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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 metabolic syndrome (MetS) is a clustering of metabolic abnormalities that increase the risk of developing atherosclerotic cardiovascular disease and type 2 diabetes. The exact etiology remains unclear, but it is known to be a complex interaction between genetic, metabolic, and environmental factors. Among environmental factors, dietary habits are of central importance in the prevention and treatment of this condition. However, there is currently no firm consensus on the most appropriate dietary recommendations. General recommendations include decreasing obesity, increasing physical activity, and consuming an anti-atherogenic diet, and have traditionally focused on low total fat intake. A major problem with the focus on low fat is that high-carbohydrate diets can contribute to increasing triglyceride and decreasing high-density lipoprotein (HDL) concentrations. Low-carbohydrate diets have been popular in recent years. However, such diets are typically higher in saturated fat and lower in fruits, vegetables, and whole grains than national dietary recommendations. More recently the quality of carbohydrate has been studied in relation to MetS, including a focus on dietary fiber and glycemic index. Similarly, there has been a move from limiting total fat to a focus on the quality of the fat, with evidence of beneficial effects of replacing some carbohydrate with monounsaturated fat. Other nutrients examined for possible importance include calcium, vitamin D, and magnesium. Together, the evidence suggests that the components of diet currently recommended as "healthy" are likely also protective against MetS, including low saturated and trans fat (rather than low total fat) and balanced carbohydrate intake rich in dietary fiber, as well as high fruit and vegetable intake (rather than low total carbohydrate); and the inclusion of low-fat dairy foods. Accelerating research on gene-diet interactions is likely to contribute interesting information that may lead to further individualized dietary guidance in the future.
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PMID:Nutritional strategies in the prevention and treatment of metabolic syndrome. 1733 84

The importance of family history of type 2 diabetes (FHD) as a risk factor for atherosclerotic cardiovascular disease (ASCVD) remains controversial. A report of diabetes in parents and siblings was used to establish FHD in a cohort of 1,005,230 Koreans aged 30-95 years insured by the National Health Insurance Corporation who had a biennial medical evaluation during 1992-1995. ASCVD morbidity and mortality from 1993 to 2005 were examined in relation to FHD and other ASCVD risk factors. The risk of ischemic heart disease (IHD) increased significantly (19%) in men with FHD but not in women. A strong interaction was observed between FHD and personal history of diabetes for the occurrence of ASCVD; men with both diabetes and FHD were at significantly increased risk of developing IHD, cerebrovascular disease and ASCVD with hazard ratios (HR) of 2.28, 2.07, and 2.12, respectively, compared to those who had neither FHD nor type 2 diabetes. Corresponding risks were 2.64, 2.03, and 2.10 in women, respectively. This study demonstrates that risk of ASCVD is increased among those with diabetes and a family history of diabetes; suggesting that genetic factors associated with occurrence of familial diabetes may increase risk of ASCVD beyond the risk among people without FHD.
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PMID:Family history of diabetes and risk of atherosclerotic cardiovascular disease in Korean men and women. 1749 25

The metabolic syndrome and type 2 diabetes are insulin-resistant states which are commonly associated with an atherogenic dyslipidaemia involving mild to moderately elevated triglycerides, a preponderance of small, dense low-density lipoprotein (LDL) particles and low levels of high-density lipoprotein cholesterol (HDL-C). In addition, there is a spectrum of qualitative changes in the lipoprotein profile, particularly in the functional capacity of HDL to facilitate cellular cholesterol efflux and to protect LDL against oxidative modification. Together, these quantitative and qualitative anomalies promote elevated oxidative stress, endothelial dysfunction and inflammation, which drive the development of premature atherosclerotic cardiovascular disease. Moreover, recent evidence indicates that this dyslipidaemic profile may play a critical role in the development and progression of diabetic microvascular disease. An integrated therapeutic approach to correct both the quantitative and qualitative changes characteristic of diabetic dyslipidaemia clearly constitutes a priority for reduction of both macrovascular and microvascular risk.
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PMID:Metabolic syndrome and type 2 diabetes: lipid and physiological consequences. 1793 58

Metabolic syndrome is considered a hyperinsulinemic and inflammatory state closely associated to endothelial dysfunction causing an increased incidence of ischemic cardiovascular events and high mortality. The main objective of the present study was to determine whether leukocitary and soluble cell adhesion molecules were altered in patients with metabolic syndrome in comparison with control subjects. Cell adhesion molecules, mainly of leukocitary location, have been not previously evaluated in specifically designed cross-sectional studies involving male patients with metabolic syndrome. Moreover, other circulating markers of different candidate atherogenic risk parameters were also studied and the potential existence of a progressive relation between the number of metabolic syndrome components and the above mentioned biomarkers was analyzed. Thirty one male patients with metabolic syndrome (ATPIII definition) and 56 male control subjects were studied. We evaluated different markers of insulin resistance, inflammation and atherosclerosis, as well as protective factors. Patients with metabolic syndrome showed (a) hypoadiponectinemia (4551 +/- 2302 ng/ml vs. 5865 +/- 2548 ng/ml, respectively; p<0.05), (b) an atherogenic lipid and lipoprotein profile, (c) altered HDL chemical composition accompanied by higher cholesteryl ester-triglyceride interchange carried out by CETP, (d) diminished Lp-PLA(2) activity (6.5 +/- 1.9 vs. 7.3 +/- 2.2, p<0.05, respectively), antioxidant enzyme related with LDL oxidation, which was positively associated with QUICKI and negatively with VCAM-1 and lymphocyte CD18, and (e) high soluble (VCAM-1: 17 +/-5 vs. 13 +/- 4 ng/ml, respectively; p<0.0005) and leukocyte adhesion molecule expression (monocyte CD54: 52 +/- 15 vs. 45 +/-12 arbitrary units, respectively; p<0.0005; and lymphocyte CD49d: 312 +/- 56 vs. 284 +/- 64 arbitrary units, respectively; p < 0.05). The increment in leukocyte and soluble cell adhesion molecules, crucial for leukocyte interaction with the endothelium and migration into the artery wall, in combination with the other disorders described above reinforce the presence of a clinical status with high propensity to type 2 diabetes and atherosclerotic cardiovascular disease.
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PMID:Alterations in cell adhesion molecules and other biomarkers of cardiovascular disease in patients with metabolic syndrome. 1809 67

In children and adults, weight gain is accompanied by the early and more aggressive manifestations of well-recognized risk factors for atherosclerotic cardiovascular disease (CVD). Because insulin resistance and the later development of type 2 diabetes mellitus also accompany weight gain, the term cardiometabolic risk is now commonly used to describe this emerging global health problem. Weight loss will improve cardiometabolic risk. However, less is known about the effect of weight loss on the development of disease and, most importantly, type 2 diabetes and CVD outcomes in the form of death, myocardial infarction, and stroke. This review describes current clinical research that uses health-promoting lifestyle interventions, new drugs, and even surgery, which are all aimed at weight loss, reduction in disease manifestations, and improved outcomes. These anticipated data are essential for the future development of effective CVD prevention strategies. Results are awaited with great interest.
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PMID:Weight reduction and cardiovascular and metabolic disease prevention: clinical trial update. 1815 45

Low serum 25 hydroxyvitamin D3 (vitamin D3) is known to perturb cellular function in many tissues, including the endocrine pancreas, which are involved in obesity and type II diabetes mellitus (TIIDM). Vitamin D3 insufficiency has been linked to obesity, whether obesity is assessed by body mass index (BMI) or waist circumference (waist). Central obesity, using waist as the surrogate, is associated with the metabolic syndrome (MetSyn), insulin resistance, TIIDM and atherosclerotic cardiovascular disease (CVD). We tested how vitamin D3 was related to measures of fat mass, MetSyn markers, haemoglobin A1c (HbA1c) and MetSyn in a cross-sectional sample of 250 overweight and obese adults of different ethnicities. There were modest inverse associations of vitamin D3 with body weight (weight) (r = -0.21, p = 0.0009), BMI (r = -0.18, p = 0.005), waist (r = -0.14, p = 0.03), [but not body fat % (r = -0.08, p = 0.24)], and HbA1c (r = -0.16, p = 0.01). Multivariable regression carried out separately for BMI and waist showed a decrease of 0.74 nmol/L (p = 0.002) in vitamin D3 per 1 kg/m2 increase in BMI and a decrease of 0.29 nmol/L (p = 0.01) per 1 cm increase in waist, with each explaining approximately 3% of the variation in vitamin D3 over and above gender, age, ethnicity and season. The similar relationships of BMI and waist with vitamin D3 may have been due to associations between BMI and waist, or coincidental, where different mechanisms relating hypovitaminosis D3 to obesity occur concurrently. Previously reviewed mechanisms include that 1) low vitamin D3, may impair insulin action, glucose metabolism and various other metabolic processes in adipose and lean tissue 2) fat soluble-vitamin D3 is sequestered in the large adipose compartment, and low in serum, 3) obese people may be sensitive about their body shape, minimising their skin exposure to view and sunlight (not tested). We showed evidence for the first theory but no evidence to support the second. In the current study, serum vitamin D3 was inversely related to weight, BMI and markers of TIIDM (large waist, raised HbA1c) but not to adipose mass nor to MetSyn per se.
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PMID:Relationships of low serum vitamin D3 with anthropometry and markers of the metabolic syndrome and diabetes in overweight and obesity. 1822 57

The main components of the metabolic syndrome (MS) are abdominal obesity, atherogenic dyslipidemia, raised blood pressure, insulin resistance with or without glucose intolerance, and proinflammatory and prothrombotic states. The clustering of these metabolic risk factors significantly increases the risk of type 2 diabetes and promotes vascular endothelial dysfunction, inflammation, and increased oxidative stress. The net result is an increase in the risk of atherosclerotic cardiovascular disease. Therefore, management of MS is of utmost importance, especially considering its rapidly increasing prevalence in a population with rising obesity rates and its significant cardiovascular implications. The primary management of this syndrome involves the correction of the underlying risk factors--obesity, physical inactivity, and an atherogenic diet--with lifestyle modifications including increased physical activity and dietary modification. Smoking cessation also should be encouraged. However, pharmacologic therapies are often required to address cardiovascular risk factors. These agents can be categorized broadly into 1) anorectic agents, 2) insulin-sensitizing agents, 3) statins, and 4) renin-angiotensin system antagonists. Emerging therapies include adipokines, endocannabinoid inhibitors, and metabolic modulators, such as perhexiline and trimetazidine. To date, these therapies have not been shown to normalize the metabolic and cardiovascular burden of MS, and there still is no single therapeutic agent for its management.
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PMID:Management of the metabolic syndrome in cardiovascular disease. 1832 5

Metabolic syndrome is a cluster of interrelated cardiometabolic risk factors that are associated with an increased risk for both type 2 diabetes and atherosclerotic cardiovascular disease. These risk factors include visceral obesity, atherogenic dyslipidemia (elevated triglycerides and low HDL cholesterol), elevated blood pressure, dysglycemia (pre-diabetes or diabetes) and a prothrombotic and proinflammatory state. The condition is progressive, beginning with borderline risk factors, and worsens over time. Primary treatment is lifestyle therapy--weight loss, increased physical activity and antiatherogenic diet. But, as the metabolic syndrome progresses, drug therapy directed at individual risk factors may be needed.
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PMID:Metabolic syndrome: an evolving concept. 1833 69

The metabolic syndrome is a constellation of metabolic risk factors and physical conditions that are accompanied by an enhanced propensity toward the development of type 2 diabetes, atherosclerosis, and cardiovascular disease. It presents a combination of atherosclerosis risk including atherogenic dyslipidemia, hypertension, elevated plasma glucose, hypercoagulability, and a proinflammatory state. The 2 major underlying risk factors for the metabolic syndrome are obesity and insulin resistance. Exacerbating factors are physical inactivity, advancing age, and endocrine and genetic factors. Associated hyperinsulinemia, hyperglycemia, and elevated adipokine levels (adipose cytokines) lead to vascular endothelial dysfunction, an abnormal lipid profile, hypertension, and vascular inflammation, all of which promote the development of atherosclerotic cardiovascular disease. In this 2-part series, the authors present an up-to-date and detailed systematic review of the literature on this important topic.
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PMID:The metabolic syndrome and cardiovascular disease: Part I. 1860 51

Adiposity-associated inflammation and insulin resistance are strongly implicated in the development of type 2 diabetes and atherosclerotic cardiovascular disease. This article reviews the mechanisms of adipose inflammation, because these may represent therapeutic targets for insulin resistance and for prevention of metabolic and cardiovascular consequences of obesity. The initial insult in adipose inflammation and insulin resistance, mediated by macrophage recruitment and endogenous ligand activation of Toll-like receptors, is perpetuated through chemokine secretion, adipose retention of macrophages, and elaboration of pro-inflammatory adipocytokines. Activation of various kinases modulates adipocyte transcription factors, including peroxisome proliferator-activated receptor-gamma and NFkappaB, attenuating insulin signaling and increasing adipocytokine and free fatty acid secretion. Inflammation retards adipocyte differentiation and further exacerbates adipose dysfunction and inflammation. Paracrine and endocrine adipose inflammatory events induce a local and systemic inflammatory, insulin-resistant state promoting meta-bolic dyslipidemia, type 2 diabetes, and cardiovascular disease. Developing therapeutic strategies that target both adipose inflammation and insulin resistance may help to prevent type 2 diabetes and cardiovascular disease in the emerging epidemic of obesity.
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PMID:Adipose inflammation, insulin resistance, and cardiovascular disease. 1897 44


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