Altered adipose tissue metabolism in offspring of dietary obese rat dams
Altered adipose tissue metabolism in offspring of dietary obese rat dams
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DOI：
10.1042/cs20100534
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发表时间：
2011-07-01
期刊：
影响因子：
6
通讯作者：
Narce, Michel
中科院分区：
文献类型：
--
作者：
Benkalfat, Nassira Batoul;Merzouk, Hafida;Narce, Michel
为了进一步研究发育规划的机制，我们分析了母亲营养过剩和产后高脂肪喂养对后代脂肪组织代谢的影响。在妊娠期和哺乳期，断奶后继续标准饲料或自助式饮食，测定食堂饮食喂养的母鼠的后代血清脂联素、瘦素和 TAG [三酰甘油（甘油三酯）] 水平、脂肪组织 TAG、脂肪酸和酶活性的出生后变化。与断奶时（第 21 天）和成年期的对照幼鼠相比，肥胖大鼠的肥胖程度更高（+35% 至 85%），血清葡萄糖、胰岛素、瘦素、脂联素和 TAG 水平显着升高（P < 0.01），脂肪组织 LPL（脂蛋白脂肪酶）和 GPDH（3-磷酸甘油脱氢酶）活性显着升高（P < 0.01） （第 90 天）。脂肪HSL（激素敏感性脂肪酶）活性仅在第90天时增加（P < 0.05），而FAS（脂肪酸合酶）活性保持不变。与对照组相比，肥胖幼仔血清和脂肪TAG中SFA（饱和脂肪酸）和MUFA（单不饱和脂肪酸）的比例以及Delta（9）去饱和指数显着增加（P < 0.05），而PUFA（多不饱和脂肪酸）则减少（P < 0.01）。断奶时的食堂饮食导致肥胖大鼠出现更严重的异常。总之，母亲营养过剩会导致后代脂肪组织代谢发生永久性变化。从断奶到成年，后代的这些预先存在的改变在高脂肪饮食下变得更加恶化。因此，脂肪因子和酶可以提供潜在的治疗靶点，并且该领域的新研究可以构成改善早期营养过剩影响的策略。
To investigate further the mechanisms of developmental programming, we analysed the effects of maternal overnutrition and of postnatal high-fat feeding on adipose tissue metabolism in the offspring. Postnatal changes in serum adiponectin, leptin and TAG [triacylglycerol (triglyceride)] levels, adipose tissue TAGs, fatty acids and enzyme activities were determined in offspring of cafeteria-diet-fed dams during gestation and lactation, weaned on to standard chow or on to cafeteria diet. Obese rats showed higher adiposity (+35% to 85%) as well as a significant increase in serum glucose, insulin, leptin, adiponectin and TAG levels (P < 0.01) and adipose tissue LPL (lipoprotein lipase) and GPDH (glycerol-3-phosphate dehydrogenase) activities (P < 0.01), compared with control pups at weaning (day 21) and at adulthood (day 90). Adipose HSL (hormone-sensitive lipase) activity was increased only at day 90 (P < 0.05), and FAS (fatty acid synthase) activity remained unchanged. The proportions of SFAs (saturated fatty acids) and MUFAs (mono-unsaturated fatty acids) and the Delta(9)-desaturation index were significantly increased (P < 0.05), whereas PUFAs (polyunsaturated fatty acids) were decreased (P < 0.01) in serum and adipose TAGs of obese pups compared with controls. The cafeteria diet at weaning induced more severe abnormalities in obese rats. In conclusion, maternal overnutrition induced permanent changes in adipose tissue metabolism of the offspring. These pre-existing alterations in offspring were worsened under a high-fat diet from weaning to adulthood. Consequently, adipose adipokines and enzymes could provide a potential therapeutic target, and new investigations in this field could constitute strategies to improve the impact of early-life overnutrition.