Unknown,Transcriptomics,Genomics,Proteomics

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Leptin and the Placental Response to Maternal Food Restriction during Early Pregnancy

ABSTRACT: Concentrations of leptin decline during food restriction. This study was designed to test the hypothesis that some of the effects of maternal food restriction on placental development are mediated by the loss of leptin. Mice were randomized to 3 treatment groups on day 1.5 of pregnancy: (1) ad libitum fed (control) (2) 50% food restriction (restricted) (3) 50% food restriction with leptin replacement (1Âµg/g body weight/day) (leptin). On day 11.5 placentas were collected, and two placentas from each mother were pooled for microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Laura Schulz

PROVIDER: E-GEOD-38095 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Leptin and the placental response to maternal food restriction during early pregnancy in mice.

Schulz Laura Clamon LC Schlitt Jessica M JM Caesar Gerialisa G Pennington Kathleen A KA

Biology of reproduction 20121116 5

Several studies have demonstrated that maternal undernutrition or overnutrition during pregnancy can have negative consequences for the health of children born to these pregnancies, but the physiological mechanisms by which this occurs are not completely understood. During periods of food restriction, concentrations of leptin decline, whereas leptin is elevated in obesity, suggesting that it may play a role in the response to altered nutrition during pregnancy. This study compares placental deve ...[more]

PMID: 22993381

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Project description:Caloric Restriction in Leptin Deficiency Worsens Myocardial Steatosis: Failure to Upregulate PPAR gamma and Thermogenic Glyecrolipid/Fatty Acid Cycling Growing evidence supports an anti-lipotoxic role for leptin in preventing inappropriate peripheral tissue lipid deposition. Obese, leptin deficient ob/ob mice develop left ventricular (LV) hypertrophy and myocardial steatosis with increased apoptosis and decreased longevity. Here we investigated the cardiac effects of caloric restriction in leptin deficiency. Echocardiography was performed on C57Bl/6 wild-type mice (WT) and 7-month-old ob/ob mice fed ad lib, leptin-repleted (LR-ob/ob), or calorie-restricted (CR-ob/ob) for four weeks. Ventricular tissue was examined by electron microscopy (EM), mitochondrial coupling assay, and microarray expression profiling. LR and CR-ob/ob mice showed decreased body weight, heart weight, and LV wall thickness compared to ad lib ob/ob mice. LV fractional shortening was decreased in ad lib ob/ob mice, but restored to WT levels in LR and CR groups. However, EM revealed severe cardiac steatosis in the CR-ob/ob group compared to only moderate steatosis in ad lib ob/ob . Despite marked cardiac steatosis, CR (like LR) restored mitochondrial coupling to WT levels. CR up-regulated genes associated with oxidative stress and cell death, changes suggestive of cardiac lipotoxicity. LR, but not CR was shown to induce core genes involved in glycerolipid/free fatty acid cycling, a highly thermogenic pathway that can reduce intracellular lipid stores. LR, but not CR up-regulated and restored PGC1 and PPARto wild type levels; CR paradoxically further suppressed cardiac PPAR. Thus, leptin is essential in protecting the heart from lipotoxicity, and the inability to up-regulate the thermogenic glycerolipid/free fatty acid cycling pathway may impair the response of leptin deficient animals to the lipotoxic stress of calorie restriction. 6 month aged ob/ob mice were either leptin repleted with osmotic mini-pumps, calorie restricted to match the caloric intake of the leptin repleted mice, or fed ad lib for one month. 6-8 month C57Bl/6J mice were aged to serve as controls.

Dataset Information

Leptin and the Placental Response to Maternal Food Restriction during Early Pregnancy

Publications

Leptin and the placental response to maternal food restriction during early pregnancy in mice.

Similar Datasets

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