Is type 2 diabetes genetic or environmental,free glucose meter medicaid 401k,gene mutation linked to type 2 diabetes - Videos Download

First of all, there is no true answer to the question of which type of diabetes is genetic. Some examples to support this evidence is, that families who have type 2 diabetes usually share the same lifestyle such as eating habits, exercise habits, as well as being overweight, which has been known to be one of the leading causes of type 2 diabetes. So to answer the question of which type of diabetes is genetic, the short answer is there is a high probability that type 2 diabetes will have a stronger predisposition to get it, compared to type 1 diabetes.
In other words, there is a predisposition of getting both type 1 and type 2 diabetes, but the type 2 diabetes has a bigger chance to run in the same family.
While we are not sure which type of diabetes is genetic for sure, or what triggers type 1 or type 2 diabetes to occur if you have a family member who suffers from it, the most important thing is to know that prevention is key especially in type 2 diabetes since studies have shown that diet and regular exercise can prevent it from happening, or in some cases reverse the symptoms. Recent Commentspatrice thompson on Free Diabetic Supplies – How to Get Them?munnaamalai on Type 1 vs Type 2 Diabetes ChartJessica I. An as-yet-undefined immunologic insult occurs in an individual with genetic predisposition and initiates a chronic low-grade immunologic process (priming).
A schematic representation of proposed integration of mechanisms by the protein products of type 1 diabetes (T1D) loci that are involved in adaptive immunity, and for which the direction of the functional effect of the T1D-associated variants is known or suspected.
ANN ARBOR—New research from a large international team of scientists offers a more complete picture of the genes responsible for type 2 diabetes, demonstrating that previously identified common alleles shared by many in the world are the biggest culprits—not the less common variants some scientists had hypothesized might play a large role in who gets the disease. The researchers also identified a novel variant specific to East Asians through their study that analyzed the genes of individuals from five ethnic groups, making this the largest multi-ethnic genetic sequencing study published to date.
Led by researchers at the University of Michigan School of Public Health, the Wellcome Trust Centre for Human Genetics at the University of Oxford, the Broad Institute of MIT and Harvard, and the Massachusetts General Hospital, more than 300 scientists from 22 countries used DNA from 120,000 individuals to pinpoint genes and their variants, which influence the disease that impacts 10 percent of the world's population. The team identified a novel association between type 2 diabetes and a variant in the gene PAX4, present only in individuals from East Asia, including Korea, China and Singapore. The researchers completed whole genome sequencing of more than 2,600 people and exome sequencing of 13,000, complemented with genome- or exome-wide array genotyping of 111,000 people. Those studied included individuals with ancestral origins in Europe, South and East Asia, the Americas and Africa.
This in-depth look at the genetics of type 2 diabetes addresses the century-old debate of whether genetic differences that influence predisposition to common diseases, like diabetes, are ones that are widely shared within populations, or whether they are more likely to be rare or unique events, specific to an individual and his or her family. Type 2 diabetes is a major threat to global public health as deaths from the disease continue to rise rapidly, along with its complications including blindness, kidney failure, heart attack, stroke and amputation. Data and discoveries generated through this project are available through the type 2 diabetes genetics portal developed as part of the Accelerating Medicines Partnership.
This research was supported by more than 60 funding organizations with primary contributions from the National Institutes of Health (National Institute of Diabetes, Digestion and Kidney Disease, National Human Research Genome Institute and Office of the Director) and the Wellcome Trust. Psychiatric researchers have discovered a genetic link between depression and type 2 diabetes. Dr Carol Kan and her team from the Institute of Psychiatry, Psychology and Neuroscience at King’s College London have been investigating the extent to which the co-occurrences could be due to interactions between genetic and environmental risk factors using two approaches; twin data and genome wide association studies (GWAS).


The findings presented this week at the Royal College of Psychiatrists’ International Congress, demonstrate that the relation between depression and type 2 diabetes may be genetic in origin and could have significant clinical importance. People with depression may be up to 60 per cent more at risk of developing type 2 diabetes and those with type 2 diabetes are around 15 per cent more at risk of developing depression, according to previous research.
Scientific studies have consistently shown a two-way epidemiological association between type 2 diabetes and depression which were reflected in previous studies.
The mechanisms underlying the association between both conditions are still unclear, although common biological pathways have been implicated in the development of the two. This is one of the most common questions asked by people who are diagnosed with diabetes, or with parents who have children with diabetes.
Researchers have found that although there is a predisposition for someone to have a diabetes, there are other factors other than genetics that may trigger the diabetes to occur. If one twin get a diabetes, the other one will likely to have it as well, although the possibility differs depending on which type of diabetes it is. This means that if you have a family member with type 2 diabetes, you have a bigger chance of getting it too if you do not take extra measures in preventing it from happening. What researchers have not found out is the triggers that might shed a clue to why some identical twins both get it, and some others do not, even though they have the exact same genes. The initiating events involve infiltration of innate immune cells (such as monocytes and natural killer cells with autoreactive B cells) (orange ovals) into the pancreatic islets.
Molecules in green actively participate in T cell activation through T cell receptor (TCR) signalling or downstream events, whereas red indicates inhibitors of these processes. The majority of these were common variants, found in all human populations, and most had previously been detected by other genome-wide association studies. They also demonstrated that variants in the gene TM6SF2, previously linked to hepatic steatosis (commonly known as "fatty liver"), influences risk of type 2 diabetes. Type 2 is the most common form of the diabetes; it impacts the body's ability to regulate glucose (or sugar). Precision medicine relies on the deep understanding of the genetic architecture of a disease. While this large range of genetic risk may challenge our efforts at precision medicine, our consortium also offers a publicly accessible dataset, unprecedented in scope, for researchers around the world to advance our molecular understanding of type 2 diabetes," said co-lead author Jason Flannick, senior group leader at the Broad Institute of Harvard and MIT and research associate at the Massachusetts General Hospital.
As you probably already know, there are two type of diabetes, type 1 diabetes and type 2 diabetes.
The reason is because even though type 1 diabetes and type 2 diabetes has different causes, but there is a bigger chance for both types of diabetes to happen if some family members also have it. The principal site of antigen presentation is thought to be the pancreatic lymph node where islet antigens are presented by antigen-presenting cells (white ovals) to T cells (brown dots). Arrows in grey boxes show the functional effect (whether an increase or a decrease) on the protein by the T1D risk allele in the genes that encode these proteins.


In addition to its genetic components, environment and behavior play major roles in who gets the disease, with obesity, excessive stress and an inactive lifestyle among the contributors. Our work provides this key information for type 2 diabetes," said lead author Christian Fuchsberger, who worked on the research as a postdoctoral fellow at U-M and now is at the Center for Biomedicine at the European Academy in Bolzano, Italy. On the other hand, type 2 diabetes twin will have a bigger chance of 75%, if the other twin has it. However, if your family member suffers from type 1 diabetes, your probability of getting it is slightly lower compared to type 2 diabetes. In the case of human leukocyte antigens (HLAs) of the major histocompatibility complex (MHC), reduced function by risk alleles is not proven but is widely suspected. Combined with other risk factors such as smoking, high cholesterol and high blood pressure, people with type 2 diabetes have a much higher risk of cardiovascular disease. As TCR activation is involved in both tolerance and immune attack, the prevailing effect of signalling alterations on autoimmunity risk is not immediately obvious. However, this is not a true evidence that this is purely genetic, because it is very common in families to share the same lifestyle which is probably causing someone to have type 2 diabetes. Where known, T1D-associated alleles impair T cell activation through a loss-of-function of activators or a gain-of-function of inhibitors. The process specifically targets insulin-producing β-cells (light blue circles), while other endocrine cells (red circles) within the islet are spared. In the lymph nodes, the cycle of antigen presentation, activation of adaptive immune cells, licensing of effector T cells and epitope spreading continues with the loss of β-cells over time. In the presence of inflammation (for example, active insulitis, perhaps initiated by innate immune events) and increased antigen abundance (for example, ?-cell apoptosis from viral infection), the same partial loss-of-function could be overridden by the stronger signals in T cells that have previously escaped self-tolerance for the same antigen. There is evidence for a regenerative attempt of β-cells in the midst of the islet inflammation (dark blue circles).
In addition, defective interleukin 2 (IL-2) signalling will compromise the function of regulatory T cells. Tertiary lymphoid organs are thought to develop within the islets, which may lead to amplification of the adaptive immune response.
Regulatory T cells (yellow dots) may arrest this process in its early and late stages but are not able to contain the amplified process in the late stages despite an increase in their numbers. The loss of metabolic function at presentation may be both functional and anatomic, because immune therapies can restore cells that have lost the capacity to produce insulin but have not been destroyed.



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