Type 1 diabetes vs type 2 diabetes diagnosis nice,what is the science behind type 2 diabetes,m trapezius wiki - PDF Review

First and foremost, there are two types of Diabetes, and they are very different from one another. Diabetes is a serious health condition that not only affects your lifestyle, but puts you at risk for other health conditions including high blood pressure, stroke, and nerve damage.  Many Americans are at risk for type 2 diabetes, and the numbers are growing yearly. One change that I always recommend to my clients when we discuss lifestyle-eating, and healthy living options that can be made, is to give up soda.
People often look at me, horrified.  They would rather I ask them to nibble on a pigs ear!  Here are some facts for you about regular and diet sodas and what they do to your body and your mind.
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Genes Involved in Type 1 DiabetesMarina Bakay1, Rahul Pandey1 and Hakon Hakonarson1, 2[1] Center for Applied Genomics, Children’s Hospital of Philadelphia, Pennsylvania, USA[2] Department of Pediatrics, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA1. Huang et al., 2012 re-analyzed the original 2007 WTCCC study by using the 1000 Genomes imputation and reported refined variant rs1265564 in Cut-like homeobox 2 (CUX2) region for association with T1D.
Y Agata, A Kawasaki, H Nishimura, T Honjo, 1996Expression of the PD-1 antigen on the surface of stimulated mouse T and B-lymphocytes. T Awata, E Kawasaki, S Tanaka, Japanese Study Group on Type 1 Diabetes Genetics (2009Association of type 1 diabetes with two loci on 12q13 and 1613and the influence coexisting thyroid autoimmunity in Japanese.
N Bottini, L Musumeci, A Alonso, T Mustelin, 2004A functional variant of lymphoid tyrosine phosphatase is associated with type I diabetes. Cambi A & Figdor CG (2003Dual function of C-type lectin-like receptors in the immune system. B Coulie, J Tack, R Bouillon, J Janssens, 1998Hydroxytryptamine-1 receptor activation inhibits endocrine pancreatic secretion in humans.
Cudworth AG & Woodrow JC1975Evidence for HL-A-linked genes in "juvenile" diabetes mellitus. W Dontje, R Schotte, T Cupedo, B Blom, 2006Delta-like1-induced Notch 1 signaling regulates the human plasmacytoid dendritic cell versus T cell lineage decision through control of GATA-3 and Spi-B. EURODIAB ACE Study Group2000Variation and trends in incidence of childhood diabetes in Europe. In order to have optimal health you will want to eat foods that maintain a stable blood sugar.
When you reduce your carbohydrate intake enough you will inevitably have to increase your fat consumption. Not only is Fat consumption and ketosis good for fat loss, it is also excellent for mental performance. For many athletes they have been told that carbohydrates are absolutely necessary for athletic performance.
There is an emerging field of research that shows the potential for ketosis preventing and possibly curing cancer (1). There is no doubt that there are many benefits to living in a state of ketosis and I have personally enjoyed them with my own experience. The field of research on ketosis will continue to develop over the years and I think it has excellent health benefits and possibilities. Please note: If you have a promotional code you'll be prompted to enter it prior to confirming your order.
If you subscribe to any of our print newsletters and have never activated your online account, please activate your account below for online access. When it comes to preventing and treating high blood pressure, one often-overlooked strategy is managing stress.
Low back pain has many different causes, including the normal wear and tear that comes with aging. Mobility — the ability to move purposefully around your environment — is vitally important to health and well-being. If a growth or mole looks like a melanoma, the doctor will take a biopsy to confirm the diagnosis.
An overactive bladder (also known as urge incontinence) causes a sudden urge to urinate, even when your bladder isn't full.
It might seem like retirement is a time to take it easy and devote yourself to gardening, golfing, and napping.
Sleep shortfalls can lead to a range of health problems, from being more likely to catch a cold or gain weight to increased risk of developing heart disease or diabetes.
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The authors, Phil Edwards and Ian Roberts, said: a€?When it comes to food consumption, moving about in a heavy body is like driving around in a gas guzzler.
Many people engage in a variety of defenses and excuses when faced with the diagnosis of Type 2 Diabetes. Whether the patient is diagnosed with Type 1 or Type 2, the health care issues involved are painful and costly.  Peripheral neuropathy is a painful and difficult to treat complication of diabetes. Immune and Non-immune T1D genes are depicted in a concept map representing the components of the immune system.
Introduction The prevalence of diabetes is increasing worldwide and to date it impacts the lives of approximately 200 million people (Steyn et al., 2009).
Immune components in T1DThe immune system is well organized and well regulated with a basic function of protecting the host against pathogens.
I Bell, Horita S & Karam JH (1984A polymorphic locus near the human insulin gene is associated with insulin-dependent diabetes mellitus. G Clayton, 2009Prediction and interaction in complex disease genetics: experience in type 1 diabetes. Simple carbohydrates are the worst and generate massive spikes in blood sugar and subsequent insulin. When blood sugar is stable your body is getting all it needs for various functions and fueling the brain.
Despite popular media and conventional wisdom, in almost every study low carbohydrate diets dominate.
Your body will switch from using sugar as a primary fuel source to using fat as a primary fuel source. The theory is that cancer relies on glucose as its energy source; remove the energy source and the cancer dies. If you are considering trying a ketogenic diet you should figure out what your objectives are and what you want to achieve. In order to post comments, please make sure JavaScript and Cookies are enabled, and reload the page.
Unfortunately, ignoring the information isn’t an answer that will help or resolve anything.
The discovery of T1D susceptibility genes started as early as 1974 with just six genes identified by 2006 shown in red. This places the immune system in a vital position between healthy and diseased states of the host.
G Clayton, P Concannon, Type 1 Diabetes Genetics Consortium (2009Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes.
Q Qu, K Wang, H Hakonarson, 2011A Genome-wide, meta-analysis of six type 1 diabetes cohorts identifies multiple associated loci. C Ferreira, R Gentz, T Curran, 1989The product of a fos- related gene, Fra-1, binds cooperatively to the AP-1 site with Jun: transcription factor AP-1 is comprised of multiple protein complexes. D Cooper, C Wallace, 2012Long-range DNA looping and gene expression analyses identify DEXI as an autoimmune disease candidate gene.
A Van Heel, 2010Multiple common variants for celiac disease influencing immune gene expression. A raised level of blood sugar is actually quite damaging and generates systemic inflammation. Ketosis is actually preferable for endurance athletes as it prolongs energy by utilizing both glycogen and body fat stores. Many people will find it very easy to adhere to the ketogenic diet and achieve very good results.
When levels of glucose in the blood rise (for example, after a meal), the pancreas produces more insulin. The advent of GWAS led to flurry of novel genes associated with T1D reaching the excess of 40 by 2009 and almost 60 by 2012.
Its protective task is regulated by a complex regulatory mechanism involving a diverse army of cells and molecules of humoral and cellular factors working in concert to protect the body against invaders. CUX2 gene has been shown to directly regulate the expression of NeuroD (Iulianella et al., 2008). Your body converts dietary and body fat into ketone bodies, which are actually the preferred fuel source for many organs and muscles in your body (1) including the brain.

A wide variety of evidence suggests that the ketogenic diet could have beneficial disease-modifying effects in epilepsy and also in a broad range of neurological disorders characterized by death of neurons. Cancer is now being considered to be a disease of metabolic dysfunction rather than previously viewed as a genetic abnormality.
T1D is a complex trait that results from the interplay between environmental and genetic factors.
Both quantitative PCR and immunohistochemical analysis confirmed the presence of the HTR1A in human pancreas (Asad et al., 2012). A Todd, 2008Meta-analysis of genome-wide association study data identifies additional type 1 diabetes risk loci.
Fat theoretically has a glycemic index of zero and will have almost no effect on blood sugar. If you have restricted your carbohydrate intake or have exercised rigorously these storages sites will have capacity.
In the state of ketosis many people find their energy levels will remain stable and that fat very easily melts off your body. Blood flow to the brain also increases during ketosis and has been shown to increase by 39%.
Weight lifters and sprinters will still require carbohydrates to replace glycogen stores after intense workouts. Innate immunity is comprised of physical, chemical, and microbiological barriers to the entry of antigen, and the elements of immune system (DC, macrophages, mast cells, NK cells, neutrophils, monocytes, complements, cytokines and acute phase proteins), which provide immediate host defense. The study suggests that HTR1A may affect T1D susceptibility by modulating the initial autoimmune attack or either islet regeneration, insulin release, or both. Eating a diet of predominantly protein and fat, with some complex carbohydrates (like vegetables) will help maintain a stable blood sugar. However, if they are full your body has no choice but to convert the excess blood sugar into body fat. But will still have comparable performance simply using the glycogen stores within the body. You may do just as well by having a low-moderate carbohydrate intake in the form of complex carbohydrates which have a low glycemic index. The epidemiological data showing differences in geographic prevalence is one clear indicator, with populations of European ancestry having the highest presentation rate. Adaptive immunity is the hallmark of the immune system of higher animals with T and B cells as the key cellular players that provide more specific life-long immunity.
The HTR1A gene is known to encode for a G-protein coupled receptor specific for serotonin, which mediates cellular signaling via the amine serotonin (Barnes & Sharp, 1999).
Sugar can be viewed as rocket fuel for quick spontaneous power and fat as a wood burning stove for long consistent energy.
It is something you can experiment with to see how you feel and perform and get a better sense of what it is like.
In T1D this system breaks down: insulin-producing ?-cells are subjected to specific attack by the host immune system.
The HTR1A receptor is mainly known to mediate signal transduction in neurons in the central nervous system (Lesurtel et al., 2008). Imagine the storage sites are your gas tank in your car, you can only fill it up so much and if you keep pumping when the tank’s full, gasoline will overflow and spill everywhere. T1D develops at all ages and occurs through the autoimmune destruction of pancreatic ?-cells with resulting lack of insulin production. To better understand the etiology of T1D, a plethora of research has been done to link the systematic destruction of ?-cells and the role of the immune system. However, serotonin is also produced in pancreatic islets of several different species (Sundler et al., 1980). The immune system participates in ?-cell destruction through several of its components including natural killer (NK) cells, B lymphocytes, macrophages, dendritic cells (DC), and antigen-presenting cells (APCs). Studies in rodent islets show inhibition of insulin secretion by serotonin (Zawalich et al., 2004).
Studies in human and animal models have shown that both innate and adaptive immune responses participate in disease pathogenesis, possibly reflecting the multifactorial nature of this autoimmune disorder. Further linkage analysis and candidate gene association studies revealed additional loci associated with T1D.
Sumatriptan (serotonin agonist) has an inhibitory effect on insulin secretion in humans (Coulie et al., 1998). In this review, we provide an update on genome-wide association studies (GWAS) discoveries to date and discuss the latest associated regions added to the growing repertoire of gene networks predisposing to T1D.2.
Starting in 2007, GWAS have increased the number of loci be associated with T1D to almost 60. Mohanan et al., 2006 reported a decrease in expression of HTR1A with increased insulin release during pancreatic regeneration.
In Figure 1 we present 59 T1D susceptibility loci as where we have classified them into loci harboring non-immune (14) vs. Before genome-wide association studies Historically, prior to GWAS, only six loci had been fully established to be associated with T1D.
Hence polymorphisms in the HTR1A gene may affect insulin release and T-cell activity, thereby increases the risk of developing T1D. This cluster of homologous cell-surface proteins is divided into class I (A, B, C) and class II (DP, DQ, RD).
The HLA genes encode highly polymorphic proteins, which are essential in self versus non-self immune recognition.
The advent of GWAS led to flurry of novel genes associated with T1D reaching the excess of 40 by 2009 and almost 60 by 2012.The complex crosstalk between innate and adaptive immune cells has major impact on the pathogenesis and development of T1D as illustrated in Figure 2.
Conclusions This chapter provides a summary of recent advances in the identification of multiple variants associated with T1D. The class I molecules are ubiquitously expressed and present intracellular antigen to CD8+ T cells. The initiation phase (Phase I) of T1D development takes place in the pancreas where conventional dendritic cells (cDCs) capture and process ?-cell antigens.
Genome wide association studies have revolutionized the field of autoimmune mediated disorders. Class II molecules are expressed mainly on professional APCs: DCs, macrophages, B-lymphocytes and thymus epithelium. Class II molecules are composed of A and B chains, and present antigens to CD4+ T cells, which promote inflammation by secreting cytokines upon recognition of their specific targets. GWAS has contributed greatly by expanding the number of established genetic variants to 57 genes.
Approximately half of the genetic risk for T1D is conferred by the genomic region harboring the HLA class II genes primarily HLA-DRB1, -DQA1 and -DQB1 genes). Migration of activated cDCs to the draining lymph node primes pathogenic islet antigen-specific T cells. In 1984, insulin (INS) gene encoded on chromosome 11p15 was identified as second loci linked with T1D (Bell et al., 1984). For the first time there is real consensus on the role of specific genetic factors underpinning T1D pathogenesis.
In 1996, the cytotoxic T-lymphocyte-associated protein 4 (CTLA4) gene encoded on chromosome 2q33 was recognized as third loci (Nistico et al., 1996). B cells present ?-cell antigen to diabetogenic T cells and secrete autoantibodies in response.
The discoveries of genetic factors involved in the pathogenesis of T1D through GWAS present the first step in a much longer process leading to cure. In 2004, a protein tyrosine phosphatase, non-receptor type 22 (PTPN22) gene encoded on chromosome 1p13, was found to be associated with susceptibility to T1D in another case-control study (Bottini et al., 2004). The activation of islet antigen-specific T cells can be inhibited by cDCs through engagement of programmed cell death ligand 1 (PDL1). Genes uncovered using this approach are indeed fundamental to disease biology and will define the key molecular pathways leading to cure of T1D. Vella et al., 2005 reported interleukin 2 receptor alpha (IL2RA) gene as fifth T1D loci on chromosome 10p15. However, such genome wide scans can lack coverage in certain regions where it is difficult to genotype so it is possible that other loci with reasonable effect sizes remain to be uncovered. These DCs promote expansion of regulatory T (TReg) cells through the production of indoleamine 2,3-dioxygenase (IDO), IL10, transforming growth factor-? (TGF?) and inducible T cell co-stimulator ligand (ICOSL). To date most of T1D-associated variants have been discovered utilizing cohorts of European ancestry because the SNP arrays were designed to optimally capture the haplotype diversity in this ethnicity.
Phase III: In the pancreas, ?-cell can be killed by diabetogenic T cells and NK cells through the release of interferon-? (IFN?), granzymes and perforin, as well as by macrophages through the production of tumour necrosis factor (TNF), IL-1? and nitric oxide (NO).

Novel SNP arrays are needed with the same degree of capture in diverse populations to elucidate the full role of each locus in a worldwide context.
GWAS of T1DThe advent of GWAS in the mid-2000s has changed the situation dramatically, increasing the pace and efficiency of discovery for the T1D associated loci, by a factor of ten. IL12 produced by cDCs sustains the effector functions of activated diabetogenic T cells and NK cells. The next challenge is to resolve the specific causal variants and determine how they affect the expression and function of these gene products. The critical platform for this work was laid by the HapMap project (International HapMap Consortium, 2003, 2005). TReg cells that inhibit diabetogenic T cells and innate immune cells through IL10 and TGF? can prevent ?-cell damage. The Next-Generation Sequencing (NGS) technology has opened new avenues to elucidate the role of coding and noncoding RNAs in health and disease and would speed up the identification of causative gene variants in T1D. The GWAS approach has been made possible by the development of high-density genotyping arrays.
Tolerogenic pDCs stimulated by iNKT cells could also control diabetogenic T cells through IDO production. No doubt, the in vitro and in vivo biology of these genes will be fascinating areas of exploration for many scientists. The genome is laid out in discrete linkage disequilibrium (LD) blocks with limited haplotype diversity within each of these blocks. Only after fully uncovering the functional context of T1D associated genes; these findings will show promise of use for preventive strategies. Therefore, a minimal set of single nucleotide polymorphisms (SNPs) can detect almost all common haplotypes present, thus improving genotyping accuracy and reducing cost. The first full-scale GWAS for T1D were published in 2007 by our group (Hakonarson et al., 2007) and The Wellcome Trust Case-Control Consortium (WTCCC, 2007). It is established that C-type lectins function both as adhesion and pathogen recognition receptors (PPRs) (Cambi & Figdor, 2003). We examined a large pediatric cohort of European descent using the Illumina HumanHap 550 BeadChip platform.
In addition, CLEC16A is almost exclusively expressed in immune cells including DCs, B-lymphocytes and NK cells. The design involved 561 cases, 1,143 controls and 467 triads in the discovery stage, followed by a replication effort in 939 nuclear families. Our 2007 GWAS in a large pediatric cohort of European descent identified CLEC16A as a novel T1D susceptibility gene within a 233-kb linkage disequilibrium block on chromosome 16p13.
In addition to finding the “usual” suspects, including an impressive 392 SNPs capturing the very strong association across the major histocompatibility complex (MHC), we identified significant association with variation at the KIAA0350 gene, which we replicated in an additional cohort. Three common non-coding variants of the CLEC16A gene (rs2903692, rs725613 and rs17673553) reached genome-wide significance for association with T1D (Hakonarson et al., 2007).
Todd et al., 2007 confirmed these findings, using 4,000 cases, 5,000 controls and 3,000 T1D families as well as association reported in the WTCCC study to the 12q13 region. The 2007 WTCCC study independently discovered CLEC16A (formally known as KIAA0350) as a T1D susceptibility locus associated with the non-coding variant rs12708716. Recently, Davison et al., 2012 reported intron 19 of the CLEC16A gene behaves as a regulatory sequence, which affects the expression of a neighboring gene dexamethasone-induced (DEXI).
Meta-analyses of T1D GWAS datasetsIn order to get the most from GWAS and to increase the statistical power, several independent research groups carried out meta-analyses using datasets from different investigative groups. While it is clear that intron 19 of CLEC16A is highly enriched for transcription-factor-binding events, more functional studies are needed to advance from GWAS to candidate causal genes and their biological functions. To find causal variant of CLEC16A gene we sequenced the 16p13 region in 96 T1D patients and found 10 new non-synonymous SNPs resulting in one stop-codon, two splice site mutations, and 7 amino acid changes (unpublished data). The SNPs with lowest nominal P-values were taken forward for further genotyping in an additional British cohort of 6,000 cases, 7,000 controls and 2,800 families. The studies are under way to examine if these changes are correlated with CLEC16A expression and if these SPNs are present in control group. Kim et al., 2010 characterized ema as an endosomal membrane protein is required for endosomal trafficking and promotes endosomal maturation.
The study included samples from WTCCC, 20070, the GoKind study (Mueller et al., 2006) and controls and family sets from Type 1 Diabetes Genetics Consortium (T1DGC). Expression of human orthologue of ema ‘CLEC16A’ rescued the Drosophila mutant demonstrating conserved function of the protein. A recent study by the same group also reported its requirement for the growth of autophagosomes and proposed that the Golgi is a membrane source for autophagosomal growth, and that ema facilitates this process (Kim et al., 2012). Expression of CLEC16A rescued the autophagosome size defect in the ema mutant, suggesting that regulation of autophagosome morphogenesis may be one of the fundamental functions of CLEC16A.
Targeted follow-up of 53 SNPs in 1,120 affected trios uncovered three new loci associated with T1D that reached genome wide significance.
Another recent study elucidated the dynamic expression changes and localization of CLEC16A in lipopolysaccharide (LPS) induced neuroinflammatory processes in adult rats. The most significantly associated SNP (rs539514, P = 5.66x10-11) resided in an intronic region of the LMO7 (LIM domain only 7) gene on 13q22.
In vitro studies indicated that the up-regulation of CLEC16A might be involved in astrocyte activation following LPS challenge (Wu et al., 2012).
The third most significantly associated SNP (rs924043, P = 8.06x10-9) was in an intergenic region on 6q27, where the region of association is approximately 900kb and harbors additional genes including WDR27, C6orf120, PHF10, TCTE3, C6orf208, LOC154449, DLL1, FAM120B, PSMB1, TBP and PCD2. These latest associations add to the growing repertoire of gene networks predisposing to T1D. Targeted follow-up of 53 SNPs in 1,120 affected trios uncovered three novel loci associated with T1D that reached genome-wide significance (Bradfield et al., 2011). LMO7 is a multi-domain mammalian protein with a calponin homology (CH) domain, a discs-large homologous regions (DHR) domain, and a LIM domain.
Mice with homozygous deletions of LMO7 display retinal, muscular, and growth retardation (Semenova et al., 2003). In cultured rat ascites hepatoma cells, the upregulation of LMO7 correlates with the ability of transforming growth factor ? (TGF?) to enhance the invasiveness of these cells (Nakamura et al., 2005). Although the function of LMO7 does not clearly relate to the etiology of T1D, LMO7 is expressed in pancreatic islets and thus is a possible biological candidate at this locus (Kutlu et al., 2009). EFR3B is an 817 amino acid protein that exists as three alternatively spliced isoforms and belongs to the EFR3 family. A number of genetic diseases have been linked to genes on chromosome 2 including Harlequin icthyosis, lipid metabolic disorder sitosterolemia, and Alstrom syndrome.
Location of SNP rs478222 in the intronic region of EFR3B gene makes it a good candidate, however the 2q23 region harbors additional multiple genes, including NCOA1, C2orf79, CENPO, ADCY3, DNAJC27, POMC, and DNMT3A. C2orf79 is peptidyl-tRNA hydrolase domain containing 1 (PTRHD1) predicted protein with unknown function.Centromere protein O (CENPO) gene encodes a component of the interphase centromere complex.
The protein is localized to the centromere throughout cell division and is required for bipolar spindle assembly, chromosome segregation and checkpoint signaling during mitosis (Okada et al., 2006). This protein catalyzes the formation of the secondary messenger cyclic adenosine monophosphate (cAMP) and is highly expressed in human placenta, testis, ovary, and colon (Ludwig & Seuwen, 2002). Wong et al., 2000 reported the presence of adenylyl cyclase 2, 3, and 4 in olfactory cilia. DNA (cytosine-5)-methyltransferase 3 alpha (DNMT3A) gene encodes a protein that functions as a de-novo methyltransferase that can methylate unmethylated and hemimethylated DNA with equal efficiencies (Yanagisawa et al., 2002).
The region of association is approximately 900kb and harbors multiple genes including PHF10, TCTE3, DLL1, FAM120B, PSMB1, TBP, and PDCD2.
Su et al., 2006 reported pancreatic regeneration in chronic pancreatitis requires activation of the notch-signaling pathway.
Family with sequence similarity 120B (FAM120B) gene encodes protein belonging to the constitutive coactivator of peroxisome proliferator-activated receptor gamma (PPARG) family.
This gene encodes TBP, the TATA-binding protein a transcription factor that functions at the core of the DNA-binding multiprotein transcription factor IID (TFIID). In addition, despite not reaching the genome wide significance, our study observed evidence for association at three additional loci containing the candidate genes LOC100128081, TNFRSF11B and FOSL2 (Bradfield et al., 2011). Of these, it is notable that the tumor necrosis factor receptor superfamily, member 11B (TNFRSF11B) is a strongly associated locus with bone mineral density, also discovered in GWAS, and the locus harboring LOC100128081 has also been reported in the context of a GWAS of SLE.
FOS-like antigen 2 (FOSL2) gene encodes a leucine zipper protein that dimerizes with the JUN family proteins and forms the transcription factor complex activator protein 1 (AP-1).

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