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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 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

The object of this review is to provide the definitions and criteria for diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS), and convey current knowledge of the causes of permanent disability or mortality from complications of these conditions, of the risk factors for DKA and HHS, and of early indicators and contemporary treatment of suspected cerebral edema. The frequency of DKA at onset of type 1 diabetes mellitus (DM1) varies from 10-70%, depending on availability of health care and frequency of diabetes. At the onset of type 2 diabetes (DM2), DKA occurs in 5-52%. One study reported HHS in approximately 4% of new patients with DM2. Recurrent DKA rates are equally dependent on variability in medical services and socio-economic circumstances, and are estimated to be eight episodes per 100 patient years, with 20% of patients accounting for 80% of the episodes. Mortality for each episode of DKA internationally varies from 0.15-0.31%, with idiopathic cerebral edema accounting for two-thirds or more of this mortality. Other causes of death or disability include untreated DKA or HHS, hypokalemia, hypophosphatemia, hypoglycemia, other intracerebral complications, peripheral venous thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure, sepsis, aspiration pneumonia, and other pulmonary complications. Population-based studies from the UK, Australia, the USA, and Canada report cerebral edema incidence in DKA of 0.5-2.0%. Published information does not support the notion that treatment factors are causal in cerebral edema. Younger age, greater severity of acidosis, degree of hypocapnia, and severity of dehydration have been suggested as risk factors in several studies. Bimodal distribution of the time of onset of cerebral edema and wide variation in brain imaging findings suggest the variability and likely multiple causation of the clinical picture. Functional brain scanning has indicated that DKA is accompanied by increased cerebral blood flow suggesting that the predominant mechanism of edema formation is a vasogenic process. A method of monitoring for diagnostic and major and minor signs of cerebral edema has been proposed and tested which indicates that intervention will be required in five individuals to provide early intervention for a single case of cerebral edema. The preferred intervention of mannitol infusion has typically been accompanied by intubation and hyperventilation, but recent evidence indicates outcome is adversely affected by aggressive hyperventilation. The prevention of DKA and HHS at the onset of diabetes mellitus requires a high degree of awareness and suspicion by primary care providers; prevention of recurrent DKA necessitates a diligent team effort.
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PMID:Hyperglycemic crises and their complications in children. 1731 23

The prevention of type 2 diabetes mellitus (DM2) is a major health issue. The DREAM trial is a multinational, multicentre, prospective double-blind study of 5269 patients with an increased risk of developing diabetes. The results show that treatment with rosiglitazone reduces the risk of developing diabetes in this relatively healthy population. The success is achieved at the expense of side effects such as increased weight gain and a higher incidence of non-fatal congestive heart failure. The DREAM trial provides interesting data that may have major implications, but at the same time raises a number of questions that need to be addressed. The ADOPT study shows the benefits of rosiglitazone over glyburide in de novo DM2.
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PMID:[The pharmacological prevention and treatment of diabetes mellitus; significance of 2 recent, large studies for the use of rosiglitazone]. 1755 22

The aim of this prospective study was to research features of insulin resistance and metabolic syndrome in offspring of diabetic parents and to find out whether there is a risk of developing type 2 diabetes mellitus (DM) in these children. Study participants were 30 children of parents with type 1 DM (DM1) (Group I) and 11 children of parents with type 2 DM (DM2) (Group II) who were being followed up in the Diabetes Department of Haseki Research and Training Hospital. The results were compared with a control group of 17 children in the same age group (Group III). There were no statistically significant differences between the Group I and the control group in fasting blood glucose, oral glucose tolerance test values, 1st 2nd and hour insulin, homeostasis model assessment (HOMA) values, body mass index (BMI), systolic and diastolic blood pressure, and lipid parameters, i.e. HDL-cholesterol, LDL-cholesterol, VLDL-cholesterol, total cholesterol, and triglycerides. Fasting, 1st and 2nd hour blood insulin levels, HOMA values, BMI, and systolic blood pressure values were significantly higher in Group II compared to the control group (p < 0.05). There were no statistically significant differences between Group II and the control group in lipid parameters, fasting blood glucose, OGTT values, or diastolic blood pressure. We conclude that in our population there is a tendency of insulin resistance and metabolic syndrome in the offspring of parents with DM2, and a risk for developing DM2. Thus, children of patients with DM2 should be followed up so as to recognize early metabolic defects of glucose metabolism and to plan effective preventive efforts to reduce cardiovascular and atherosclerotic risk factors.
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PMID:Insulin resistance and metabolic syndrome in children of parents with diabetes mellitus. 1745 Oct 82

The incidence of obesity, cardiometabolic syndrome (CMS), and type 2 diabetes mellitus (DM2), as well as their devastating cardiovascular consequences, keep rising with increasing human and economical costs. For a long time, insulin resistance has been the main player in the pathogenesis and treatment of DM2, but every day more knowledge is gained about the central role of beta-cell failure, not only in the appearance of hyperglycemia but also in the failure of the pharmacological therapy. beta-Cell failure implies impairment of glucosestimulated insulin secretion and loss of beta-cell mass. Hyperglycemia, elevated circulating fatty acids, inadequate local activation of renin angiotensin system, and chronic low grade inflammation are conditions that coexist in the CMS and DM2 that turn out to be deleterious for the beta-cell functioning and existance. Excessive oxidative stress secondary to increased production of reactive oxygen species and decreased availability of antioxidants is a possible common converging point of the multiple noxious stimuli. Activation of the NADPH oxidase complex secondary to angiotensin II stimulation is of interest, as its pharmacological blockade has beneficial effects. New knowledge about the intimate mechanisms of oxidative-stress induced beta-cell failure will provide new therapeutic targets against CMS and DM2.
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PMID:The expanding role of oxidative stress, renin angiotensin system, and beta-cell dysfunction in the cardiometabolic syndrome and Type 2 diabetes mellitus. 1750 16

To investigate the relative role of the adiponectin and leptin in the insulin resistance (IR) and obesity we studied plasma levels of these adipocytokines in obese and insulin resistant postmenopausal (PM) females with type 2 diabetes (DM2) during 6 months of Metformin therapy. We recruited 26 PM women, between the ages of 50 and 67 (59,7+/-8,1 years). These women had a BMI of 36,6+/-1,8 kg/m2. After baseline measurements Metformin therapy has been initiated (1700+/-2550 mg per day). Duration of therapy was 6 months. The results of investigations of adipocytokines after Metformin 6 months therapy shown that circulating adiponectin levels were significantly increased (19,1+/-6,0 vs. 16,1+/-3,9 ng/ml, p=0,008) together with significant reduction of BMI (35,9+/-1,9 vs. 36,6+/-1,8 kg/m2, p=0,005) and IR (3,05+/-0,89 vs. 3,96+/-0,70, p<0,001). The magnitude of the change in adiponectin levels positively correlated with the magnitude of BMI reduction (r=0,4784, p=0,013) and IR reduction (r=0,5779, p=0,002). Any significant correlation did not observed between changes of leptin levels and BMI, leptin levels and IR. In summary, our data suggest that hypoadiponectinemia in PM may be explained by only IR because the amelioration of whole-body insulin action by 6-month Metformin therapy leads to increase of plasma adiponectin levels; leptin levels did not significantly change after 6-month Metformin therapy.
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PMID:Effect of metformin therapy on plasma adiponectin and leptin levels in obese and insulin resistant postmenopausal females with type 2 diabetes. 1752 1

Heart disease is the leading cause of death in patients with insulin resistance and type 2 diabetes (DM2). Even in the absence of coronary artery disease and hypertension, functional and structural abnormalities exist in patients with well-controlled and uncomplicated DM2. These derangements are collectively designated by the term diabetic cardiomyopathy (DCM). Changes in myocardial energy metabolism, due to altered substrate supply and utilization, largely underlie the development of DCM. Insulin is an important regulator of myocardial substrate metabolism, but also exerts regulatory effects on intracellular Ca2+ handling and cell survival. The current paper reviews the multiple functional and molecular effects of insulin on the heart, all of which ultimately seem to be cardioprotective both under normal conditions and under ischemia. In particular, the dismal consequences of myocardial insulin resistance contributing to the development of DCM will be discussed.
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PMID:Myocardial insulin action and the contribution of insulin resistance to the pathogenesis of diabetic cardiomyopathy. 1755 6

The purpose of the study was to evaluate the effects of hyperhomocysteinemia (HHC) on vascular-thrombocyte and coagulation hemostasis and the development of coronary artery disease (CAD) in patients with type 2 diabetes mellitus (DM2). DM 2 patients with or without CAD were examined; high incidence of HHC (40.3%) was revealed. The level of homocysteine was significantly higher in DM2 patients with CAD vs. non-CAD subjects. Among patients with DM2 and CAD the level of the amino acid was elevated in 77.1% of cases with a history of myocardial infarction. In patients with DM2, CAD, and HHC, vascular-thrombocyte hemostasis factors were found to be hyperactive, while anticoagulatory ones were suppressed. These changes in the hemostatic system in HHC increase the probability of thrombus formation and CAD progress.
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PMID:[Hyperhomocysteinemia in coronary artery disease and hemostasis disorders in patients with type 2 diabetes mellitus]. 1766

Diabetes mellitus is associated with end-organ complications in the peripheral and central nervous system. It is unknown if these complications share a common aetiology, and if they co-occur in the same patient. The aim of the present study was to relate different measures of peripheral neuropathy in patients with type 2 diabetes mellitus (DM2) to cognition and brain MRI. A standardized neurological examination and questionnaire, neuropsychological examination and brain MRI were performed in 122 patients with DM2 and 56 matched controls. Measures of peripheral neuropathy were vibration threshold, a sensory examination sum score and the Toronto Clinical Neuropathy Scoring System. Neuropsychological test scores were expressed in standardized z-values across five predetermined cognitive domains. White matter lesions and cortical and subcortical atrophy were rated on MRI. Overall 38% of the patients with DM2 and 12% of the controls were classified as having any neuropathy (p<0.001). Patients with DM2 had a lower performance on the neuropsychological tests, more white matter lesions (p<0.01) and more atrophy (p<0.01) than controls. Within the DM2 group none of the measures of peripheral neuropathy was related to MRI abnormalities or cognitive dysfunction (linear regression analyses, adjusted for age, education, sex). We conclude that peripheral neuropathy in patients with DM2 is not related to cognitive dysfunction and brain abnormalities. This indicates that central and peripheral neurological complications of DM2 might have different etiologies.
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PMID:Peripheral and central neurologic complications in type 2 diabetes mellitus: no association in individual patients. 1785 Aug 22

Fatty acids, having intimate relationship with type 2 diabetes mellitus (DM2), are not only the main energy source as nutrients, but also signaling molecules in insulin secretion. In this work, we developed a two-step rapid method to comprehensive profiling of esterified fatty acid (EFA) and non-esterified fatty acid (NEFA) using KOH-CH3OH to methylate EFA followed by H2SO4-CH3OH to methylate NEFA. Its applications to fatty acids profiling of type 2 diabetic patients and health controls were also presented. The t-test results informed that 16 NEFAs and 7 EFAs had distinct differences between type 2 diabetes and health controls. Furthermore, quantitative alterations of fatty acids in plasma of type 2 diabetic patients treated with rosiglitazone were obtained by this method. Our research results indicated that the dynamic changes of NEFAs are various. Some decreased linearly, such as C18:0, C18:3n-6 and C22:6, and some changed nonlinearly, such as C18:3n-3 and C22:4. All results informed that fatty acid profiles could provide comprehensive and accurate information for not only discrimination between DM2 patients and health controls, but also evaluation alterations of fatty acids during therapeutic process.
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PMID:Simultaneously quantitative measurement of comprehensive profiles of esterified and non-esterified fatty acid in plasma of type 2 diabetic patients. 1788 Sep 34


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