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Science, Technology and Medicine open access publisher.Publish, read and share novel research. Impact of Genetic Polymorphisms on Insulin ResistanceEvrim Komurcu-Bayrak[1] Department of Genetics, Institute for Experimental Medicine, Istanbul University, Turkey1.
Bianco AC, Maia AL, da Silva WS, Christoffolete MA.2005Adaptive activation of thyroid hormone and energy expenditure. On the plus side the 20 Minute Meals app includes detailed step-by-step photos for each recipe Haskell library aace diabetes guidelines ppt would encourage use o Type lazy-evaluation. However modern doctors routinely give insulin to people with type 2 diabetes simply because it reducs blood sugar levels. Blending aloe vera gel in a blender and drinking it once This is about the basics techniques etc. For women free fatty acids (ffa) a link between obesity and insulin resistance with type 2 diabetes is it a good idea to start insulin if you ae trying to conceive? I once watched a guy scoop corn out with his bare hand instead of asking for a spoon from the staff. General overview of genetic and environmental factors contributing to the development of insulin resistance and type 2 diabetes. IntroductionThe identification of DNA polymorphisms in human populations is an important step towards understanding the contribution of functional genetic variants to predisposition of diseases or clinical phenotypes.
Dunaif, 1995Hyperandrogenic anovulation (PCOS): a unique disorder of insulin action associated with an increased risk of non-insulin-dependent diabetes mellitus. Diabetic Ketoacidosis Warning Signs diabetes hereditary or not symptoms of diabetes uk One of the test for nephrogenic diabetes insipidus most common diabetes and pregnancy medscape complications is diabetic neuropathy which is a form of nerve damage that results from the effects of high blood sugar levels upon nerve fibers throughout the body.
It is important to know diabetes care center uknapolis the name of the diabetes drug you are taking INSULIN How it works Examples Insulin lowers blood fat induced insulin resistance and atherosclerosis glucose (blood sugar). The number of injections of insulin taken each day depends on the needs of the individual and the type of insulin used.
The answer is probably because it is the only drug that reliably youtube penyakit diabetes drops blood sugars below the level that cause secondary insulin resistance. Louisiana diabetes tracker apps Department of State Civil Service – Baton leading cause of insulin resistance Rouge LA.
The combination of genetic predisposition (genetic polymorphisms effecting free fatty acid metabolism, insulin signalling, adipokines and cytokines) and some environmental factors such as excessive dietary intake and physical inactivity results with the occurrence of adipocytogenesis, lipodystrophy and obesity which increase the development risk of insulin resistance. Approach to the determination of the predisposition uses polymorphisms as marker for a disease in an affected DNA population compared to a control DNA population.
Isulin resistance in obese individuals may also be associated with high does canine diabetes cause blindness levels of plasma leptin and low levels of adiponectin. Magnesium can be found in foods such as dry roasted almonds spinach cashews peanut butter and baked potatoes. Researhers from Italy have found a statistically significant association between enteroviral infection and diagnosis of type-1 diabetes in children.
The Joy of Diabetes book is a diabetic handbook that embraces living with Type 1 Diabetes (Juvenile Diabetes) & Type 2 Diabetes. Insulin resistance predates pancreatic beta cell dysfunction and plays the crucial role in the pathogenesis of type 2 diabetes. Subsequently, the polymorphisms statistically associated with the disease group may be directly informative or linked to the probable causative variant.
Consequently sick people have extremely high insurance rates or simply can’t buy coverage. Resultant increase of proinflammatory mediators and imbalance in adipokines reduced eNOS expression. Christov, 2003Testosterone supplementation in men with type 2 diabetes, visceral obesity and partial androgen deficiency.
Pretty easy to put together took two of us about an hour and a half with only a few swear words involved! This large variant set might not represent the variants causative of disease because it was performed in genomes of only a limited number of individuals. Sacchettini, 1996A polymorphism in the human intestinal fatty acid binding proteins alters fatty acid transport across Caco-2 cells. Do you have tips on diabetes type 2 best diet type 2 diabetes symptoms numbness Symptoms of Diabetes: Diabetes Signs That Are Common to Men Mango Peach Yogurt Smoothie Recipe. For this reason, the discovery genetic variation in regions of functional DNA sequence in the genomes of individuals with disease is important for disease-gene association studies. Yoon, 2001The A54T polymorphism at the intestinal fatty acid binding protein 2 is associated with insulin resistance in glucose tolerant Caucasians. The resultant adiposity and release of free fatty acids caused mitochondrial dysfunction and paradoxical reduction in oxidative phosphorylation and increase in the formation of oxidative free radicals. Conde, 2008Influence of Lys656Asn polymorphism of the leptin receptor gene on insulin resistance in nondiabetic obese patients. A lytic cycle where its DNA is reproduced quickly by host cells and bursts going on to infect more cells or a lysogenic cycle wehre it incorporates itself into your chromosomes and multiplies as your cells divide waiting until it decides to go lytic.
For arthritics, D-Phenylalanine was shown to be especially effective at reducing inflammation associated with osteoarthritis by research conducted by Seymour Ehrenpreis at the University of Chicago. Therefore, recently, genome-wide association (GWA) or candidate gene approaches are used in the understanding of the molecular genetic background of complex polygenic disease. Maia, 2010Association of the type 2 deiodinase Thr92Ala polymorphism with type 2 diabetes: case-control study and meta-analysis. This causes the development of type 2 diabetes which along with central adiposity amplifies the risk of cardiovascular diseases in metabolic syndrome. Mather, 2005Insulin and endothelin in the acute regulation of adiponectin in vivo in humans. Bouchard, 1999Linkages and associations between the leptin receptor (LEPR) gene and human body composition in the Quebec Family Study. Vicente, 2006Leptin receptor Lys656Asn polymorphism is associated with decreased leptin response and weight loss secondary to a lifestyle modification in obese patients. Soler, 1997The TNF-alpha gene Nco I polymorphism influences the relationship among insulin resistance, percent body fat, and increased serum leptin levels. Insulin resistance is caused by the reduced ability of peripheral target tissues to respond properly to insulin stimulation. Perez-Bravo, 2004Intestinal FABP2 A54T polymorphism: association with insulin resistance and obesity in women. Insulin resistance predates beta cell dysfunction and plays the crucial role in the pathogenesis of type 2 diabetes. Ogihara, 2006Effects of angiotensin II type 1 receptor gene polymorphisms on insulin resistance in a Japanese general population: the Tanno-Sobetsu study.


Saruta, 2004Novel resistin promoter polymorphisms: association with serum resistin level in Japanese obese individuals. Parker, 2004Mitochondrial superoxide: production, biological effects, and activation of uncoupling proteins.
Lupien, 1993Apolipoprotein E polymorphism modifies relation of hyperinsulinemia to hypertriglyceridemia.
Botnia, Group, 2007Variation in GYS1 interacts with exercise and gender to predict cardiovascular mortality.
Pedersen, 2007Studies of the common DIO2 Thr92Ala polymorphism and metabolic phenotypes in 7342 Danish white subjects. Kim, 2009Type 2 deiodinase expression is induced by peroxisomal proliferator-activated receptor-gamma agonists in skeletal myocytes. Ordovas, 2003Obesity modulates the association among APOE genotype, insulin, and glucose in men.
Oka, 2007Involvement of apolipoprotein E in excess fat accumulation and insulin resistance. Pedersen, 2003Mutational analysis of the UCP2 core promoter and relationships of variants with obesity. Romero, 2010Relation of-55CT polymorphism of uncoupling protein 3 gene with fat mass and insulin resistance in morbidly obese patients. Given the crucial roles of pathways in the pathogenesis of liver and muscle insulin resistance, understanding the molecular mechanism of insulin resistance is vital for the development of new and more effective therapies for metabolic disorders. Prochazka, 1995An amino acid substitution in the human intestinal fatty acid binding protein is associated with increased fatty acid binding, increased fat oxidation, and insulin resistance. The homeostasis model assessment (HOMA) index for insulin resistance was calculated as the product of fasting plasma insulin (in microunits per milliliter) and fasting plasma glucose (in millimoles per liter), divided by 22.5 (Matthews et al. Bouchard, 2000Associations between the leptin receptor gene and adiposity in middle-aged Caucasian males from the HERITAGE family study. Genetic and epidemiological studies strongly suggest that insulin resistance is, at least in part, genetically determined.
Matsuzawa, 1999Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity.
Boehnke, 2004Variation in the resistin gene is associated with obesity and insulin-related phenotypes in Finnish subjects. The numerous genes have been suggested as a potential candidate gene for insulin resistance, but the findings of these studies were controversial. This chapter is to provide an overview of our recent understanding of genetic predisposition to insulin resistance.
It is aimed to summarize the results of the recent studies about the genetics of insulin resistance.
The polymorphisms of the FABP genes Fatty acid-binding proteins (FABPs) are members of a superfamily of lipid-binding proteins.
These tissue specific proteins (FABP1-4) play the physiological role in the uptake, intracellular metabolism and excretion of long-chain fatty acids (LCFA) (Zimmerman & Veerkamp, 2002). The polymorphisms of these genes have been studied in several metabolic phenotypes such as obesity, metabolic syndrome, hypertriglyceridemia and insulin sensitivity (Mansego et al. Roche, 2010Gene-nutrient interactions in the metabolic syndrome: single nucleotide polymorphisms in ADIPOQ and ADIPOR1 interact with plasma saturated fatty acids to modulate insulin resistance. 2012).The liver FABP (FABP1) is an abundant cytosolic lipid-binding protein that regulates lipid transport and metabolism. In this study, it has been shown that carriers of the allele A of this polymophism had HOMA index values higher than homozygotes GG.
However, none of the other analyzed variants in FABP2, FABP3 and FABP4 genes were associated with type 2 diabetes and insulin resistance in this study (Mansego et al.
2012).The intestinal FABP (FABP2) plays a key role in the absorption and intracellular transport of dietary LCFA (Weiss, 2002). Therefore, the FABP2 gene has been suggested as a possible candidate gene for type 2 diabetes and insulin resistance.
Furthermore, the linkage analysis of the FABP2 locus with insulin resistance was also found in a study in Mexican Americans who were of a mixed American-Indian and -European ancestry (Mitchell et al., 1995). However, sib-pair analysis failed to detect any linkage of the FABP2 locus or the Ala54Thr polymorphism with diabetes-related phenotypes in other ethnic groups.
However, the findings of this study would need to be confirmed in studies involving a larger number of subjects. A number of conflicting and inconclusive studies have investigated the possible association of the FABP2 Ala54Thr polymorphism with insulin resistance. A meta-analysis of these published studies has suggested that the Thr54 allele of the FABP2 Ala54Thr is weakly associated with a higher degree of insulin resistance, higher fasting insulin and blood glucose level. As gender and ethnicity probably were important variables in determining associative risk with insulin resistance and type 2 diabetes, Zhao et al. The polymorphisms of the ELOVL6 geneElongase of long chain fatty acids family 6 (ELOVL6) is expressed in lipogenic tissues.
This enzyme specifically catalyze the elongation of saturated and monounsaturated fatty acids with 12, 14 and 16 carbons.
A population-based study has suggested that the genetic variations in the ELOVL6 gene are related with insulin resistance. In this population from southern Spain, carriers of the minor alleles of the rs9997926 and rs6824447 polymorphisms had a lower risk of having high HOMA index, whereas carriers of the minor allele rs17041272 had a higher risk of being insulin resistant.
The polymorphisms of the APOE geneApolipoprotein E (ApoE) is primarily involved in plasma lipid homeostasis.
ApoE is involved in excess fat accumulation and energy metabolism, including the regulation of food intake and energy expenditure. Therefore, excess fat accumulation via an apoE-dependent pathway might play a role in the development of insulin resistance (Kypreos et al., 2006). In a cross-sectional study, the impacts of these polymorphisms have been analyzed on lipid, apolipoprotein, glucose, and serum insulin concentrations in the TARF cohort, a representative of Turkish adults. On the other hand, a large population-based family study related with type 2 diabetes found a relationship for the polymorphisms of the APOE gene and the nearby muscle glycogen synthase (GYS1) gene on chromosome 19 with cardiovascular mortality, independently of each other (Fredriksson et al., 2007). Other functional polymorphisms in the GYS1 gene may relate to developing insulin resistance. The polymorphisms of the UCP genesUncoupling protein 2 and 3 (UCP2 and UCP3) play an important role in human energy homeostasis (Brand et al., 200 4) and have been considered candidate genes for obesity, type 2 diabetes and insulin resistance. Thus, UCP2 and UCP3 are involved in regulating ATP synthesis, generation of reactive oxygen species and glucose-stimulated insulin secretion by pancreatic ? cells. However, Andersen et al has found an association between this variant and obesity in Danish individuals and established case-control studies.


This study has shown that the -866G-allele was associated with elevated fasting serum insulin levels and insulin resistance (HOMA index) and decreased insulin sensitivity in Danish subjects (Andersen et al., 2012).
Furthermore, in a study performed with a Spanish group of 193 obese children and adolescents and 170 controls, Ochoa et al. The polymorphisms of the ADRB genes?-adrenoceptors (ADRB1, ADRB2, ADRB3) in the sympathetic nervous system play a role in regulating energy expenditure and lipolysis. ADRBs gene variation is an intense area of investigation because ?-adrenoceptors are well described in organ system distribution, catecholamine-mediated physiological processes, disease states and treatment targets (Eisenach & Wittwer, 2010). One of the most studied polymorphism (rs1801253) in the ADRB1 gene encode for arginine or glycine in amino acid 389 (Arg389Gly).
In 238 healthy young Caucasians and African-Americans, Gly389 carriers had a higher level of insulin and insulin resistance than non-carriers, and this allele was more prevalent in the subjects with higher body mass index (BMI; Lima et al. In previous studies, it has been found that this polymorphism was associated with serum insulin levels and insulin resistance (HOMA index) but, no association with obesity among Swedish women (Mottagui-Tabar et al., 2008). However, there are limited number of studies evaluating the association between these genes and insulin resistance. In larger scale studies with different populations should be performed for these genes to support the association between genotype and phenotype.4. The polymorphisms of the APM1, ADIPOR1, and ADIPOR2 genesAdiponection is an adipokine secreted by adipocytes.
The polymorphisms in adiponectin (APM1,ADIPOQ, ACRP30) gene, and its receptors (ADIPOR1 and ADIPOR2) are strongly associated with metabolic syndrome, obesity, type 2 diabetes and, insulin resistance. Furthermore, administration of thiazolidinediones (TZD), an insulin-sensitising class of drugs, to insulin-resistant subjects significantly increased the plasma adiponectin levels, and this effect was correlated with the amelioration of insulin resistance in these subjects (Maeda et al., 2001). In a study from Menzaghi et al, a haplotype of the adiponectin gene was associated with several features of insulin resistance in nondiabetic individuals, including low serum adiponectin levels (Menzaghi et al., 2002). The reasons for partially discrepant results between polymorphisms in these genes and metabolic measures could be due to the different genetic background of the studied populations or environmental interactions, particularly dietary factors. The polymorphisms of the D2 and TSHR genesThyroid hormones are known to upregulate the expression of glucose transporter type 4 (GLUT4) in skeletal muscle, and consequently increase glucose uptake (Weinstein et al., 1994). Thyroxine (T4), a major secretory product of the thyroid gland, needs to be converted to triiodothyronine (T3) to exert its biological activity. Type 2 deiodinase (D2) catalyzes T4 to T3 conversion, and plays a critical role in maintaining intracellular T3 levels in specialized tissues, such as the anterior pituitary and brown adipose tissue (Bianco et al., 2005). Thr92Ala polymorphism of D2 gene showed an association with lower glucose disposal rate in nondiabetic subjects and also a higher prevalence of insulin resistance in Pima Indians and Mexican–Americans (Mentuccia et al., 2002).
In addition, this polymorphism was associated with greater insulin resistance in type 2 diabetes patients and with lower enzyme activity in thyroid tissue samples (Canani et al., 2005). A previous study has investigated the association between serum thyroid parameters and the TSHR Asp727Glu polymorphism in nondiabetic elderly men. Carriers of the Glu727 allele had also a significantly higher glucose, insulin, HOMA index and leptin levels, but no association with serum TSH levels (Peeters et al., 2007).
The polymorphisms of the SHBG geneSome studies have suggested that the polymorphisms in genes encoding sex hormones may be effective on the development of insulin resistance. Moreover, polycystic ovarian syndrome was associated with higher risk of type 2 diabetes and insulin resistance in women (Dunaif, 1995).
The polymorphisms of the LEP and LEPR genesLeptin (LEP), a hormone secreted by adipocytes, and its receptor (LEPR) are other candidate genes for insulin resistance. However, the roles of leptin and its receptor in the development of metabolic traits in the general population are less clear. The polymorphisms of the RBP4 geneRetinol-binding protein 4 (RBP4) is an adipokine with potential contribution to systemic insulin resistance (Yang et al., 2005). The polymorphisms of the RETN geneResistin (RETN), a hormone secreted by adipocytes, has been examined as candidate gene for obesity and type 2 diabetes and insulin resistance. These conflicting findings have made it difficult to determine a role for resistin in insulin resistance. The reasons for discrepant results are not known, and may reside in the different genetic background of the studied populations or the different-designed studies.5. Hypertension is related to insulin resistance and a number of studies have reported an association between RAS gene polymorphisms and hypertension (Sugimoto et al. However, further studies are required to confirm the impact of these candidate gene polymorphisms in the larger and different populations.6. The polymorphisms of the TNF-? gene Tumor necrosis factor alpha (TNF-?) is a multifunctional proinflammatory cytokine and also an adipokine produced in adipocytes. In addition, the TNF-? affects lipid metabolism and may lead to hypertriglyceridemia by decreasing hepatic lipoprotein lipase activity and by increasing hepatic de novo fatty acid synthesis (Zinman et al., 1999). A meta-analysis of many published studies including different populations has suggested that -308A TNF-? gene variant is associated with increased risk of developing obesity compared with controls and significantly higher systolic arterial blood pressure and plasma insulin levels (Sookoian et al., 2005). TNF-? -857C>T polymorphism is also associated with obese type 2 diabetes (Kamizono et al. 2000) and insulin resistance in Japanese diabetic subjects with adiponectin +276GG genotype (Ohara et al., 2012). Other genetic or environmental factors may play important roles in modulating the relationships.7. ConclusionThe insulin resistance is highly heritable and originates from the interactions of multiple genes and environmental factors. Figure 1 shows the main factors contributing to the development of insulin resistance and type 2 diabetes. Until now, goal of many studies was to use a candidate gene approach to identify genes associated with insulin resistance and several genes have been investigated in many association-based studies. These discrepant results might be due to differences in the study populations and design of these studies. In addition, the candidate gene polymorphisms have been searched in a number of small-scale studies with variable results. Limited number meta-analyses have been done to demonstrate the effect of several candidate gene polymorphisms on insulin resistance.
On the other hand, the use of genome-wide association (GWA) studies will identify novel polymorphisms related to insulin resistance.



Current treatment for diabetic neuropathy 356.9
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