Maternal nutritional history predicts obesity in adult offspring independent of postnatal diet
Maternal nutritional history predicts obesity in adult offspring independent of postnatal diet
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DOI：
10.1113/jphysiol.2008.163477
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发表时间：
2009-02-15
影响因子：
5.5
通讯作者：
Vickers, M. H.
中科院分区：
文献类型：
--
作者：
Howie, G. J.;Sloboda, D. M.;Vickers, M. H.
母体营养的显著改变可能会导致后代的长期代谢后果，特别是肥胖、瘦素和胰岛素抵抗。尽管在这种情况下，孕产妇营养缺乏已经得到了很好的描述，但关于高脂肪（HF）营养对下一代有何影响的数据相对较少。本研究调查了母体HF营养在整个母亲生命期（包括妊娠期和哺乳期）或仅限于妊娠期和哺乳期的HF营养对雄性和雌性后代生长和代谢参数的影响。将未交配过的Wistar大鼠分配到三个实验组之一：（1）对照组（Cont）：母鼠在其一生中以及整个妊娠期和哺乳期饲喂标准食物饮食;（2）母体高脂肪（MHF）组：母鼠从断奶直至整个妊娠期和哺乳期饲喂HF饮食;以及（3）妊娠期和哺乳期高脂肪（PLHF）：母鼠在其整个生命期内饲喂普通饲料直至受孕，然后在整个妊娠期和哺乳期内饲喂HF饲料。断奶时，在研究的剩余时间（160天）内，所有后代均喂食普通饲料或HF饲料。两组间的窝仔数和性别比无显著差异。与对照组后代相比，MHF和PLHF后代的体重显著降低，出生时为低瘦素血症和低胰岛素血症。然而，作为成年人，普通饲料喂养的MHF和PLHF后代比对照后代显著更肥胖（在第150天进行DEXA扫描，对于母体HF饮食，P < 0.001）。正如预期的那样，断奶后HF饮食导致所有组的肥胖增加;然而，MHF和PLHF后代总是比Cont后代显着更肥胖。高胰岛素血症和高瘦素血症抑制了MHF和PLHF后代的肥胖增加（P < 0.001; MHF和PLHF vs Cont）。值得注意的是，一生的HF营养产生了类似的后代表型，HF营养仅限于妊娠和哺乳期，因此表明母体HF营养的产后后遗症发生独立于孕前饮食。这些数据进一步强化了母体营养在这些关键发育窗口期的重要性，并表明母体HF喂养可完全独立于出生后营养诱导雄性和雌性后代明显肥胖表型。
Significant alterations in maternal nutrition may induce long-term metabolic consequences in offspring, in particular obesity and leptin and insulin resistance. Although maternal nutrient deprivation has been well characterized in this context, there is a relative paucity of data on how high fat (HF) nutrition impacts on the subsequent generation. The present study investigated the effects of maternal HF nutrition either throughout the mother's life up to and including pregnancy and lactation or HF nutrition restricted to pregnancy and lactation, on growth and metabolic parameters in male and female offspring. Virgin Wistar rats were assigned to one of three experimental groups: (1) controls (Cont): dams fed a standard chow diet throughout their life and throughout pregnancy and lactation; (2) maternal high fat (MHF) group: dams fed a HF diet from weaning up to and throughout pregnancy and lactation; and (3) pregnancy and lactation high fat (PLHF): dams fed a chow diet through their life until conception and then fed a HF diet throughout pregnancy and lactation. At weaning, all offspring were fed either a chow or HF diet for the remainder of the study (160 days). Litter size and sex ratios were not significantly different between the groups. MHF and PLHF offspring had significantly lower body weights and were hypoleptinaemic and hypoinsulinaemic at birth compared to Cont offspring. As adults however, chow-fed MHF and PLHF offspring were significantly more obese than Cont offspring (DEXA scanning at day 150, P < 0.001 for maternal HF diet). As expected a postweaning HF diet resulted in increased adiposity in all groups; MHF and PLHF offspring, however, always remained significantly more obese than Cont offspring. Increased adiposity in MHF and PLHF offspring was paralleled by hyperinsulinaemia and hyperleptinaemia (P < 0.001; MHF and PLHF versus Cont). It is of interest that a lifetime of HF nutrition produced a similar offspring phenotype to HF nutrition restricted to pregnancy and lactation alone, thus suggesting that the postnatal sequelae of maternal HF nutrition occurs independent of preconceptional diet. These data further reinforce the importance of maternal nutrition during these critical windows of development and show that maternal HF feeding can induce a markedly obese phenotype in male and female offspring completely independent of postnatal nutrition.