein restriction promotes transient hyperphagia, whereas severe protein restriction induces hypophagia, with alterations in meal patterns. Protein restriction enhances energy expenditure that is partly attenuated by propranolol, but not ondansetron. Moderate to severe protein restriction decreases gains in body weight, lean and fat mass, decreased postprandial glucose and leptin, but increased fibroblast growth factor-21 concentrations. Protein-matching retains lean mass suggesting that intake of dietary protein, but not calories, is important for preserving lean mass. Notably, protein restriction increases the protein and/or transcript abundance of key amino acid sensing molecules in liver and intestine (PERK, eIF2α, ATF2, CHOP, 4EBP1, FGF21), and upregulated thermogenic markers (β2AR, Klotho, HADH, UCP-1) in brown adipose tissue.
Low-protein diets promote hyperphagia and sympathetically mediated increase in energy expenditure, prevent gains in tissue reserves, and concurrently upregulate hepatic and intestinal amino acid sensing intermediaries and thermogenic markers in brown adipose tissue.
限制膳食蛋白质会引起多食和增加能量消耗；然而，对于这些反应是否是由于碳水化合物含量增加的结果，了解较少。本研究旨在确定固定碳水化合物含量的蛋白质稀释饮食对能量平衡、激素以及组织中蛋白质感知和产热关键标志物的影响。
将肥胖易感大鼠（每组 13-16 只）随机分为含有固定碳水化合物（52%卡路里）和不同蛋白质浓度的饮食：15%（对照）、10%（轻度蛋白质限制）、5%（中度蛋白质限制）或 1%（重度蛋白质限制）蛋白质卡路里，或与 5%蛋白质相匹配的蛋白质，持续 21 天。给予普萘洛尔和昂丹司琼分别探究交感和 5-羟色胺能系统在饮食引起的能量消耗变化中的作用。结果发现，轻度至中度蛋白质限制会促进短暂的多食，而重度蛋白质限制会引起食欲减退，并改变进食模式。蛋白质限制会增加能量消耗，而普萘洛尔可部分减弱这种作用，但昂丹司琼则无影响。中到重度蛋白质限制会减少体重、瘦体重和脂肪量的增加，降低餐后血糖和瘦素水平，但增加成纤维细胞生长因子 21 浓度。蛋白质匹配保留瘦体重，表明摄入蛋白质而不是卡路里对维持瘦体重很重要。值得注意的是，蛋白质限制会增加肝脏和肠道中关键氨基酸感应分子（PERK、eIF2α、ATF2、CHOP、4EBP1、FGF21）的蛋白和/或转录丰度，并上调棕色脂肪组织中的产热标志物（β2AR、Klotho、HADH、UCP-1）。
低蛋白饮食会促进多食和交感神经介导的能量消耗增加，防止组织储备增加，同时上调肝脏和肠道中的氨基酸感应中间产物和棕色脂肪组织中的产热标志物。
