During epididymal transit, spermatozoa acquire new proteins. Some of these newly acquired proteins behave as integral membrane proteins, including glycosylphosphatidylinositol (GPI)-anchored proteins. This suggests that the secreted epididymal proteins are transferred to spermatozoa by an unusual mechanism. Within the epididymal lumen, spermatozoa interact with small membranous vesicles named epididymosomes. Many proteins are associated with epididymosomes and the protein composition of these vesicles varies along the excurrent duct and differs from soluble intraluminal proteins. Some epididymosome-associated proteins have been identified and their functions in sperm maturation hypothesized. These include P25b, a zona pellucida binding protein, macrophage migration inhibitory factor, enzymes of the polyol pathway, HE5/CD52, type 5 glutathione peroxidase, and SPAM1 or PH-20. The electrophoretic patterns of proteins associated to epididymosomes are complex and some of these proteins are transferred to defined surface domains of epididymal spermatozoa. Epididymosomes collected from different epididymal segments interact differently with spermatozoa. This protein transfer from epididymosomes to spermatozoa is time-dependent, temperature-dependent and pH-dependent, and is more efficient in the presence of zinc. Some proteins are segregated to lipid raft domains of epididymosomes and are selectively transferred to raft domains of the sperm plasma membrane. Some evidence is presented showing that epididymosomes are secreted in an apocrine manner by the epididymal epithelial cells. In conclusion, epididymosomes are small membranous vesicles secreted in an apocrine manner in the intraluminal compartment of the epididymis and play a major role in the acquisition of new proteins by the maturing spermatozoa.
During the epididymal maturation, spermatozoa interact with different populations of epididymosomes and sequentially acquire some epididymosome-associated proteins critical to sperm functions. Although very few proteins associated with epididymosomes have been identified, the physiological importance of these vesicles in the sperm maturation remains unclear. To document these relevant issues, lipid and protein analysis of epididymosomes from caput and cauda epididymal fluids was determined. Lipid analysis revealed a particular composition of specific phospholipids in these vesicles; the levels of phosphatidyl-ethanolamine, phosphatidyl-inositol and phosphatidyl-choline being higher in caput epididymosomes. From the 555 and 438 proteins identified in caput- and cauda-derived epididymosomes, respectively, 231 proteins were identified in both types of epididymosome. Proteins exclusively identified in caput and cauda epididymosomes are mainly enzymes and transporter molecules. The presence of several glycan-modifying enzymes is the hallmark of the caput epididymosomes proteome. Among the common proteins in both types of epididymosome, a subset of Rab and SNARE proteins implicated in vesicle trafficking and membrane fusion were identified. Together, these data suggest that epididymosome-associated proteins are involved in various molecular functions suggesting that during the epididymal transit, spermatozoa interact with different populations of epididymosomes, which could modify the male gamete in a sequential manner.
In white women in their mid-30s, the prevalence of the metabolic syndrome is 3- to 5-fold increased in those with a history of PIH in their first pregnancy. This emphasizes the importance of long-term follow-up assessment for cardiovascular risk factors in these women.
Abstract-Insulin resistance syndrome has been observed in women with hypertensive disease of pregnancy, but few studies evaluated the presence of the syndrome a few years after delivery. The objective of this study was to evaluate the presence of insulin resistance and its metabolic alterations in these women compared with those who had a normal pregnancy. We performed an observational study in 168 women with previous hypertensive disease of pregnancy and 168 control subjects with normal pregnancy contacted, on average, 7.8 years after their first delivery (mean age: 34.8 years). Complete blood lipid profile, insulin, glucose, homocysteine, adipokins, and markers of inflammation were measured. Also, an oral glucose tolerance test was performed in 146 case and 135 control subjects. Case subjects were more overweight compared with control subjects. We found significantly lower high-density lipoprotein cholesterol and adiponectin levels and higher apolipoprotein (apo) apoB/apoA1 ratio, homocysteine, leptin, and insulin levels among case subjects compared with control subjects (PՅ0.004). Also, case subjects were more insulin resistant in the basal state estimated by homeostasis assessment model 2, as well as in the nonbasal state as estimated by insulin sensitivity indices calculated from the oral glucose tolerance test. Finally, in a multivariate regression model, leptin, apoB/apoA1 ratio, waist circumference, adiponectin, and free fatty acids explained 40% of homeostasis assessment model 2 variance. Young women with previous hypertensive disease of pregnancy show signs of insulin resistance within the first decade after delivery. These findings suggest that insulin resistance may be the link between hypertensive disease of pregnancy and increased cardiovascular risk later in life. Key Words: hypertension Ⅲ insulin resistance Ⅲ obesity Ⅲ preeclampsia Ⅲ gestational hypertension Ⅲ cardiovascular diseases Ⅲ dyslipidemia H ypertensive disease of pregnancy (HDP) appears after the 20th week of gestation in women and is classified into 2 main groups: the nonproteinuric group, including gestational hypertension (GH) and transient hypertension, and the preeclampsia (PE) group characterized by proteinuria, returning to normal values in the postpartum period. All together, they occur in Ϸ8% of pregnancies. 1 Epidemiological data suggest that women with previous HDP are at increased risk of cardiovascular disease (CVD) later in life. [2][3][4] Also, review articles proposed that insulin resistance could play a role bridging HDP to long-term CVD, but data are lacking to validate the hypothesis. 5,6 During normal pregnancy, insulin resistance progresses until the third trimester to facilitate the transfer of glucose to the fetus, and insulin returns to a normal level after delivery. However, in women suffering from HDP, recent data indicate that insulin resistance and the associated metabolic disturbances, such as dyslipidemia and hyperinsulinemia, are more pronounced compared with pregnant women without this complication. 7,8 A...
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