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We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. Type II diabetes mellitus (T2DM) is a widespread metabolic disorder characterized by insulin resistance precipitating abnormally high blood glucose levels. The worldwide rise in type II diabetes mellitus (T2DM) is a public health issue that must be addressed. The main mechanisms through which epigenetics acts to affect cell phenotype and biological processes are DNA methylation and histone modifications (Bramswig and Kaestner, 2012). As Russell notes, there are many specific means by which a histone is modified, including methylation, phosphorylation, or ubiquitination at varying locations within the complex. These epigenetic alterations, of which much is known through various studies in vitro, have also been shown in vivo to be associated with environmental influences, not least of which is the intrauterine environment and its impact on a developing fetus (Bramswig and Kaestner, 2012). A current focus in the field of epigenetics is the exploration of metabolic changes within the intrauterine environment and their implication on the development of risk factors associated with T2DM postnatally.
A clear relationship has been found between exposure to famine in utero and the development of an atherogenic lipid profile as an adult. Interestingly, a more recent look into the same Dutch famine data found only women to have significantly increased lipid profiles, an assessment of total cholesterol, LDL, and HDL. Furthermore, a cohort study carried out on 513,501 women from 1989 to 2003 found that maternal weight gain throughout pregnancy increases the birthweight of children independently of genetic factors (Ludwig and Currie, 2010).
The means by which this occurs is further complicated by the existence of so called endocrine-disrupting chemicals (EDCs) that have the capacity to influence most if not all aspects of adipose tissue growth, from undifferentiated stromal cells to mature adipocytes, a phenomenon that is especially detrimental to children and young adults who are physiologically in the midst of a time of intense adipocyte hyperplasia (Janesick and Blumberg, 2011).
While coronary artery disease (CAD) itself is not a direct risk factor for T2DM, CAD is associated with high blood pressure, which is an identified risk factor for the development of T2DM.
While exposure to famine early in gestation seems to have the largest impact on future lipid profiles and the development of CAD, it was found that mid- to late-exposure to famine in utero appears to have the largest effect on glucose tolerance (Ravelli et al., 1998). These results further solidify earlier explorations of a potential association between events experienced prenatally in varying intrauterine environments and the significant effects that exposure has on metabolic control systems. What has been a source of confusion is the complex timing by which epigenetic mechanisms exert their influence on DNA transcription.
Notably, varying methylation patterns at this same IGF2 locus were also observed in adults exposed in utero to the Dutch famine depending upon the timing of their prenatal exposure. The results found from studying the effect of prenatal nutrition on lipid profiles, obesity, and glucose handling have interesting implications for the development of T2DM in adults.
Given the recent findings and discrepancies in current studies discussed earlier, more work is needed to determine the influence that timing of gestational exposure to various intrauterine insults has on future T2DM development.
Tobi et al., working off previous studies that had shown hypomethylation of the IGF2 DMR to be a result of exposure to famine during gestation, decided to look at the patterns of 15 other possible genes implicated in metabolic and cardiovascular disease in 60 people conceived during the Dutch famine. Recently, this epigenetic interaction has been suggested to exert its effects even earlier, by presenting a likely regulatory influence on the onset of embryonic genome activation (EGA) prior to implantation (Vassena et al., 2011).
Similarly, epigenetics can also influence the developmental process later in the fetal development timeline, as seen in already-differentiated β cells. Sugar-sweetened soft drinks are a major source of excess calories and glycemic load in the diet. Epidemiologic studies have provided substantial evidence that regular consumption of soft drinks not only contributes to weight gain and obesity, but also increases risk of type 2 diabetes and the metabolic syndrome.
The deleterious effects of soft drinks on diabetes are not entirely explained by body weight. Emerging evidence suggests that soft drink consumption is also associated with increased risk of coronary heart disease. This data provides mounting evidence that sugar-sweetened beverages not only contribute to positive energy balance and obesity, but also to type 2 diabetes and cardiovascular risk.
The HCL system is designed to automatically control blood glucose levels with minimal input or supervision from patients or caregivers. The HCL system logged a glucose reading every 5 minutes during the trial, but patients still had to occasionally calibrate the sensors and take mealtime or corrective insulin doses. After some 12,400 patient-days, the study showed, there were no incidents of diabetic ketoacidosis, severe hypoglycemia or serious device-related adverse events.
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Medical Design & Outsourcing covers the technical advancements in design, development, and contract manufacturing of medical devices and equipment. A 7-year-old boy presented with a solitary, nearly circular, very pruritic inflammatory facial lesion. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. While the onset of T2DM is known to be the consequence of a multifactorial interplay with a strong genetic component, emerging research has demonstrated the additional role of a variety of epigenetic mechanisms in the development of this disorder. According to the International Diabetes Federation, there were 366 million people living with diabetes in 2011, and this number is expected to rise to 552 million by 2030 (Whiting et al., 2011). DNA methylation involves DNA methyltransferases modifying cytosines to create 5-methylcytosine, with the majority of this action occurring in CpG islands found in multiple protein-coding gene promoter regions throughout the human genome. However, one of the most extensively studied is that of acetylation and deacetylation of the histone tails, a delicate balance that serves to alter the charge of the histone core, ultimately determining the ease by which DNA transcription can occur. Here, we focus on this environmental link, its epigenetic impact, and the molecular implications of those epigenetic alterations as points of further exploration by researchers and novel therapeutic intervention by clinicians seeking to proactively care for patients at risk for T2DM.
The impact of maternal nutrition on lipid profiles, impaired glucose handling, high blood pressure, and obesity, among other risk factors for T2DM, are areas of interest at this time. This discrepancy may be due to the fact that earlier studies neglected to look at men and women groups separately in their analyses and also did not include sibling controls.
Much of this arises from the physiological response of the fetus to overnutrition, with normal maternal insulin resistance associated with pregnancy becoming exaggerated in obese states and increasing the shunting of vital nutrients to the growing fetus. As Janesick and Blumberg note, these EDCs, including a wide range of both natural and man-made substances such as pharmaceuticals, pesticides, and plasticizers like bisphenol A, possess the ability to modulate important cellular-signaling pathways via epigenetic alterations (2011).
Therefore, it is not uncommon for a person with T2DM to also suffer from CAD as the two diseases are intimately linked through this association.

For example, the specific regulatory action on the differentially methylated region (DMR) of the insulin-like growth factor II (IGF2) and H19 promoters early in gestation may have long-term effects and may not be susceptible to further epigenetic modification via environmental or age-related stimuli as was previously thought (Heijmans et al., 2007).
Individuals who were conceived before the German-imposed famine and, thus, exposed to the associated effects of malnutrition on the mother later in their gestation period had similar methylation patterns to those who were not exposed to famine at all.
These are well-appreciated risk factors for T2DM, and exposure to famine during pregnancy was found to increase all of these risk factors. Changes in methylation were seen in six of these 15 candidate genes in people conceived during the famine compared to their siblings. During the first few cycles of cellular mitosis post-fertilization, the embryo relies primarily on mRNA and protein inherited from the mother in order to carry out the rapid division and high metabolic activity characteristic of this stage of development. It appears that the deleterious effects of soft drinks are not entirely mediated through BMI.
Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. Sugar-sweetened beverages and incidence of type 2 diabetes mellitus in African American women. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community.
Patients showed lower percentages of low blood sugar at night while using the HCL system, and mean HBA1c levels fell. Heritable epigenetic modifications, such as DNA methylation and histone modifications, play a vital role in many important cellular processes, including pancreatic cellular differentiation and maintenance of normal β-cell function.
T2DM is a chronic and largely preventable disease defined by high blood glucose resulting from insulin resistance and is characterized by risk factors such as family history of disease, obesity, high blood pressure, and high low-density lipoprotein (LDL) and low high-density lipoprotein (HDL) levels (American Diabetes Association, 2013). Methylation of cytosines in these areas is associated with repression of transcription (Russell, 2010). For example, HDACs are capable of deacetylating amino-terminal lysine residues on histone tails, permitting the positively charged lysine residues of the histone to bind more tightly to the negatively-charged DNA wrapped around it. With this in mind, the Dutch famine from 1944 to 1945 and the great amount of data collected from individuals who felt its effects firsthand offers a unique study cohort to delve into this topic, with a very brief shortage of food lasting only 5 months juxtaposed against a backdrop of adequate nutrition before and after. High LDL levels are recognized by the American Diabetes Association as a major risk factor for the development of T2DM (American Diabetes Association, 2013).
These results suggest that controlling mechanisms for obesity must be separate from those influencing BMI (Ravelli et al., 1998). The fetus, in turn, secretes its own insulin in response, increasing glucose uptake, and fat storage, and thus causing the increased birth weights of babies born under these conditions (Ludwig and Currie, 2010). Whether through normal physiological responses to extraordinary circumstances or by exogenous substances interacting with the fetal epigenome, it is clear that there is much more at stake here.
As such, the development of CAD offers yet another glimpse into a individual's underlying susceptibility to the development of T2DM. Furthermore, the persons with the greatest level of glucose intolerance were the most likely to be obese. In a study comparing the extent of methylation at specific CpG islands in human adolescent and middle aged twins, it was found that no significant distinguishing epigenetic marks could be attributed to differences in age at these particular loci but, instead, revealed an astonishing consistency in the methylation status, once methylated, of the IGF2 and H19 promoters (Heijmans et al., 2007).
Therefore, they propose that epigenetic modifications occurring during embryological development tend to exert a greater phenotypic influence on the organism and are more stable in relation to the length of their influence (Heijmans et al., 2007).
However, those who were conceived in the midst of the famine saw an ensuing hypomethylation at CpG islands within this important promoter site and was readily observed even 60 years later at the time data from the cohort study was originally released (Heijmans et al., 2008). However, the timing of exposure to famine and the effect it has, overall, on fetal metabolic development is less clear. Indeed, as others have noted previously, such an integration must also incorporate information regarding more conventional regulators of gene transcription known to play a pivotal role in immediate cellular response to changing environmental stimuli. Hypermethylation was observed in the GNASAS, MEG3, IL10, ABCA1, and LEP proximal promoters; hypomethylation was observed in the INSIGF promoter. One of the first genes transcribed by the fetal genome, POU5F1 is expressed even before EGA occurs through a recombination of maternally-inherited mRNA up until the 2-cell stage. One potential explanation is that the high glycemic load of soft drinks increases insulin demand and in the long-run, may lead to beta-cell failure. Recent studies have found possible epigenetic mechanisms to explain observed risk factors, such as altered atherogenic lipid profiles, elevated body mass index (BMI), and impaired glucose tolerance (IGT), for later development of T2DM in children born to mothers experiencing both famine and hyperglycemic conditions.
This gene silencing occurs through direction prevention of transcriptional promoter binding as well as the recruitment of transcriptional repressors (Bramswig and Kaestner, 2012). This tighter binding allows for more compact wrapping around the structural scaffolding provided by the histones. Additionally, the short time period over which the starvation conditions were experienced inevitably creates for interesting study parameters in which pregnant mothers were exposed to these harsh conditions at different trimesters in their pregnancy (Roseboom et al., 2000). While further work is needed to determine the reasons why varying exposures lead to these differences, it is quite apparent that exposure to famine during pregnancy leads to an overall increased risk for obesity and increased BMI as adults, both of which are important risk factors for the development of T2DM. When it comes to pregnancy, healthcare personnel, mothers, and society at large must be aware that any deviation from ideal fetal development conditions will have implications on both immediate maternal and fetal health as well as on the long-term wellness of the child as he or she moves into adulthood.
An increased rate of CAD in offspring was found to be positively related to maternal exposure to famine while pregnant (Painter et al., 2006). It is important to note that IGT was found in adults of all body types with prenatal exposure, suggesting that the underlying mechanism for IGT was not secondary to obesity but, rather, the cause of it (Ravelli et al., 1998). By measuring global histone acetylation levels in various metabolic states, her group was able to show that ATP-citrate lyase (ACL), a metabolically important enzyme critical in the conversion of glucose-derived citrate into acetyl-CoA, was needed for histone acetylation.
These findings challenge other studies that suggested the possibility of global epigenetic pliancy arising through the influence of environment, diet, and age (Fraga et al., 2005).
Intuitively, such an early alteration to genetic expression in cells of a developing fetus carries with it enormous implications for the cells that are to arise after subsequent mitotic events. Although this is not exactly correlative with the hypermethylation observed in offspring born to GDM mothers, the study suggests a time of critical importance early in embryological development for epigenetic influence with the potential for lasting regulatory action on this specific portion of the human genome.
Highest increased rates of atherogenic lipid profiles, obesity, and CAD were found with early exposure, while highest increased rates of glucose intolerance and T2DM itself were found in mid- to late-exposure.
This is no small task, especially considering the vast unknown that the realm of epigenetics still poses as well as the substantial ethical obstacles to studying these alterations in humans, but by delving ever deeper in this particular field, science will be one step ever closer to understanding the true mechanisms by which organisms respond, survive, and thrive in an incredibly complex and dynamic world (McGraw et al., 2013). When compared to individuals that were exposed later in gestation, methylation changes in IL10, GNASAS, and INSIGF were found to be time-sensitive. Interestingly, this pre-EGA translation of maternal mRNA involves two waves of activity, the first involving the translation of protein products that persist throughout this critical stage of development, suggesting that they have important regulatory roles in the initiation of EGA, while the second wave is highlighted by protein breakdown in order to feed the rapidly developing cells (Vassena et al., 2011). This process is only relieved by the activation of fetal genomic transcription, which carries out the transcription of this important regulator for the remainder of embryonic development.

It was found that under certain conditions, such as intrauterine hyperglycemia typical to gestational diabetes mellitus (GDM), these genes are epigenetically downregulated through the addition of methyl groups at CpG islands within highly variable DMRs of their promoter regions (Ding et al., 2012). Because high-fructose corn syrups contained in soft drinks contain roughly 45% glucose and 55% fructose, the overall glycemic index of soft drinks is only moderate due to the low glycemic index of fructose. Food and Drug Administration for its new HELIO automated immunofluorescence (IFA) system with AESKUSLIDES ANA HEp-2-Gamma Assay. It is suggested that these epigenetic influences happen early during gestation and are less susceptible to the effects of postnatal environmental modification as was previously thought, highlighting the importance of early preventative measures in minimizing the global burden of T2DM. Epigenetics, or the heritable changes in gene expression that occur without changes in the primary DNA sequence, has recently been proposed as a route through which this process occurs (Russell, 2010).
Repressors that bind to methylated CpG islands then initiate the cascade that ultimately results in the second primary mechanism of epigenetic regulation: histone modifications and the recruitment of histone deacetyltransferases (HDACs) (Russell, 2010). Genes located within this area of tighter binding are, therefore, transcriptionally repressed as the transcription machinery is unable to access the gene promoter (2010).
Meticulous records and census data spanning several decades reveal the far-reaching impact that prenatal diet during different trimesters has on the offspring's health in adulthood.
Based on these findings, it is thought that prenatal exposure to famine may have sex-specific outcomes (Lumey et al., 2009).
Similar to the trends seen with lipid profiles and BMI, persons exposed to famine early in pregnancy were more likely to develop CAD as adults than those exposed in mid- to late-pregnancy, with a mean age of diagnosis at 47 years of age for those exposed early during the first trimester and a mean age of diagnosis at 50 years for those exposed later in the developmental process.
Interestingly, this acetylation coincided with times of plentiful glucose supply, tipping the balance to favor global histone acetylation over HDAC-induced deacetylation, allowing for the expression of specific metabolic genes as well as promote cellular differentiation into adipocytes (Wellen et al., 2009).
A more recent look into the epigenetic footprint of DNA taken from a cohort of monozygotic twins goes one step further by suggesting that DNA promoter regions with the greatest level of regulatory action retained the most stable methylation patterns while those loci that were considered not as important functionally showed a greater level of variability in epigenetic imprinting (Kaminsky et al., 2009).
Studies conducted after the publishing of the glucose intolerance results expressed contrasting perspectives and highlighted that exposure early in gestation, specifically the first trimester, was most significant for future risk (Heijmans et al., 2008).
Also, alteration of the methylation status in INSIGF, GNASAS, and LEP were sex-specific with methylation at GNASAS and LEP being specific for men (Tobi et al., 2009). However, when trimethylation at H3K27 is removed and the PcG-mediated repression of that gene is released, that particular locus is primed for transcription. Once this occurs, other pluripotency genes such as NANOG, SOX2, KLF4, and ZFP42, begin to be expressed in a sequential manner, hinting at a hierarchical scheme by which pluripotency is acquired in a developing human embryo with POU5F1 playing the role of master regulator which, when properly expressed, paves the way for the expression of other pluripotency genes (Vassena et al., 2011).
However, overall blood glucose response is not only determined by the glycemic index value of a food, but also by its amount of carbohydrate. Interestingly, persons exposed in mid- to late-pregnancy did not have a significantly increased risk for developing CAD than the control group (Painter et al., 2006).
As glucose intolerance and obesity are major hallmarks of T2DM, this insight is promising for further elucidation of epigenetic influence on future development of chronic disease, in general, and T2DM, specifically. With this discovery, epigenetic influence on a global level is now believed to occur prior to birth with more subtle changes to loci of lesser significance occurring throughout life (Kaminsky et al., 2009). In conjunction with other recent studies that have stressed the importance of early exposure to adverse events in utero, the emphasis that Ravelli et al.
These results support previous findings that exposure to famine has timing- and sex-specific effects on a developing embryo.
This work deals primarily with discovering additional avenues, specifically in altering the epigenome of cells already differentiated, from which to circumvent the ethical obstacles imposed on research using pluripotent cells. Thus, the concept of glycemic load, which is the product of the glycemic index value of a food and its carbohydrate content, has been used to represent the quality and quantity of carbohydrates consumed. Although we were unable to get an exact number out of him, John Klein, Medtronic’s new Chief Procurement Officer, told us the company managed a growing universe of “tens of thousands” of suppliers. Regardless of when it occurs and to whom, it is clear that prenatal exposure to famine during gestation increases the risk of developing an atherogenic lipid profile later in life, possibly through epigenetic mechanisms, thereby increasing the risk for the person developing T2DM. This has interesting implications on the development of T2DM, as these findings would indicate that there are molecular events that occur specifically early in gestation that are highly susceptible to the state of maternal health and nutrition. This implies a significant role for epigenetic mechanisms early in the regulation of stem cell differentiation into pancreatic endocrine cells. However, this early epigenetic influence on genomic activation could 1 day prove to have ramifications not only for somatic cells reprogramming but for more targeted and preventative epigenetic therapeutic interventions as well.
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