View clinical trials related to Lipid Profile.
Filter by:Lipid profile of full-term infants on different regimens. The aim of the study is to compare infant's lipid profiles on different feeding regimen during the first 6 months of life and its correlation with their mothers' lipid profiles (exclusive breastfeeding and mixed feeding) and to compare infants' lipid profiles on different feeding regimen with each other (including those on exclusive formula feeding).
Obese women have a higher prevalence of infertility than their lean counterparts. Obesity is a risk factor for anovulation , including in response to gonadotropin treatment .Further, even in women who are cycling regularly, obesity is associated with increased time-to-pregnancy and decreased chance of natural pregnancy. During obesity or periods of overnutrition, lipid accumulates in nonadipose tissues, notably skeletal muscle, liver, heart, and pancreas due to cellular uptake of exogenous fatty acids, triglycerides, and cholesterol as well as de novo lipogenesis in response to elevated glucose. The accumulation of intracellular lipid leads to high levels of free fatty acids that are subject to oxidative damage and the formation of cytotoxic and highly reactive lipid peroxides, which ultimately are detrimental to intracellular organelles, particularly the endoplasmic reticulum (ER) and mitochondria. Exposure of the ER to high levels of free fatty acids and lipid peroxides causes structural alterations that perturb ER function and lead to accumulation of unfolded proteins and calcium release. Failure of the UPR to reestablish ER homeostasis can lead to apoptosis .When mitochondria are exposed to high levels of free fatty acids, these can become oxidized by mitochondrial reactive oxygen species, forming lipid peroxides that damage essential proteins and uncouple mitochondrial function. This results in mitochondrial damage, which can cause further accumulation of lipids that cannot be catabolized, disrupted cellular homeostasis, and ultimately apoptosis . The cellular mechanisms by which obesity causes decreased conception rates are not known. Based on extensive evidence of obesity-induced lipotoxicity in other cells, it was hypothesized that obesity results in the activation of lipotoxicity pathways in the ovary. It was shown that lipid accumulation, ER stress, mitochondrial dysfunction, and apoptosis occur in ovarian cells and the oocyte in response to a high-fat diet. The aim of our study was to evaluate the influence of high BMI on oocytes, granulose cells and metabolites in the follicular fluid.