Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The insulin resistance syndrome, also referred to as the metabolic syndrome or syndrome X, is associated with a primary cellular defect in insulin action (insulin resistance) and a compensatory increase in insulin secretion. The combination of insulin resistance and subsequent hyperinsulinaemia causes a number of metabolic and cardiovascular changes that result in a syndrome typically characterised by type 2 diabetes, obesity, dyslipidaemia, coronary artery disease and hypertension. Moreover, disturbances in sleep (sleep apnoea) and ovarian dysfunction are also characterised by insulin resistance. The pathophysiological basis for these disturbances reflects the impact of variable genetic and environmental influences. At a molecular level, insulin resistance involves defects of insulin signalling such as reduced insulin receptor tyrosine kinase activity and reduced post-receptor phosphorylation steps that impinge on metabolic and vascular effects of insulin.
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PMID:The insulin resistance syndrome: physiological considerations. 1746 39

The metabolic syndrome (also referred to as syndrome X or the insulin resistance syndrome) has emerged as an important cluster of risk factors for atherosclerotic disease. Patients with the syndrome also are at increased risk for developing type 2 diabetes mellitus. Common features are central (abdominal) obesity, insulin resistance, hypertension, and dyslipidemia. Weight reduction deserves first priority in individuals with abdominal obesity and the metabolic syndrome. Both weight reduction and maintenance of a lower weight are best achieved by a combination of reduced caloric intake and increased physical activity. Dietary patterns close to the Mediterranean diet and rich in fruit and vegetables, and high in monounsaturated fats are negatively associated with features of the metabolic syndrome. Some recent studies dealing specifically with the effect of interventions on the resolution of the metabolic syndrome have demonstrated a 25% net reduction in the prevalence of the syndrome following lifestyle changes mainly based on nutritional recommendations. Similar rates of resolution have been obtained with drugs, such as rosiglitazone and rimonabant. The favourable benefit/hazard ratio makes Mediterranean-style diets particularly promising to reduce the cardiovascular burden associated with the metabolic syndrome.
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PMID:Mediterranean diet and the metabolic syndrome. 1787 92

The metabolic syndrome also called syndrome X, is a constellation of interrelated risk factors of metabolic origin--metabolic risk factors--that appear to share insulin resistance as a possible pathogenetic factor that directly promote the development of atherosclerotic cardiovascular diseases and increase the risk for developing type 2 diabetes mellitus. The recommended first step for treatment of metabolic syndrome is lifestyle modifications such as weight loss, aerobic exercise, smoking cessation, and improved diet which independently improve insulin resistance and slow progression to type 2 diabetes mellitus. Even though success achieved through lifestyle modification is limited, the significance of it cannot be overemphasized. Specific dietary changes that are appropriate for addressing different aspects of the syndrome include reducing saturated fat intake to lower insulin resistance, reducing sodium intake to lower blood pressure, and reducing high-glycemic-index carbohydrate intake to lower triglyceride levels. Furthermore, drugs able to reduce insulin resistance, such as metformin and thiazolidinediones, already in the therapeutic armamentarium of type 2 diabetes, could be used in subjects with the metabolic syndrome as a preventive measure.
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PMID:Metabolic syndrome: are we at risk? 1809 42

Insulin resistance is being recognized increasingly as the basis for the constellation of metabolic abnormalities that make up the metabolic syndrome, or Syndrome X. Insulin resistance is also the primary risk factor for the development of type 2 diabetes mellitus, which is currently reaching epidemic proportions by affecting more than 170 million people worldwide. A combination of environmental and genetic factors have led to a dramatic rise in visceral adiposity, the predominant factor causing insulin resistance and type 2 diabetes. Visceral adiposity is also the major risk factor for the development of Sleep Apnea (SA)--an association that has fueled interest in the co-morbidity of SA and the metabolic syndrome, but hampered attempts to ascribe an independent causative role for Sleep Apnea in the development of insulin resistance and type 2 diabetes. Numerous population and clinic-based epidemiologic studies have shown associations, often independent of obesity, between SA (or surrogates such as snoring) and measures of glucose dysregulation or type 2 diabetes. However, treatment of SA with continuous positive airway pressure (CPAP) has not been conclusive in demonstrating improvements in insulin resistance, perhaps due to the overwhelming effects of obesity. Here we show that in lean, otherwise healthy mice that exposure to intermittent hypoxia produced whole-body insulin resistance as determined by the hyperinsulinemic euglycemic clamp and reduced glucose utilization in oxidative muscle fibers, but did not cause a change in hepatic glucose output. Furthermore, the increase in insulin resistance was not affected by blockade of the autonomic nervous system. We conclude that intermittent hypoxia can cause acute insulin resistance in otherwise lean healthy animals, and the response occurs independent of activation of the autonomic nervous system.
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PMID:Metabolic consequences of intermittent hypoxia. 1826 87

The metabolic syndrome (also known as syndrome X, insulin resistance syndrome, dysmetabolic syndrome, deadly quartet and plurimetabolic syndrome) is a cluster of factors associated with increased risk of developing coronary heart disease and/or type 2 diabetes. Several recent studies reviewed in the present paper have indicated an association between the metabolic syndrome and periodontitis, and suggest that people exhibiting several components of metabolic syndrome should be encouraged to undergo a periodontal examination. Further investigations are required to clarify the mechanisms of the relationship between metabolic syndrome and periodontal disease in men, and to determine whether oral health care in individuals exhibiting metabolic syndrome has the potential to reduce the incidence of various systemic diseases.
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PMID:Metabolic syndrome and periodontal diseases. 1936 79

Absence of meal-induced insulin sensitization (AMIS) results in a predictable progression of dysfunctions, including postprandial hyperglycemia, compensatory hyperinsulinemia, resultant hyperlipidemia, increased oxidative stress, and obesity, progressing to syndrome X and diabetes. To test the 'AMIS syndrome' hypothesis we used 3 known means of producing graded and progressive changes in meal-induced insulin sensitization in rats. We used an aging model (9, 26, and 52 weeks), associated with a slow development of AMIS; a low-dose sucrose supplement model to accelerate the development of AMIS; and an antioxidant cocktail (S-adenosylmethionine, vitamin E, and vitamin C) to protect against the effect of the sucrose on meal-induced insulin sensitization. Adiposity was assessed from weighed regional fat masses and bioelectrical impedance. AMIS developed with age, was increased by sucrose supplementation, and was inhibited by the antioxidant cocktail. AMIS correlated with postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, and with adiposity (r2 = 0.7-0.8) regardless of age or nutrient status. The range of degrees of AMIS, established over time with these models, afforded the tool with which to test the AMIS syndrome and further the argument that AMIS is the first metabolic defect that cumulatively leads to a predictable series of homeostatic disturbances and dysfunctions, including obesity and type 2 diabetes.
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PMID:Obesity, syndrome X, and diabetes: the role of HISS-dependent insulin resistance altered by sucrose, an antioxidant cocktail, and age. 2005 13

Syndrome X is a combination or co-occurrence of several known cardiovascular risk factors (including central obesity, dyslipidemias, fatty liver disease, hyperinsulinemia, insulin resistance, and hypertension) that affects at least one in five people in developed countries. Syndrome X shortens life and increases morbidity by contributing to the development of both diabetes and cardiovascular disease. Type 1 or 2 diabetes affects approximately 170 million people globally and these numbers are rapidly rising. In patients with diabetes, vascular diseases develop early and progress at an accelerated rate. It has recently become evident that glucose-6-phosphate dehydrogenase (G6PD), the rate limiting enzyme in the pentose-phosphate pathway and its reaction products play key roles in regulating vascular function. Epidemiological studies have also shown that G6PD deficiency markedly reduces retinopathy and mortality due to cardiovascular diseases in males from certain Mediterranean regions. Conversely, G6PD expression and activity are upregulated in rat and mouse models of obesity, hyperglycemia and hyperinsulinemia, and a role for G6PD in the development of insulin resistance in type 2 diabetes has been proposed. Unfortunately, there are no selective drugs available to validate the hypothesis that G6PD and its products are involved in the development of Syndrome X in humans. This review discusses the potential mechanisms by which G6PD could be implicated in vascular diseases in Syndrome X and the need to develop new approaches, including new drugs and molecular tools, to ameliorate diabetes-induced vascular dysfunction and vasculopathies.
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PMID:Targeting the Pentose Phosphate Pathway in Syndrome X-related Cardiovascular Complications. 2071 18

Serum- and glucocorticoid-inducible kinase 1 (SGK1) is expressed following cell stress and exposure to a variety of hormones including glucocorticoids and mineralocorticoids. It is activated by insulin and growth factors via phosphatidylinositol-3-kinase and the 3-phosphoinositide-dependent kinase PDK1. SGK1 enhances the activity of a variety of ion channels such as ENaC, TRPV5, ROMK, KCNE1/KCNQ1 and ClCKb; carriers such as NHE3, NKCC2, NCC and SGLT1; as well as the Na+/K+-ATPase. SGK1 contributes to Na+ retention and K+ elimination of the kidney as well as mineralocorticoid stimulation of salt appetite. A certain SGK1 gene variant (combined polymorphisms in intron 6 [I6CC] and in exon 8 [E8CC/CT]) is associated with moderately enhanced blood pressure. The SGK1 gene variant has been shown to affect 3%-5% of whites and some 10% of Africans. The gene variant sensitizes the carriers to the hypertensive effects of hyperinsulinemia. Moreover, the SGK1 gene variant is associated with increased body mass index, presumably a result of enhanced SGLT1 activity with accelerated intestinal glucose absorption. Obesity predisposes the carriers of the gene variant to development of type 2 diabetes. Moreover, SGK1 stimulates coagulation. Thus, SGK1 may participate in the pathogenesis of metabolic syndrome or syndrome X, a condition characterized by the coincidence of essential hypertension, procoagulant state, obesity, insulin resistance and hyperinsulinemia.
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PMID:SGK, renal function and hypertension. 2117 Aug 69

The metabolic syndrome (or syndrome X) is a constellation of risk factors including insulin resistance, hypertension, dyslipidemia, and central obesity that predispose to the development of cardiovascular disease and type 2 diabetes in adult life. Insulin resistance is believed to be a critical pathophysiological event early in the disease process, impacting both skeletal muscle metabolic function and vascular responses. Adverse changes in insulin sensitivity have been found to originate in utero; for instance, prenatal events such as placental insufficiency/oxidative stress leading to altered fetal growth trajectories are associated with increased rates of metabolic syndrome in adult life. Such intrauterine insults result in reduced skeletal muscle mass in conjunction with altered insulin signaling, decreased oxidative fibers, and impaired mitochondrial function. These developmental disturbances set the stage for development of muscle triglyceride accumulation and depressed insulin sensitivity in childhood. Abnormalities of vascular structure and function arising from deprived intrauterine conditions that are exacerbated by insulin resistance account for the progression of hypertension from childhood to adulthood. Arterial changes initiated in utero include reduced endothelial nitric oxide (NO) bioavailability, vascular smooth muscle cell proliferation and inflammation, events leading to endothelial dysfunction, and atherosclerosis that are present in those destined for metabolic syndrome. In addition, the hypertensive phenotype that is a hallmark of metabolic syndrome may also be traced to blunted kidney development and renin-angiotensin system activation in growth-restricted offspring. The summative impact of these intrauterine programmed changes in terms of influencing adult health and disease encompasses dietary and lifestyle factors introduced postnatally. Establishing novel therapeutic interventions aimed at preventing and/or reducing in utero-induced insulin resistance and vascular dysfunction warrants investigation because the numbers of low birthweight babies continue to increase.
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PMID:In utero origins of adult insulin resistance and vascular dysfunction. 2171 Mar 97

Gynostrmma pentaphyllum seed oil (GPSO), extracted from G. pentaphyllum seeds, is rich in conjugated linolenic acid, which is a special fatty acid consisting of cis-9, trans-11, trans-13 isomers. Type 2 diabetes mellitus (T2DM) is characterized by hyperglycemia resulting from insulin resistance, and is usually accompanied by hypertension, hyperlipidemia, atherosclerosis (i.e., the metabolic syndrome, or syndrome X), and polycystic ovarian disease. This study aimed to investigate the effect of GPSO on T2DM hepatic lipid metabolism and the underlying mechanism involving level of protein expression. In the experiment, the model of T2DM was established. Kunming male mice were fed with a high-fat diet and injected with streptozocin, in which the exploration of detailed mechanism in the therapy of T2DM was targeted. The results showed that the ability of oral glucose tolerance was improved in the GPSO group. Biochemical indices also revealed that GPSO had a positive effect on hypoglycemic activity, suggesting that GPSO could promote the expression of glucose transporter 4 in liver and skeletal muscle.
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PMID:Conjugated fatty acid-rich oil from Gynostrmma pentaphyllum seed can ameliorate lipid and glucose metabolism in type 2 diabetes mellitus mice. 2894 7


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