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膳食镁可预防果糖诱导的大鼠胰岛素抵抗。

Dietary magnesium prevents fructose-induced insulin insensitivity in rats.

作者信息

Balon T W, Jasman A, Scott S, Meehan W P, Rude R K, Nadler J L

机构信息

Department of Diabetes, Endocrinology, and Metabolism, City of Hope National Medical Center, Duarte, CA 91010.

出版信息

Hypertension. 1994 Jun;23(6 Pt 2):1036-9. doi: 10.1161/01.hyp.23.6.1036.

DOI:10.1161/01.hyp.23.6.1036
PMID:8206589
Abstract

Increased dietary fructose may produce insulin insensitivity and elevate blood pressure in rats. It is possible that the reduced magnesium content of the high-fructose commercial diet used in some studies may play a role in these abnormalities because it is known that magnesium deficiency can produce insulin insensitivity and increased angiotensin II action in humans. To study this, we maintained rats for 9 weeks on either a normal control diet, a standard high-fructose diet, or the same high-fructose diet supplemented with magnesium. Glucose uptake was assessed using a perfused rat hindquarter preparation sequentially with 0, 900, and 120,000 pmol/L of added insulin. Basal serum glucose, plasma insulin, and basal glucose uptake in the absence of insulin were similar among all three groups. However, insulin sensitivity, defined as glucose uptake in the presence of 900 pmol/L insulin minus basal, was depressed in the high-fructose compared with the control group (1.02 +/- 0.38 to 1.77 +/- 0.57 mumol/g per hour, P < .05). In contrast, the high-fructose group supplemented with normal magnesium had similar insulin sensitivity as the control group (2.09 +/- 0.69 mumol/g per hour). Total serum magnesium was reduced in the high-fructose group compared with control or high-fructose plus magnesium-supplemented groups. Blood pressure and fasting insulin levels were also lower in the magnesium-supplemented group. These results suggest that magnesium deficiency and not fructose ingestion per se leads to insulin insensitivity in skeletal muscle and changes in blood pressure.

摘要

饮食中果糖增加可能会使大鼠产生胰岛素抵抗并升高血压。一些研究中使用的高果糖商业饮食中镁含量降低,这可能在这些异常情况中起作用,因为已知镁缺乏会导致人类胰岛素抵抗和血管紧张素II作用增强。为了研究这一点,我们将大鼠分别用正常对照饮食、标准高果糖饮食或添加镁的相同高果糖饮食喂养9周。使用灌注大鼠后肢标本,依次加入0、900和120,000 pmol/L胰岛素来评估葡萄糖摄取。三组大鼠的基础血清葡萄糖、血浆胰岛素以及无胰岛素时的基础葡萄糖摄取情况相似。然而,与对照组相比,高果糖组在900 pmol/L胰岛素存在下的葡萄糖摄取量减去基础值所定义的胰岛素敏感性降低(从1.77±0.57 μmol/g每小时降至1.02±0.38 μmol/g每小时,P <.05)。相比之下,补充正常镁的高果糖组具有与对照组相似的胰岛素敏感性(2.09±0.69 μmol/g每小时)。与对照组或补充镁的高果糖组相比,高果糖组的总血清镁降低。补充镁的组血压和空腹胰岛素水平也较低。这些结果表明,镁缺乏而非果糖摄入本身导致骨骼肌胰岛素抵抗和血压变化。

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