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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The medical community faces an emerging epidemic of type 2 diabetes mellitus (DM2) in children and adolescents with a disproportionate increase among certain ethnic groups. DM2 represents one arm of the metabolic syndrome and parallels an increasing prevalence of obesity. The metabolic syndrome includes insulin resistance, hyperlipidemia, and hypertension with a consequent risk of early cardiovascular disease. Thus, treatment of DM2 and the metabolic syndrome poses a challenge for pediatric endocrinologists and represents a huge public health issue. This review presents information about treatment of childhood DM2 with emphasis on indications for the use of insulin in management and normalization of blood glucose.
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PMID:The management of type 2 diabetes mellitus in children and adolescents. 1575

Type 1 diabetes mellitus (DM1) commonly occurs in childhood, although many pediatric centers are now seeing more cases of type 2 diabetes (DM2). Kidney failure caused by either type of diabetes is uncommon during childhood, but these years of hyperglycemia contribute to long-term complications. All children with diabetes warrant screening of glomerular filtration rate, blood pressure, and urine albumin excretion. Screening should begin after 5 years of DM1 or at puberty. A similar screening strategy should start at the time of diagnosis of DM2. Atypical features such as dipstick positive proteinuria or active urine sediment may warrant referral to a nephrologist for evaluation, including biopsy. The first line of treatment in either form of diabetes is achieving the best glycemic control possible. Patients developing microalbuminuria or hypertension should receive antiangiotensin II drugs. Adult studies suggest blood pressure goals should be lower in diabetes than in the general population. Although direct evidence is not yet available in children, achieving blood pressure below the 90th percentile for age, height, and gender seems prudent. Longitudinal studies and new screening tests may allow detection of susceptible children earlier in the course of DM1 or DM2, perhaps allowing prevention of diabetic kidney disease.
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PMID:Pediatric aspects of diabetic kidney disease. 1582 59

Cardiovascular disease (CVD) and Type 2 diabetes mellitus (DM2), once conceived as different entities, share common origins and pathways. Increased activity of the renin-angiotensin-aldosterone-system, insulin resistance, chronic low-grade inflammation and oxidative stress collectively contribute to endothelial dysfunction and atherosclerosis, which manifest clinically as CVD. Nowadays, it is possible to identify and intervene in high-risk populations even before the clinical diagnosis of DM2. The control of dietary patterns and increased physical activity is completely feasible, as well as the management of hypertension and dyslipidaemia. Pharmacological interventions targeted at blocking renin-angiotensin-aldosterone-system and sensitising to insulin have a role in the prevention of DM2 and CVD, and are avidly explored worldwide. In the near future, ongoing trials should provide data that will allow us to better treat patients with the cardiometabolic syndrome and diabetes in order to reduce CVD morbidity and mortality.
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PMID:Insights into the emerging cardiometabolic prevention and management of diabetes mellitus. 1621 82

Type II diabetes mellitus (DM2) is associated with an increased risk of cognitive dysfunction and dementia. The increased risk of dementia concerns both Alzheimer's disease and vascular dementia. Although some uncertainty remains into the exact pathogenesis, several mechanisms through which DM2 may affect the brain have now been identified. First, factors related to the 'metabolic syndrome', a cluster of metabolic and vascular risk factors (e.g. dyslipidaemia and hypertension) that is closely linked to DM2, may be involved. A number of these risk factors are predictors of cerebrovascular disease, accelerated cognitive decline and dementia. Secondly, hyperglycaemia may be involved, through adverse effects of potentially 'toxic' glucose metabolites on the brain and its vasculature. Thirdly, insulin itself may be involved. Insulin can directly modulate synaptic plasticity and learning and memory, and disturbances in insulin signalling pathways in the periphery and in the brain have recently been implicated in Alzheimer's disease and brain aging. Insulin also regulates the metabolism of beta-amyloid and tau, the building blocks of amyloid plaques and neurofibrillary tangles, the neuropathological hallmarks of Alzheimer's disease. In this paper, the evidence for the association between DM2 and dementia and for each of these underlying mechanisms will be reviewed, with emphasis on the role of insulin itself.
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PMID:Increased risk of Alzheimer's disease in Type II diabetes: insulin resistance of the brain or insulin-induced amyloid pathology? 1624 41

Type 2 diabetes mellitus (DM2) has increased 41% in the United States, with an estimated one third undiagnosed and another 41 million with prediabetes. Hypertension affects 20% to 60% of all diabetics, contributing to up to 75% of deaths due to cardiovascular disease. These staggering statistics make it imperative that hypertensive patients who are at risk for DM2 are identified and treated early. Numerous studies have been done involving choice of antihypertensive in established diabetics, and a slowing or halting of the progression in the development of diabetes in these patients has been noticed. However, to date, nothing is conclusive. For now, following the JNC 7 guidelines of using a diuretic as monotherapy or in combination with an angiotensin-converting enzyme inhibitor (ACEI), angiotensin II-receptor blocker (ARB), beta-blocker, or calcium channel blocker may be prudent. Two current studies, the DREAM trial and the ONTARGET trial, may shed more light as to whether ACEIs or ARBs have a preferred niche in initial treatment of the hypertensive patient who is at risk for diabetes.
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PMID:Selection of antihypertensive agents in patients at risk for diabetes. 1638 3

Determination of microalbuminuria has been shown to be useful to identify patients with type 2 diabetes (DM2) at high risk of renal and cardiovascular (CV) diseases. The determination of the albumin/creatinine (Cr) ratio in an isolate sample of urine has been shown to be sufficient for the diagnosis as well as for the evaluation of the efficacy of the therapy employed to reduce microalbuminuria. Values of urinary albumin >30 mg/g of Cr or 3,4 mg/mmol of Cr are evidence of microalbuminuria. This condition is frequently associated with high blood pressure levels, which increases dramatically not only the progression of renal disease but also de risk of a CV event. Epidemiologic studies have demonstrated that the presence of microalbuminuria is predictive of higher morbi-mortality independent of the presence of other CV risk factors. It appears to reflect a generalized vascular lesion not confined to the glomeruli. The capacity of reducing blood pressure, intraglomerular pressure and the permeability of the glomerular membrane, which are important factors in the progression of renal disease, may explain the renoprotective effects of the angiotensin converting enzyme inhibitors (ACEIs) and the angiotensin II receptors blockers (ARBs). In the treatment of diabetic nephropathy, the control of blood pressure, which has to be maintained near or below 130/80 mmHg associated to the blockade of the renin-angiotensin system with ACEIs or BRAs are the best strategies to promote renal and CV protection.
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PMID:[Microalbuminuria: cardiovascular and renal risk factors underestimated in clinical practice]. 1676 97

The objective of this work was to investigate the insulin sensitivity (SI) and the beta cell function (BCF) in different glucose tolerance statuses in a comparative cross-sectional study. Eighty-four patients with different glucose tolerance statues were classified as normoglicemic-control group (NC) patients without family history of type 2 diabetes (DM2) or hypertension (HTN); normoglicemic-patients with familiar history of DM2 or HTN (FPDM2); patients with glucose intolerance (IGT group) and patients with diagnostic of DM2 <10 years (DM2 group). In each patient was obtained a clinical history and an oral glucose tolerance test (75 g) was performed. Glucose (GOD-PAP) and insulin (RIA) were quantified. Insulin Sensitivity (IS) (Whole Body Insulin Sensitivity Index), Insulin resistance (IR) (HOMA) and BCF (insulinogenic index) were evaluated. The statistical analysis was realized in SPSS v. 10.0. It was found that glucose was similar among NC, FPDM2 and IGT groups. Insulin was higher in the FPDM2 (26.71 +/- 22.25 microU/mL), and IGT (34.10 +/- 34.98 microU/mL) in comparison with NC (22.83 +/- 21.26 microU/mL) (p < 0.01). IS was different among NC and IGT group (0.74 +/- 0.43 to 0.29 +/- 0.18, p < 0.05) and among IGT and DM2 (0.29 +/- 0.18 to 0.86 +/- 0.55, p < 0.001). BCF was different among the DM2 and NC (0.051 +/- 0.05 to 1.28 +/- 1.99 microU.mL/mg.dL, p < 0.05), DM2 and FPDM2 group (0.051 +/- 0.05 to 1.23 +/- 1.51 microU.mL/mg.dL, p < 0.01), DM2 and IGT (0.051 +/- 0.05 to 2.64 +/- 2.22 microU.mL/mg.dL, p < 0.001). SI was inversely related to corporal weight and IMC (r = -0.38, p = 0.001 and r = -0.33, p = 0.004, respectively). BCF was related to age (r = -0.27, p = 0.016), the area under curve of glucose (r = -0.30, p = 0.010) and body weight (r = 0.34, p = 0.002). In conclusion, the decrease of glucose tolerance was associated with the lowering of Insulin Sensitivity (IS). The beta cell function (FCB) was lower in the diabetic patients group in comparison with the TGA and FPDM2 groups. These measurements need to be included in patients with high risk for early identification and changes in life style to protect the normal functioning of beta cell and to prevent the onset of IGT or DM2.
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PMID:[Insulin sensitivity and beta cell function in different glucose tolerance status]. 1688 77

The term intrauterine growth restriction (IUGR) is assigned to newborns with a birth weight and/or birth length below the 10th percentile for their gestational age and whose abdominal circumference is below the 2.5th percentile with pathologic restriction of fetal growth. IUGR is usually due to maternal, fetal, or placental factors. However, many IUGR cases have unknown underlying cause. Recent studies focus on new factors that can influence fetal development and birth outcome like the timing and the type of fetal nutrition, maternal psychosocial stress and personality variables, 11beta-hydroxysteroid dehydrogenase type 2 placental activity, the activity of the neuroendocrine system that mediates the effects of psychosocial stress, and the role of proinflammatory cytokines and of oxidative stress. Data have shown that IUGR is associated with a late life increased prevalence of metabolic syndrome, a condition associating obesity with hypertension, type 2 diabetes mellitus (DM2), and cardiovascular disease. Recent data demonstrated that the diabetes-associated mortality appears to be disproportionately concentrated among individuals of abnormal birth weight.
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PMID:Causes of intrauterine growth restriction and the postnatal development of the metabolic syndrome. 1730 40

Numerous population studies confirm the high prevalence of hypertension in type II diabetic (DM2) subjects and that intensive antihypertensive treatment is more beneficial to diabetic than to nondiabetic hypertensive subjects, yet not many of these are specific to Spain. To assess the degree of blood pressure (BP) control and the effects of antihypertensive drugs in the medical management of hypertension in diabetic patients in specialist care centres throughout Spain, we studied the socio-demographic, clinical and relevant laboratory parameters of 796 hypertensive patients with DM2 (mean age 66.09 (95% confidence interval (CI): 64.08-68.10). The percentage of diabetic patients responding positively to BP control measures was lower when compared to the nondiabetic population in both Spain and Europe. The degree of control was poorer for systolic than for diastolic BP, yet 40.6% of the patients were only on monotherapy. The fact that antihypertensive treatment was modified in only 40% of the poorly controlled patients was also highly significant and could be attributed to a nonstringent use of clinical guidelines. Among the other differences between well-controlled and poorly controlled patients, we found that well-controlled patients presented with lower levels of cholesterol and triglycerides, a lower prevalence of excess weight/obesity, and a greater prevalence of cardiovascular and/or cerebrovascular disease despite having a greater percentage of patients on antiplatelet therapy. Better application of therapeutic guidelines and the prevention and treatment of compounding factors could improve the response rate to BP control measures in poorly controlled patients.
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PMID:Blood pressure, antihypertensive treatment and factors associated with good blood pressure control in hypertensive diabetics: the Tarmidas study. 1746 Jul 9

Twenty to forty percent of type-2 diabetic patients (DM2) present nephropathy. Genetic polymorphism of Apolipoprotein E (Apo E) has been proposed as a risk factor in the development and progression of diabetic nephropathy. The purpose of the study was to evaluate the relationship between Apo E polymorphism and presence of nephropathy in DM2 patients. We studied 85 DM2 patients with a similar nutritional state, environmental and socioeconomic condition and more than 10 years of evolution. They were grouped in DM2 patients with kidney complications (n=56) and without kidney complications (n=29; control group). Apo E genotype was determined by restriction fragment-length polymorphism analysis. A plasmatic biochemical characterization was performed on all the subjects studied. The 85 DM2 patients had arterial hypertension in treatment. The nephropathy diabetic group showed differences (p<0.001) in BMI, systolic blood pressure, glycemia, cholesterol (total, HDL and LDL), HbA1c and creatinine. The e4 allelic frequency was 8% in the nephropathy group versus 25.9% in the control group. Apo e3 allele and E3/3 genotype frequency were higher and E3/4 genotype was lower in the nephropathy group than in controls. These groups also showed differences in total, HDL and LDL cholesterol. DM2 patients without nephropathy presented a higher frequency of e4 allele. These results could suggest a protective role of e4 allele in the development and progression of diabetic nephropathy.
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PMID:Relationship between Apolipoprotein E polymorphism and nephropathy in type-2 diabetic patients. 1748 71


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