Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA.
Nutrients. 2013 Aug 21;5(8):3311-28. doi: 10.3390/nu5083311.
Methylglyoxal is a precursor to advanced glycation endproducts that may contribute to diabetes and its cardiovascular-related complications. Methylglyoxal is successively catabolized to D-lactate by glyoxalase-1 and glyoxalase-2. The objective of this study was to determine whether dietary fructose and green tea extract (GTE) differentially regulate methylglyoxal accumulation in liver and adipose, mediated by tissue-specific differences in the glyoxalase system. We fed six week old male Sprague-Dawley rats a low-fructose diet (10% w/w) or a high-fructose diet (60% w/w) containing no GTE or GTE at 0.5% or 1.0% for nine weeks. Fructose-fed rats had higher (P < 0.05) adipose methylglyoxal, but GTE had no effect. Plasma and hepatic methylglyoxal were unaffected by fructose and GTE. Fructose and GTE also had no effect on the expression or activity of glyoxalase-1 and glyoxalase-2 at liver or adipose. Regardless of diet, adipose glyoxalase-2 activity was 10.8-times lower (P < 0.05) than adipose glyoxalase-1 activity and 5.9-times lower than liver glyoxalase-2 activity. Adipose glyoxalase-2 activity was also inversely related to adipose methylglyoxal (r = -0.61; P < 0.05). These findings suggest that fructose-mediated adipose methylglyoxal accumulation is independent of GTE supplementation and that its preferential accumulation in adipose compared to liver is due to low constitutive expression of glyoxalase-2.
甲基乙二醛是糖基化终产物的前体，可能导致糖尿病及其心血管相关并发症。甲基乙二醛被相继分解为 D-乳酸，由 1 型和 2 型醛糖酶完成。本研究旨在确定膳食果糖和绿茶提取物（GTE）是否通过组织中醛糖酶系统的特异性差异，对肝脏和脂肪组织中甲基乙二醛的积累产生不同的调节作用。我们用 9 周的时间，用不含 GTE 或含 0.5%或 1.0%GTE 的低果糖（10%w/w）或高果糖（60%w/w）饲料喂养 6 周龄雄性 Sprague-Dawley 大鼠。果糖喂养的大鼠脂肪中甲基乙二醛含量较高（P<0.05），但 GTE 没有影响。果糖和 GTE 对血浆和肝甲基乙二醛也没有影响。果糖和 GTE 也未影响肝脏和脂肪中 1 型和 2 型醛糖酶的表达或活性。无论饮食如何，脂肪中的 2 型醛糖酶活性比 1 型低 10.8 倍（P<0.05），比肝脏中的 2 型低 5.9 倍。脂肪中的 2 型醛糖酶活性与脂肪中的甲基乙二醛呈负相关（r=-0.61；P<0.05）。这些发现表明，果糖介导的脂肪甲基乙二醛积累与 GTE 补充无关，其在脂肪中的优先积累与肝脏相比，是由于其 2 型醛糖酶的低组成性表达。
