Venu Lagishetty, Padmavathi Inagadapa J N, Kishore Yedla D, Bhanu Nandiwada V, Rao Kalashikam R, Sainath Pothaganti B, Ganeshan Manisha, Raghunath Manchala
Division of Endocrinology and Metabolism, National Institute of Nutrition, Hyderabad, India.
Obesity (Silver Spring). 2008 Jun;16(6):1270-6. doi: 10.1038/oby.2008.72. Epub 2008 Mar 27.
We investigated the long-term effects of maternal/postnatal magnesium (Mg) restriction on adiposity, glucose tolerance, and insulin secretion in the offspring and the probable biochemical mechanisms associated with them.
Female weanling Wistar/NIN (WNIN) rats received a control diet or 70% Mg-restricted (MgR) diet for 9 weeks and mated with control males. A third of the restricted dams were shifted to control diet from parturition. Half of the pups born to the remaining restricted dams were weaned on to control diet, while the other half continued on MgR diet. Various parameters were determined in the offspring at 18 months of age.
The percentage of body fat increased, lean body mass (LBM) and fat free mass (FFM) decreased in restricted offspring and were irreversible by rehabilitation. While glucose tolerance and insulin resistance (IR) were comparable among groups, glucose-stimulated insulin secretion and basal glucose uptake by the diaphragm were significantly decreased in restricted offspring and not corrected by rehabilitation. Plasma leptin was lower, and tumor necrosis factor-alpha (TNF-alpha) was higher in restricted offspring, whereas expression of fatty acid synthase (FAS) and fatty acyl transport protein 1 (FATP 1) was higher in liver and adipose tissue. While changes in FAS and FATP 1 were not correctible by rehabilitation, those in leptin and TNF-alpha were corrected by rehabilitation from parturition but not from weaning. Tissue oxidative stress and antioxidant status were comparable among groups.
Results indicate that maternal and postnatal Mg status is important in the long-term programming of body adiposity and insulin secretion in rat offspring.
我们研究了母体/产后镁（Mg）限制对后代肥胖、糖耐量和胰岛素分泌的长期影响以及与之相关的可能生化机制。
雌性断乳Wistar/NIN（WNIN）大鼠接受对照饮食或70%镁限制（MgR）饮食9周，然后与对照雄性大鼠交配。三分之一的限制饮食母鼠从分娩时开始改为对照饮食。其余限制饮食母鼠所生幼崽的一半断奶后改为对照饮食，而另一半继续食用MgR饮食。在后代18个月大时测定各种参数。
限制饮食后代的体脂百分比增加，瘦体重（LBM）和去脂体重（FFM）减少，且康复后不可逆。虽然各组之间的糖耐量和胰岛素抵抗（IR）相当，但限制饮食后代的葡萄糖刺激胰岛素分泌和膈肌基础葡萄糖摄取显著降低，且康复后未得到纠正。限制饮食后代的血浆瘦素较低，肿瘤坏死因子-α（TNF-α）较高，而肝脏和脂肪组织中脂肪酸合酶（FAS）和脂肪酸转运蛋白1（FATP 1）的表达较高。虽然FAS和FATP 1的变化康复后无法纠正，但瘦素和TNF-α的变化从分娩时开始康复可得到纠正，而从断奶时开始康复则不能纠正。各组之间组织氧化应激和抗氧化状态相当。
结果表明，母体和产后镁状态对大鼠后代身体肥胖和胰岛素分泌的长期编程很重要。
