maternal obesity

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Maternal Obesity And Pregnancy

Author : Per Glud Ovesen
ISBN : 9783642250231
Genre : Medical
File Size : 74. 8 MB
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A dramatic and worldwide increase is occurring in the prevalence of overweight and obesity in women of childbearing age. Obese women carry a significant excess risk of a variety of serious complications during pregnancy, and in addition, maternal obesity predisposes to obesity in the offspring. This book provides a timely update on the latest knowledge on maternal obesity and pregnancy. A very wide range of issues are covered, including macrosomia and associated shoulder dystocia; the risk of miscarriage, malformations, and complications of pregnancy; the impact of hyperglycemia; clinical management; consequences for anesthesia and ultrasound; impacts on breastfeeding, fertility, and childhood obesity; and pregnancy following gastric surgery. All of the authors are recognized experts in their fields, and the book has been designed to meet the practical needs of obstetricians, gynecologists, internists, and general practitioners.

Maternal Obesity

Author : Matthew W. Gillman
ISBN : 9781107003965
Genre : Medical
File Size : 88. 35 MB
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Afflicting more than 300 million women across the globe, obesity has profound effects on health during pregnancy and on the wellbeing of the unborn child. In the face of such a challenging pandemic, this book reviews the latest research and provides up-to-date advice on clinical management. Maternal Obesity addresses the adverse effects of obesity among women of childbearing age, including infertility, medical complications, problems in labor, and adverse birth outcomes, and it reviews evidence that the obese mother's in utero environment has long-lasting influences on the health of the developing child. Chapters cover basic, clinical, and population perspectives, providing a range of valuable information from mechanistic insight through to public health and policy implications. Invaluable for obstetricians, gynaecologists, paediatricians, general and family physicians, subspecialists in obstetric and paediatric medicine, midwives, and dietitians, as well as researchers and public health policy makers seeking to tackle the burden of maternal obesity-related illness.

Folic Acid Fortification Maternal Obesity And Neural Tube

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File Size : 38. 87 MB
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Maternal Obesity Inflammation And Insulin Resistance In

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What Are The Effects Of Maternal Obesity On Synaptic Function In The Maternal And Offspring Hippocampus

Author : Denise Lau
ISBN : OCLC:860770093
Genre :
File Size : 21. 77 MB
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Obesity is a global epidemic that is associated with several adverse health consequences. In addition, there is also a growing prevalence of obesity in pregnancy. Maternal obesity places the fetus in an abnormal in utero condition that can produce alterations in development leading to permanent programming of physiological systems. Obesity is also associated with cognitive dysfunction, which calls for investigations into its effects on the hippocampus, a brain area involved in learning and memory. Long-term potentiation (LTP), a neurophysiological correlate for learning and memory, can be examined in hippocampal slices. This study aimed to fill in the gap in literature regarding the effect of obesity on hippocampal synaptic plasticity in female rats, and maternal obesity effects on offspring hippocampal synaptic plasticity. Female Sprague-Dawley rats were fed either a control diet (CD), or a high-fat diet (HFD; 40% of calories from saturated fat) for 16 weeks. Impaired glucose tolerance and greater retroperitoneal fat pad weight indicated an obese phenotype in HFD rats; as well, the modified diet led to impaired LTP: CD rats had 10% more potentiation in amplitude, and 11% more potentiation in slope than HFD rats. Offspring were weaned onto control diet at post-natal day 21. Reduced success rates for achieving LTP, and lowered magnitudes of mean LTP in the offspring, strongly suggest that maternal obesity may have compromised hippocampal synaptic plasticity, and warrants further study.

Maternal Obesity Amp Activated Protein Kinase And Fetal Skeletal Muscle Development

Author : Junfeng Tong
ISBN : 1124228772
Genre : Ewes
File Size : 76. 66 MB
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Maternal obesity during gestation programs offspring to obesity and type 2 diabetes in adulthood. Skeletal muscle is the major peripheral tissue responsive to insulin. The prenatal stage is crucial for skeletal muscle development. AMP-activated protein kinase (AMPK) is involved in both skeletal muscle development and etiology of obesity. In this study, we investigated the effects of maternal obesity on fetal skeletal muscle development, AMPK activity, and their association with fetal origins of obesity and type 2 diabetes. Using the obese pregnant ewe model, we showed that myogenesis was attenuated and the diameter of primary muscle fibers was smaller in fetal skeletal muscle born to obese dams (OB). Wingless and Int (Wnt)/[beta]-Catenin signaling pathway promotes myogenesis and inhibits adipogenesis. The Wnt/[beta]-catenin signaling was down-regulated in OB fetal muscle, which was associated with inflammatory response in fetal muscle due to maternal obesity. Moreover, AMPK activity was reduced while the expression of adipogenic marker peroxisome proliferator-activated receptor (PPAR) [gamma] was increased in OB fetal muscle. In 3T3-L1 cell lines, pharmacological activation of AMPK inhibited the expression of PPAR[gamma] and reduced the presence of adipocytes, while pharmacological inhibition of AMPK enhanced the expression of PPAR[gamma]. These data suggest that AMPK activity is inversely related to adipogenesis in fetal sheep muscle and 3T3-L1 cells. In the diet-induced obesity mouse model, we also observed the down-regulation of AMPK activity, myogenic markers, and mitochondrial content and function, while the up-regulation of PPAR[gamma] in the skeletal muscle of offspring born to obese dams (OB). Maternal metformin administration to obese mice during gestation and lactation activated AMPK activity and prevented these changes in OB offspring skeletal muscle, which suggested that maternal administration of metformin might improve OB offspring muscle function. Besides, we investigated the role of AMPK in skeletal muscle protein degradation in C2C12 myotubes. The data showed that pharmacological activation of AMPK stimulated two muscle specific ubiquitin ligases expression, indicating that acute AMPK activation may promote muscle protein degradation. In summary, our data show that maternal obesity affects fetal skeletal muscle development which has long-term effects on offspring properties, and AMPK is a key mediator affecting fetal skeletal muscle development.

Impacts Of Maternal Obesity On Reducing Leptin Signaling In The Pituitary And Its Role In Depressing The Gh Igf1 Axis Resulting In Insulin Dysregulation And Increased Adiposity In Adult Offspring

Author : Tursunjan Nurmamat
ISBN : 1303471124
Genre : Adipose tissues
File Size : 30. 63 MB
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Obesity is a major health concern, and the world is facing a global epidemic of obesity with increasing rates. It is considered a disease state in itself, but more importantly, it is also a major risk factor for other serious diseases including type II diabetes, hypertension, non-alcoholic fatty liver disease, and coronary heart disease. Currently, obesity affects more than one third of the women of reproductive age in the United States. Not only does obesity during pregnancy lead to increased maternal health concerns, it is linked to increases in adiposity and components of the metabolic syndrome in their offspring. Both human epidemiological studies and animal models of maternal obesity have provided strong evidence for the association of maternal overnutrition/obesity during pregnancy with abnormal fetal organ development, increased offspring adiposity and insulin resistance. However, the mechanisms mediating the alterations in offspring metabolic dysfunction born to obese mothers are yet to be elucidated. Leptin, a hormone mainly produced by adipocytes, is well-known for its effect on appetite control in the hypothalamus; however, recent studies suggest that it may also play important roles in the pituitary regulating body composition. This dissertation mainly focuses on the possible role of pituitary leptin signaling in mediating the phenotype of increased adult offspring adiposity and insulin resistance programmed by in utero exposure to maternal overnutrition/obesity. Further, we investigated the effect of an early pregnancy dietary intervention on both mothers and fetuses in a sheep model of maternal obesity in search of a potential intervention strategy for obese human pregnancies. In the first experiment, we evaluated the impact of maternal obesity on offspring weight gain, adiposity and insulin resistance during an ad libitum feeding trial in adulthood. We found that both male and female offspring of overnourished/obese mothers (MO) had increased appetite, weight gain, percentage body fat and insulin resistance compared with offspring born to control fed mothers (CON). Then, we evaluated the hormonal profiles of male offspring at necropsy at the end of the feeding trial, and further determined the role of leptin signaling utilizing relevant tissue samples from the male offspring. We confirmed that pituitary leptin signaling was reduced and was associated with down-regulation of the growth hormone (GH)/insulin-like growth factor 1 (IGF1) axis in MO offspring compared with CON offspring. In the second experiment, we have evaluated the effect of reducing maternal global food intake in obese pregnant ewes to a maintenance level at day 28 of gestation which is equivalent to ~day 50 in human pregnancy. The results of this study are consistent with the concept that reducing maternal diet of obese overfed ewes to requirements from early gestation can prevent subsequent alterations in fetal growth, adiposity and glucose-insulin dynamics. Given the relative importance of maternal metabolic parameters on offspring development in humans, and the similarities between our ovine model data and those from obese pregnancies in humans, we suggest that our model could potentially lead to a better understanding of the specific control mechanisms involved.

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