Sato Kazusa, Arai Hidekazu, Mizuno Akira, Fukaya Makiko, Sato Tadatoshi, Koganei Megumi, Sasaki Hajime, Yamamoto Hironori, Taketani Yutaka, Doi Toshio, Takeda Eiji
Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima 770-8503, Japan.
J Nutr. 2007 Aug;137(8):1908-15. doi: 10.1093/jn/137.8.1908.
Excessive dietary intake of carbohydrates and fats has been linked to the development of obesity. However, the mechanism by which these dietary factors interact to bring about metabolic changes has not been elucidated. We examined the combined effects of different types of dietary carbohydrates and fats on the etiology of obesity and its complications in the Zucker fatty (fa/fa) rat, a model of obesity. Specifically, these rats were fed an isocaloric diet containing various combinations of carbohydrates [palatinose (P), an insulin-sparing sucrose analogue, and sucrose (S)] and fatty acids [oleic acid (O) and linoleic acid (L)]. After 8 wk, palatinose feeding (PO and PL) led to significant reductions in visceral fat mass, adipocyte cell size, hyperglycemia, and hyperlipidemia compared with sucrose feeding (SO and SL); pancreatic islet hypertrophy was also prevented by palatinose feeding. Linoleic-acid-fed rats (PL and SL) exhibited reduced insulin-immunoreactive staining of the pancreatic islets, enhanced macrophage infiltration in adipose tissue, and an elevated plasma tumor necrosis factor-alpha concentration when compared with oleic-acid-fed rats (PO and SO). Furthermore, sucrose and linoleic acid synergistically increased the expression of genes involved in hepatic gluconeogenesis and lipogenesis [sterol regulatory-element binding protein (SREBP)-1c and SREBP-2]. In conclusion, a diet containing palatinose and oleic acid may prevent diet-induced metabolic abnormalities. The combination of palatinose and oleic acid holds promise for a new approach to preventing and treating obesity and its complications.
饮食中碳水化合物和脂肪的过量摄入与肥胖的发生有关。然而，这些饮食因素相互作用导致代谢变化的机制尚未阐明。我们研究了不同类型的饮食碳水化合物和脂肪对肥胖 Zucker 脂肪（fa/fa）大鼠（一种肥胖模型）肥胖病因及其并发症的综合影响。具体而言，给这些大鼠喂食含各种碳水化合物组合[帕拉金糖（P），一种节省胰岛素的蔗糖类似物，和蔗糖（S）]以及脂肪酸[油酸（O）和亚油酸（L）]的等热量饮食。8 周后，与喂食蔗糖（SO 和 SL）相比，喂食帕拉金糖（PO 和 PL）导致内脏脂肪量、脂肪细胞大小、高血糖和高脂血症显著降低；喂食帕拉金糖还可预防胰岛肥大。与喂食油酸的大鼠（PO 和 SO）相比，喂食亚油酸的大鼠（PL 和 SL）胰岛胰岛素免疫反应性染色减少，脂肪组织中巨噬细胞浸润增强，血浆肿瘤坏死因子-α 浓度升高。此外，蔗糖和亚油酸协同增加参与肝脏糖异生和脂肪生成的基因[固醇调节元件结合蛋白（SREBP）-1c 和 SREBP-2]的表达。总之，含帕拉金糖和油酸的饮食可能预防饮食诱导的代谢异常。帕拉金糖和油酸的组合有望成为预防和治疗肥胖及其并发症的新方法。
