Feto-Maternal Consequences of Obesity in Pregnancy

Introduction: Potential ill effects of obesity in pregnancy pose a challenge encompassing many comorbidities that threaten the life and require special attention. Pregnancy is the most crucial event for women surrounded with multiple complexities. Obesity during pregnancy leads to life threatening events for mother as well as fetus. Purpose of the present study was to identify the feto-maternal outcomes of obesity during pregnancy. Methodology: An observational cross-section design was used. Non-probability convenient sampling was done to collect data from 170 women. Data related to predominated maternal problem during pregnancy and fetus birth was collected. Ethical considerations were followed. Data was analyzed through SPSS (version 24.0). Results: Findings revealed multiple consequences of obesity on both mother and fetus. Obesity was considered as a mainstay of feto-maternal complications and findings revealed a significant association (p-value <0.05). Conclusion: Obesity is a signal for many adverse feto-maternal outcomes during pregnancy that poses a challenge for both mother and fetus. It is concluded from this study that there is ample need to educate mothers regarding the hazardous consequences of obesity in pregnancy. Keywords: Fetus, Maternal, Consequences, Obesity, Pregnancy

Insulin Increases Adipose Adiponectin in Pregnancy by Inhibiting Ubiquitination and Degradation: Impact of Obesity

Context Circulating adiponectin levels are decreased in pregnant women with obesity or gestational diabetes, and this is believed to contribute to the insulin resistance and increased risk of fetal overgrowth associated with these conditions. However, the molecular mechanisms regulating adiponectin secretion from maternal adipose tissues in pregnancy are poorly understood. Objective We tested the hypothesis that obesity in pregnancy is associated with adipose tissue insulin resistance and increased adiponectin ubiquitination and degradation, caused by inflammation and endoplasmic reticulum (ER) stress. Methods Visceral adipose tissues were collected from lean and obese pregnant humans and mice. Total and ubiquitinated adiponectin, and markers of inflammation, ER stress, and insulin resistance were examined in adipose tissues. The role of insulin, inflammation, and ER stress in mediating adiponectin ubiquitination and degradation was examined using 3T3L-1 adipocytes. Results Obesity in pregnancy is associated with adipose tissue inflammation, ER stress, insulin resistance, increased adiponectin ubiquitination, and decreased total abundance of adiponectin. Adiponectin ubiquitination was increased in visceral fat of obese pregnant women as compared to lean pregnant women. We further observed that insulin prevents, whereas ER stress and inflammation promote, adiponectin ubiquitination and degradation in differentiated 3T3-L1 adipocytes. Conclusion We have identified adiponectin ubiquitination as a key mechanism by which obesity diminishes adiponectin secretion in pregnancy. This information will help us better understand the mechanisms controlling maternal insulin resistance and fetal growth in pregnancy and may provide a foundation for the development of strategies aimed at improving adiponectin production in pregnant women with obesity or gestational diabetes.

Overweight and obesity in pregnancy: their impact on epigenetics

Over the last few decades, the prevalence of obesity has risen to epidemic proportions worldwide. Consequently, the number of obesity in pregnancy has risen drastically. Gestational overweight and obesity are associated with impaired outcomes for mother and child. Furthermore, studies show that maternal obesity can lead to long-term consequences in the offspring, increasing the risk for obesity and cardiometabolic disease in later life. In addition to genetic mechanisms, mounting evidence demonstrates the induction of epigenetic alterations by maternal obesity, which can affect the offspring’s phenotype, thereby influencing the later risk of obesity and cardiometabolic disease. Clear evidence in this regard comes from various animal models of maternal obesity. Evidence derived from clinical studies remains limited. The current article gives an overview of pathophysiological changes associated with maternal obesity and their consequences on placental structure and function. Furthermore, a short excurse is given on epigenetic mechanisms and emerging data regarding a putative interaction between metabolism and epigenetics. Finally, a summary of important findings of animal and clinical studies investigating maternal obesity-related epigenetic effects is presented also addressing current limitations of clinical studies.