Noto Amy, Zahradka Peter, Ryz Natasha R, Yurkova Natalia, Xie Xueping, Taylor Carla G
Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, MB, Canada R3T 2N2.
Metabolism. 2007 Jan;56(1):142-51. doi: 10.1016/j.metabol.2006.09.009.
Pancreatic preservation is an important part of diabetes management that may occur with improved peripheral insulin sensitivity and attenuated low-grade adipose tissue inflammation. The objective of the current study was to determine the response of obese, insulin-resistant fa/fa Zucker rats vs lean controls to dietary conjugated linoleic acid (CLA) supplementation with respect to pancreatic islet size, insulin resistance, and markers of inflammation and adipose glucose uptake. Six-week-old fa/fa and lean Zucker rats (n = 20 per genotype) were fed either a 1.5% CLA mixture or control diet for 8 weeks. Oral glucose tolerance testing was conducted at 7.5 weeks. Fasting serum haptoglobin, insulin, and C-peptide were assayed, and select messenger RNA (mRNA) and protein markers of inflammation and glucose metabolism were measured in adipose and liver tissues. CLA-fed fa/fa Zucker rats had smaller islet cell size, improved oral glucose tolerance and insulinemia, and attenuated serum haptoglobin levels compared with control-fed fa/fa Zucker rats, despite no differences in body weight and a slightly higher visceral adipose mass. CLA did not alter insulin sensitivity or islet size in lean Zucker rats. The CLA-fed fa/fa rats also had greater adipose glucose transporter-4 mRNA and less adipose tumor necrosis factor alpha mRNA and protein compared with control-fed fa/fa rats. In contrast, other markers of inflammation and glucose metabolism including adipose macrophage inflammatory factor, macrophage inflammatory protein-2, and liver pyruvate carboxylase and pyruvate dehydrogenase kinase 4 were not significantly changed. These results suggest that CLA supplementation preserved pancreatic function in conjunction with improved peripheral glucose use and reduced inflammation in fa/fa Zucker rats.
胰腺保护是糖尿病管理的重要组成部分，可能随着外周胰岛素敏感性的提高和低度脂肪组织炎症的减轻而出现。本研究的目的是确定肥胖、胰岛素抵抗的fa/fa Zucker大鼠与瘦对照大鼠在补充膳食共轭亚油酸（CLA）后，在胰岛大小、胰岛素抵抗、炎症标志物和脂肪组织葡萄糖摄取方面的反应。六周龄的fa/fa和瘦Zucker大鼠（每种基因型n = 20）被喂食1.5%的CLA混合物或对照饮食8周。在7.5周时进行口服葡萄糖耐量测试。测定空腹血清触珠蛋白、胰岛素和C肽，并测量脂肪和肝脏组织中炎症和葡萄糖代谢的选定信使核糖核酸（mRNA）和蛋白质标志物。与喂食对照饮食的fa/fa Zucker大鼠相比，喂食CLA的fa/fa Zucker大鼠胰岛细胞尺寸更小，口服葡萄糖耐量和胰岛素血症得到改善，血清触珠蛋白水平降低，尽管体重没有差异且内脏脂肪量略高。CLA并未改变瘦Zucker大鼠的胰岛素敏感性或胰岛大小。与喂食对照饮食的fa/fa大鼠相比，喂食CLA的fa/fa大鼠脂肪组织葡萄糖转运蛋白4 mRNA含量更高，脂肪组织肿瘤坏死因子α mRNA和蛋白质含量更低。相比之下，其他炎症和葡萄糖代谢标志物，包括脂肪巨噬细胞炎症因子、巨噬细胞炎症蛋白-2以及肝脏丙酮酸羧化酶和丙酮酸脱氢酶激酶4，没有显著变化。这些结果表明，补充CLA可保护胰腺功能，同时改善fa/fa Zucker大鼠的外周葡萄糖利用并减轻炎症。
