MRC Versus Arthritis Centre for Musculoskeletal Ageing Research, School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom.
School of Biosciences, University of Birmingham, Birmingham, United Kingdom.
Clin Nutr. 2022 Aug;41(8):1623-1635. doi: 10.1016/j.clnu.2022.06.022. Epub 2022 Jun 16.
Obesity and insulin resistance are associated with an impaired sensitivity to anabolic stimuli such as dietary protein (anabolic resistance). Omega-3 polyunsaturated fatty acids (n-3 PUFA) may be protective against the deleterious effects of saturated fatty acids (SFA) on insulin resistance. However, the contribution of excess fat consumption to anabolic and insulin resistance and the interaction between SFA and n-3 PUFA is not well studied.
The primary aim of this study was to investigate the effects of an oral fat pre-load, with or without the partial substitution of SFA with fish oil (FO)-derived n-3 PUFA, on indices of insulin and anabolic sensitivity in response to subsequent dietary protein and carbohydrate (dextrose) co-ingestion.
Eight middle-aged males with overweight or obesity (52.8 ± 2.0 yr, BMI 31.8 ± 1.4 kg·m) ingested either an SFA, or isoenergetic SFA and FO emulsion (FO), or water/control (Con), 4 h prior to a bolus of milk protein and dextrose.
Lipid ingestion (in particular FO) impaired the early postprandial uptake of branched chain amino acids (BCAA) into the skeletal muscle in response to protein and dextrose, and attenuated the peak glycaemic response, but was not accompanied by differences in whole body (Matsuda Index: Con: 4.66 ± 0.89, SFA: 5.10 ± 0.94 and FO: 4.07 ± 0.59) or peripheral (forearm glucose AUC: Con: 521.7 ± 101.7; SFA: 470.2 ± 125.5 and FO: 495.3 ± 101.6 μmol·min·100 g lean mass·min [t = 240-420 min]) insulin sensitivity between visits. Postprandial whole body fat oxidation was affected by visit (P = 0.024) with elevated rates in SFA and FO, relative to Con (1.85 ± 0.55; 2.19 ± 0.21 and 0.65 ± 0.35 kJ·h·kg lean body mass, respectively), however muscle uptake of free fatty acids (FFA) was unaffected.
Oral lipid preloads, consisting of SFA and FO, impair the early postprandial BCAA uptake into skeletal muscle, which occurs independent of changes in insulin sensitivity.
ClinicalTrials.gov Identifier NCT03146286.
肥胖和胰岛素抵抗与对合成代谢刺激(如膳食蛋白质)的敏感性降低有关(合成代谢抵抗)。ω-3 多不饱和脂肪酸(n-3PUFA)可能对饱和脂肪酸(SFA)对胰岛素抵抗的有害影响具有保护作用。然而,过量脂肪摄入对合成代谢和胰岛素抵抗的贡献以及 SFA 和 n-3PUFA 之间的相互作用尚未得到很好的研究。
本研究的主要目的是研究口服脂肪负荷,无论是否用鱼油(FO)衍生的 n-3PUFA 部分替代 SFA,对随后摄入蛋白质和碳水化合物(葡萄糖)时胰岛素和合成代谢敏感性的影响。
8 名超重或肥胖的中年男性(52.8±2.0 岁,BMI 31.8±1.4kg·m)在摄入 SFA 或等热量 SFA 和 FO 乳液(FO)或水/对照(Con)4 小时后,摄入牛奶蛋白和葡萄糖。
脂质摄入(特别是 FO)损害了蛋白质和葡萄糖摄入后支链氨基酸(BCAA)在骨骼肌中的早期餐后摄取,并减弱了血糖峰值反应,但全身(Matsuda 指数:Con:4.66±0.89,SFA:5.10±0.94 和 FO:4.07±0.59)或外周(前臂葡萄糖 AUC:Con:521.7±101.7;SFA:470.2±125.5 和 FO:495.3±101.6μmol·min·100g 瘦体重·min[t=240-420min])胰岛素敏感性在各次访问之间没有差异。餐后全身脂肪氧化受访问影响(P=0.024),SFA 和 FO 相对 Con(1.85±0.55;2.19±0.21 和 0.65±0.35kJ·h·kg 瘦体重)升高,然而游离脂肪酸(FFA)的肌肉摄取不受影响。
由 SFA 和 FO 组成的口服脂质预负荷会损害餐后早期骨骼肌中 BCAA 的摄取,这与胰岛素敏感性的变化无关。
ClinicalTrials.gov 标识符 NCT03146286。