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Until now the exact mechanism of insulin secretion failure in type 2 diabetes has not been completely understood.
Type 2 diabetes occurs when insulin production from pancreatic beta cells either fails, or peripheral tissues become resistant to the hormone insulin preventing the uptake of glucose from the blood stream into cells for fuel. Designing new treatment options for type 2 diabetes has been difficult considering the exact mechanism of insulin secretion was not understood. To test the importance of Snapin in insulin secretion a drug which inhibits its production was added.
These exciting new findings will not only propel diabetic research but also help develop more accurate treatment options. People with type 1 diabetes CANNOT cordupe insulin which brings the blood sugar down so just about everything they eat causes their blood sugar to rise. Both fasting plasma glucose (FPG) and postprandial plasma glucose (PPG) are directly correlated to the risk of complications, with some evidence that postprandial might constitute a stronger risk factor for cardiovascular (CV) complications (4–9). There is compelling evidence from randomized controlled studies that improved glycemic control reduces the risk of microvascular complications but has no significant effect on macrovascular outcomes in recently diagnosed type 1 (13) and type 2 diabetes (1,11,14), as well as more long-standing type 2 diabetes (15–19). These 3 trials confirmed the benefit of intensive glycemic control on microvascular outcomes. None of the above studies independently confirmed a significant benefit of tight glycemic control on macrovascular outcomes. The unexpected higher mortality rates seen in the intensive arm of the ACCORD study and the lack of clear macrovascular benefit in the ADVANCE and VADT trials have been further reviewed. A major difficulty in attempting to use evidence-based observations to determine the value of tighter postprandial glucose control has been the lack of well-designed, long-term outcome studies where assessing postprandial glucose values is the major objective of the study.
Contrasting results from recent studies should not discourage physicians from controlling blood glucose levels. 7 DECODE Study Group, European Diabetes Epidemiology Group Is current definition for diabetes relevant to mortality risk from all causes and cardiovascular and noncardiovascular causes?
Is the increased total mortality and sudden death risk associated with the intensive glycemic treatment strategy (ACCORD – VADT) linked to hypoglycemia ? Although metformin is first-line therapy for patients with type 2 diabetes, glycemic control fails with metformin alone in many patients.
This week, our class discussed the detrimental effects of insulin resistance as seen in Type 2 diabetes mellitus. The toxic ?-amyloid plaques, typically seen in Alzheimer’s disease, can further decrease insulin activity by binding to insulin receptors. The Cobbers on the Brain blog is a component of the Neurochemistry course at Concordia College in Moorhead, MN, and written by students. Science, Technology and Medicine open access publisher.Publish, read and share novel research.
The Role of Placental Exosomes in Gestational Diabetes MellitusCarlos Salomon1, 2, Luis Sobrevia1, Keith Ashman2, Sebastian E.
Johns Hopkins researchers believe they have uncovered the molecular switch for insulin secretion. Snapin is a protein  produced in nerve cells and plays an important role in cell communication, and has also been found in pancreatic beta cells.
The initial prospective randomized controlled trials were conducted in patients with recently diagnosed diabetes. Patients were at least 55 years old with a history of major macrovascular or microvascular disease or at least 1 other risk factor for vascular disease.
However, meta-analysis of clinical trials designed to assess differences in CV outcomes in patients who had achieved lower versus higher levels of glycemia demonstrated that those treated with more intensive therapy, compared to less intensive glycemic control, were found to have a 10% to 15% reduction in the risk of major CV events, primarily because of a 15% reduced risk of MI, but with no effect on stroke, CV death or all cause mortality (26).
Several potential reasons for these findings have been suggested, including patient age, duration of diabetes, presence of CVD, history of severe hypoglycemic events, weight gain and the rapid decrease in A1C values. Most of the large outcome trials conducted so far have been mostly based on preprandial glucose and A1C targets.
Intensive glucose control, lowering A1C values to ≤7% in both type 1 and type 2 diabetes, provides strong benefits for microvascular complications and, if achieved early in the disease, might also provide a significant macrovascular benefit, especially as part of a multifactorial treatment approach.
Glycemic targets should be individualized based on age, duration of diabetes, risk of severe hypoglycemia, presence or absence of cardiovascular disease, and life expectancy [Grade D, Consensus]. Bernard Charbonell (University of Nantes, France) discussed new options in diabetes management.
An open-label randomized controlled trial was conducted, which compared add-on exenatide with add-on glimepiride in patients who had failed to achieve glycemic control with metformin alone. We recognised that there was underlying moderate-severe insulin resistance affecting muscle and the liver, and this, coupled with beta cell failure, formed the classical triumvirate (1). It has been established that Type 2 diabetes can be seen as a cofactor in the development of Alzheimer’s disease (AD). Neuronal insulin resistance contributes to the formation of these plaques as the enzyme that degrades both insulin and ?-amyloid must work to degrade increased levels of both insulin resistance prevents the normal use and breakdown of insulin.
Well, Type 2 diabetes can be caused by genetics, but also by poor diet (which causes obesity).
An increase in the incidence of gestational diabetes mellitus: Northern California, 1991-2000. The genetics of gestational diabetes mellitus: evidence for relationship with type 2 diabetes mellitus. Gestational diabetes reduces adenosine transport in human placental microvascular endothelium, an effect reversed by insulin. Morphologic and proteomic characterization of exosomes released by cultured extravillous trophoblast cells.
Specific isolation of placenta-derived exosomes from the circulation of pregnant women and their immunoregulatory consequences.
Human trophoblast-derived exosomal fibronectin induces pro-inflammatory IL-1beta production by macrophages. Human villous trophoblasts express and secrete placenta-specific microRNAs into maternal circulation via exosomes. Application of systems biology principles to protein biomarker discovery: Urinary exosomal proteome in renal transplantation. Proteomic identification of exosomal LRG1: a potential urinary biomarker for detecting NSCLC.
Mast cell- and dendritic cell-derived exosomes display a specific lipid composition and an unusual membrane organization. Analysis of antigen presenting cell derived exosomes, based on immuno-magnetic isolation and flow cytometry.
Exosome: from internal vesicle of the multivesicular body to intercellular signaling device. Comparison of ultracentrifugation, density gradient separation, and immunoaffinity capture methods for isolating human colon cancer cell line LIM1863-derived exosomes. Isolation and characterization of exosomes from cell culture supernatants and biological fluids.
Membrane vesicle release in bacteria, eukaryotes, and archaea: a conserved yet underappreciated aspect of microbial life. Microvesicles derived from human umbilical cord mesenchymal stem cells stimulated by hypoxia promote angiogenesis both in vitro and in vivo. Placenta-derived soluble MHC class I chain-related molecules down-regulate NKG2D receptor on peripheral blood mononuclear cells during human pregnancy: a possible novel immune escape mechanism for fetal survival. Review: Differential placental macrovascular and microvascular endothelial dysfunction in gestational diabetes.
Plasma kisspeptin levels in pregnancies with diabetes and hypertensive disease as a potential marker of placental dysfunction and adverse perinatal outcome. Postprandial hyperglycemia and the 2-hour post-challenge PG appears to be a better predictor of cardiovascular disease (CVD) and all-cause mortality than FPG (7). Median baseline A1C level and diabetes duration were lower than in the ACCORD trial at 7.2% and 8 years, respectively, whereas mean age was slightly higher at 66 years. The primary outcome of the study was the time from randomization to the first occurrence of a major CV event(18,19). Similarly, intensive therapy in ACCORD patients showed a favourable effect on microvascular outcomes, particularly albuminuria and diabetic retinopathy (16). Intensive glycemic control, however, was associated with more than a 2-fold increase in the risk of severe hypoglycemia (25).

Increased mortality associated with intensive treatment could not be explained by the type of pharmacological treatment, rapidity to implement the intensive strategy or weight gain (24). The insulin resistance in muscle primarily was responsible for the excessive postprandially rise in plasma glucose concentration, while insulin resistance in the liver, in combination with accelerated gluconeogenesis, resulted in an excessive rate of hepatic glucose production which led to an increase in the fasting plasma glucose concentration (2-4).
The defining characteristic of Type 2 diabetes is the body’s resistance to the effects of insulin. This means that the same amount of enzyme would be responsible for the breakdown of an increasing amount of target molecules, which it is not intended to do.
With the obesity epidemic as of late, it is generally expected that frequency of Alzheimer’s disease will skyrocket in the coming years. Exosomes are generated in the endosomal structure participating the plasma membrane in this process, and secreted via constitutive endosomal pathways involving the Golgi complex from various cell types. International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics. In the DCCT, a 10% reduction in A1C was associated with a 40% to 50% lower risk of retinopathy progression, although the absolute reduction in risk was substantially less at lower A1C levels (2). Subsequent observational data from long-term follow-up of both the DCCT and UKPDS cohorts showed a persistence of significant microvascular benefits in patients who had previously been in the intensively treated groups despite the fact that, during the subsequent follow-up period, their glycemic control became similar to that of patients who were previously in the standard arm (20–22). At inclusion, participants had a mean age of 62 years, diabetes duration of 10 years and a median baseline A1C level of 8.1%. In ADVANCE, patients in the intensive control group demonstrated a reduction in the incidence of major microvascular events, mainly through a 21% relative reduction in nephropathy (15). Hypothesis-generating secondary analysis from the ACCORD trial reported a nonsignificant trend toward lower all-cause mortality in individuals assigned to the standard arm who were younger than 65 years at baseline (27). Zschau Impact of fasting and postprandial glycemia on overall glycemic control in type 2 diabetes.
This differs from Type 1 diabetes mellitus in which insulin is simply not being produced, but can metabolized injected insulin without a problem.
As a society, the need for a quick fix has propagated and exacerbated the consumption of fast foods.
Villous chorionic explant-derived exosomes were isolated by ultracentrifugation and purified using a sucrose gradient. The exosomes contain specific proteins and miRNA as a new form of exosome-mediated intercellular communication and with different biological function.
10 ug of exosome proteins and trophoblast cell lysate were separated on 4-12% SDS-PAGE and stained with SimplyBlue™ SafeStain (Invitrogen). Rice2[1] Cellular and Molecular Physiology Laboratory (CMPL), Division of Obstetrics and Gynaecology, School of Medicine, Faculty of Medicine, Pontificia Universidad Catolica de Chile, Santiago, Chile[2] University of Queensland Centre for Clinical Research, University of Queensland, Herston, Queensland, Australia[3] Department of Obstetric and Gynaecology, Universidad de los Andes, Santiago, Chile1. Exosomes appear to play an essential role in preventing an excessive immune response and in the development of autoimmunity in human pregnancy. In the UKPDS, this relationship was directly linear, with each 1.0% (absolute) reduction in mean A1C associated with a 37% decline in the risk of microvascular complications, a 14% lower rate of myocardial infarction (MI) and a 21% reduction in deaths from diabetes (3).
The follow-up data from these 2 studies also demonstrated a beneficial effect of improved glycemic control on CV outcomes. The primary outcome in the ADVANCE trial was a composite of microvascular events (nephropathy and retinopathy) and macrovascular disease defined by major adverse CV events. A recent meta-analysis confirmed the positive impact of intensive glycemic control on microalbuminuria (25).
Similarly, the ADVANCE trial also reported a nonsignificant trend toward fewer events among younger patients in the intensive therapy group (15). Insulin resistance makes it difficult for the body to perform insulin-mediated functions such as metabolism and regulation of other cellular processes. This worsening in diet, along with people becoming more sedentary, has led to increasing obesity and also increased frequency of Type 2 diabetes.
IntroductionGestational Diabetes Mellitus (GDM) affects ~5% of all pregnancies and parallels the global increase in obesity and type 2 diabetes. Recently, it has been demonstrated that placental miRNAs circulate in the blood of pregnant women [66, 67].
In the DCCT cohort, there was a significant reduction in CV outcomes (42%) as well as non-fatal MI, stroke and CV death (57%) in previously intensively treated patients compared with those who were previously in the standard arm (23). The primary outcome of this study was a composite of major CV events: non-fatal MI, nonfatal stroke or death from CV causes.
For example, maternal plasma concentration of placental miRNA-141 increases with gestational age [66].
The intensive glucose control arm was prematurely terminated after 3.5 years due to higher mortality associated with assignment to this treatment (17,24). Compared with the UKPDS and the DCCT, which were conducted in younger individuals with recent-onset diabetes, the duration of diabetes in the ACCORD, ADVANCE and VADT trials ranged from 8 to 11.5 years.
Recently, it has been established that insulin is involved in neuronal metabolism, cell survival, longevity, and learning and memory.
It is difficult and expensive to maintain a healthy diet, but do a couple hours per day to make healthy food and exercise outweigh years of cognitive decline that will impact your family and your own quality of life?
Lifestyle changes that impact adversely on caloric balance are thought to be a contributing factor in this emerging pandemic [1, 2].
Placenta-specific miRNA-517A is released from chorionic villous trophoblasts into maternal circulation, where it may affect maternal tissues (e.g. Further emphasis of the importance of duration of diabetes was identified in a substudy of the VADT patients when measurement of the coronary calcium score, utilizing computed tomography, revealed fewer CVD events in these younger patients enrolled in the intensive treatment arm (28).
This connection to learning and memory has led to research to determine insulin’s role in Alzheimer’s disease. We, as a society, must change so as to be more conscious of our current health because it dictates our condition in the future.
The current ‘gold standard’ for the diagnosis of GDM is the oral glucose tolerance test (OGTT) at 24–28 weeks of gestation [3, 4]. The frequency of severe hypoglycemia in these trials was 2 to 3 times higher in the intensive therapy groups, and a higher mortality was reported in participants with 1 or more episodes of severe hypoglycemia in both the ACCORD (29) and the ADVANCE (30) trials, irrespective of the different treatment arms in which individual patients were allocated. The specific death of the cells in the brain’s memory center, called the hippocampus, leads to forgetfulness and inhibition of memory formation seen in Alzheimer’s disease.
Stop spending so much on unnecessary things like multiple big televisions, movies you don’t need, or the up-and-coming Xbox One.
When GDM is diagnosed in the late second or early third trimester of pregnancy the ‘pathology’ is most likely well-established and the possibility to reverse or limit potential adverse effects on perinatal outcomes may be limited [ 5].
There is a paucity of data, however characterising the release of exosome from endothelial cells during normal and pathological pregnancies.
Insulin resistance facilitates this cell death through loss of intracellular transport of important nutrients, wastes, and other molecules. Use your resources to enable your own well being as well as those for whom you are responsible. It will be important to determine if the placenta communicates with the maternal endothelium via microvesicles, and, if so, to elucidate the role and mechanism of action of exosome pathologies associated with endothelial dysfunction, such as GDM. The benefits of a healthier lifestyle are plentiful and include more energy, more efficient cognition, and increased immune system function. If such early detection tests were available, they would represent a major advance and contribution to the discipline and afford the opportunity to evaluate alternate treatment and clinical management strategies to improve health outcomes for both mother and baby. I can eat an almost unlimited amount of nuts without my blood sugar going over 100 at any point. Based upon recent technological developments and studies, we consider it realistic that a clinically useful antenatal screening test can be developed.
It remains to be elucidated how much of this “free” miRNA and mRNA is actually contained within exosomes and thereby confers stability.
Unlike diseases such as cancer where biomarkers need to be exquisitely specific, a useful antenatal screening test would ideally be highly sensitive, but not necessarily highly specific.
Indeed, the exact mechanisms involved in the release of miRNA from the placenta remain to be established. Rather than using the Glycemic Index, I urge your friend to think about food in terms of carbohydrates. The consequence of a false positive would be no worse than an erroneous triage to high-risk care. A recent study, however, reported that miRNAs are selectively packaged into microvesicles and are actively secreted [68-70].

He should experiment with different quantities and types of carbohydrates by eating and then testing his blood sugar. Effects There remains a paucity of data about the effect of placenta-derived exosomes on both fetus and mother. To date there is a paucity of data defining changes in the release, role and diagnostic utility of placenta-derived nanovesicles (e.g.
The available data, however, support a role for placental exosomes in mediating communication at the materno-fetal interface and, possibly, at the distal site within the mother.
Recent data show that trophoblast-derived exosomes induce proinflammatory cytokines such IL-1 ? in human macrophages cells [8]. The aim of this brief commentary, thus, is to review the biogenesis, isolation and role of nanovesicles; and their release from the placenta.
He may learn that he’s more tolerant of carbohydrates in the afternoon or evening than the morning. Interestingly, protein analysis revealed that exosome release from trophoblast cells increases with low oxygen tension and their exosome promote the cell migration in extravillous cytotrophoblast (HTR- 8) (Salomon et al. The Glycemic Index simply doesn’t tell us anything except for how some people without diabetes handled carbohydrates.
Exosomes and GDMExosomes released from the placentae of women with GDM may alter maternal physiology.
BiogenesisExosomes are small [40-100 nm) membrane vesicles that are released following the exocytotic fusion of multi-vesicular bodies with the cell membrane (Figure 1). While the process(es) of exosome formation remains to be fully elucidated, available data support an endosomal origin and formation by the inward budding of multi-vesicular bodies [16] (see Figure 2). Exosomes may also be directly transported from the Golgi complex to multi-vesicular bodies [14].
In pathological pregnancies characterised by compromised placental perfusion and ischaemia, such as GDM, exosome secreted from the placenta can participate in an adaptive response of the mother and fetus and so interact with target tissue and modulate different biological processes, such as immune response, cellular adhesion, development and metabolism.Exosomes have been identified in plasma under both normal and pathological conditions. Recent data, however, suggest that the release of nanovesicles from cells may represent a normal mechanism for cell-to-cell communication [17]. Packaging of exosomal contents appears to be a direct process in which the ESCRT (endosomal sorting complex required for transport) systems play a significant role [18-20].
Exosomes are released from the placenta and the concentration of exosomes in maternal plasma increases during normal pregnancy [21-23]. They contain placenta-specific proteins and miRNA and, as such, may be differentiated from maternally-derived exosomes [25]. The concentration of exosomes has been reported to increase in association with pre-eclampsia [22, 23, 26]. Composition The exosomal content is highly dependent on the origin cell and on pre-conditioning of the cell. One of the first exosomal proteomes characterised was from mesothelioma cells, in which 38 different proteins were identified [27]. Studies in cancer cells show the great variability of proteins expressed in exosomes [28-32]. This study provides the first extensive analysis of the proteome of the exosome-derived trophoblast cells [7].
The data obtained in this study, highlights the extent of putative functional interactions that may be mediated by exosomes. While the composition of exosomes appears to be cell-specific, a subset of common proteins has been identified. Among the most commonly used markers for characterisation of exosomes are tetraspanin proteins, including: CD63, CD81, CD9, and CD82. Exosomes derived from antigen-presenting cells (APC) express MHC-I and MHC-II on their surface [36-38].
Significantly, single cell types display the capacity to generate different subpopulations of exosomes. 2005 demonstrated that RBL-2H3 cells (basophilic leukemia cell line) released two main subpopulations of exosomes that can be discriminated by protein and lipid contents.
The first subpopulation contains phospholipids obtained mainly from granules and the second contains phospholipids from Golgi. In addition, proteins CD63, MHC-II, CD81-containing exosomes accounted for 47%, 32%, and 21%, respectively, of total exosomes [39, 40].3. Isolation of exosomesExosome research is a burgeoning discipline with over 2000 articles published in the last 3 years. The putative role of exosomes spans from intracellular signaling to biomarkers of disease [41].
Germane to any study seeking to elucidate the physiological or pathophysiological role of exosomes is their specific isolation. Exosomes may be further purified by differential sedimentation on sucrose gradients or sucrose-deuterium oxide (D2O) [ 7]. Alternative methods utilise size exclusion chromatography and density gradient centrifugation [44] or solid-phase immunoaffinity capture (i.e.
In the absence of specific, cell surface exosome markers, the veracity of immuno-affinity methods remains to be established.More recently a commercial kit for the isolation of the exosomes has been released (ExoQuickTM, System Biosciences).
While the commercial kit provides significant advantage with respect to processing time, the resulting preparation may not be equivalent to that obtained by ultracentrifugation and differential segmentation. In our own laboratory, parallel preparations of exosomes using both methods reveal differences in the biophysical characteristics of the exosomes isolated.
Exosome preparations isolated using the commercial kit were characterised by a great range in particle diameter (30-300 nm, as estimated by transmission electron microscopy (TEM) and have a higher protein content than similar preparations isolated using the ultracentrifugation method. The role for exosomes in cell-to-cell communicationRecently, evidence supporting a role for exosomes in cell-to-cell communication has been obtained [47, 48]. Exosome release may represent a significant, hitherto unappreciated, communication mechanism between cells, host cell and microbes [47]. For example, exosome function as a carrier of specific molecules such as mRNA and miRNA can interact with neighbouring cells or travel long distances in the bloodstream to reprogram the phenotype and regulate their function [40]. In the placenta, exosome- derived trophoblastic cells are able to reprogram monocytes to secrete specific cytokine profiles independent of cell-to-cell contact [8].
Placental-derived exosomes may also play a role in modulating immunological responses through the induction of lymphocyte apoptosis, [21, 44, 49]. In addition, in the absence of energy production, normal membrane phospholipid asymmetry is lost and amniophospholipids translocate to the outer leaflet of the cell membrane and generate a fusogenic and pro-coagulant surface.
Given that exosomes circulate in blood, these fusogenic moieties may be masked by, for example, annexin V.
In vitro effects of exposing cells to exosomal proteins has been reported and include: induction of differentiation of stem cells [51], suppression of activation of natural killer cells and macrophages [52, 53], and stimulation of cell migration [8, 54]. Putative roles of exosomes, thus, include cell differentiation, immunomodulation and migration [55].
Exosomes are not merely inert fragments of cell membrane but display capacity to affect cell function at remote loci and possibly be a source of disease biomarkers. Exosomes also contain miRNA that may transfer to other cells and alter the expression of the transcriptome and ultimately cell phenotype. They act via binding to messenger RNA and, thus, prevent the translation of the encoded protein. Previous studies have reported that miRNAs are involved in the pathogenesis of diabetes and are required for pancreatic development and the regulation of glucose-stimulated insulin secretion [50, 58]. Placental exosome release Exosomes are released by the placenta during pregnancy and their release may correlate with pregnancy outcome.
The syncytiotrophoblasts and cytotrophoblasts are the most abundant cell types of the human placenta and sense and regulate oxygen and nutritional exchange between mother and fetus during the pregnancy [61, 62]. Pathologies of pregnancy including preeclampsia, intrauterine growth restriction (IUGR) and GDM are associated with placental dysfunction [4, 63, 64] and may display differential and specific exosome release profiles.It has been established that the concentration of exosomes in maternal peripheral blood is greater than that observed in non-pregnant women [21].
In this study, exosomes of placental origin were specifically isolated from the maternal blood using anti-PLAP (anti-placental-type alkaline phosphatase) conjugated to agarose micro-beads.

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