Hovland Anders, Nestvold Torunn, Bohov Pavol, Trøseid Marius, Aukrust Pål, Berge Rolf K, Waage-Nielsen Erik, Retterstøl Kjetil, Lappegård Knut Tore
a Coronary Care Unit, Division of Internal Medicine , Nordland Hospital , Bodø , Norway.
b Department of Clinical Medicine , University of Tromsø , Tromsø , Norway.
Scand J Clin Lab Invest. 2017 Dec;77(8):628-633. doi: 10.1080/00365513.2017.1393691. Epub 2017 Oct 25.
Obesity is a global pandemic leading to increased mortality and increased risk of cardiovascular disease. Bariatric surgery is an established treatment of obesity leading to weight loss and reduction of mortality. To further elucidate how bariatric surgery improves metabolic control, we explored the fatty acid (FA) profiles in morbidly obese subjects treated with lifestyle intervention and subsequent bariatric surgery.
The intervention group consisted of 34 morbidly obese patients scheduled for bariatric surgery and the control group of 17 non-obese patients scheduled for elective laparoscopic procedures. The intervention group had to undergo lifestyle changes preoperatively. Fasting blood samples were drawn at admission, after lifestyle intervention and 1 year after bariatric surgery.
At admission, the morbidly obese patients had significantly higher levels of monounsaturated FAs (MUFAs) and lower levels of n-6 polyunsaturated FAs (PUFAs) and n-3 PUFAs than healthy controls (all p-values <.05). In the intervention group, there was a significantly lower level of total FAs after lifestyle intervention, and from admission to 1 year after surgical intervention (both, p < .05), primarily reflecting a lower proportion of saturated FAs (SFAs). Following bariatric surgery, but not after lifestyle changes, there was an increase in the proportion of n-3 PUFA (p < .05) reaching levels not significantly different from healthy controls.
Our findings suggest that a reduced proportion of the proposed anti-atherogenic n-3 PUFAs characterizes morbidly obese individuals, and that this FA profile is reversed by bariatric surgery, but not by lifestyle intervention.
肥胖是一种全球性流行病，会导致死亡率上升和心血管疾病风险增加。减肥手术是一种公认的肥胖治疗方法，可导致体重减轻和死亡率降低。为了进一步阐明减肥手术如何改善代谢控制，我们研究了接受生活方式干预及随后减肥手术的病态肥胖受试者的脂肪酸（FA）谱。
干预组由34例计划接受减肥手术的病态肥胖患者组成，对照组由17例计划接受择期腹腔镜手术的非肥胖患者组成。干预组患者术前必须进行生活方式改变。在入院时、生活方式干预后以及减肥手术后1年采集空腹血样。
入院时，病态肥胖患者的单不饱和脂肪酸（MUFA）水平显著高于健康对照组，而n-6多不饱和脂肪酸（PUFA）和n-3 PUFA水平低于健康对照组（所有p值均<.05）。在干预组中，生活方式干预后总脂肪酸水平显著降低，从入院到手术干预后1年（均p <.05），主要反映饱和脂肪酸（SFA）比例降低。减肥手术后，而非生活方式改变后，n-3 PUFA比例增加（p <.05），达到与健康对照组无显著差异的水平。
我们的研究结果表明，病态肥胖个体的特征是具有抗动脉粥样硬化作用的n-3 PUFA比例降低，并且这种脂肪酸谱通过减肥手术得到逆转，但生活方式干预不能逆转。
