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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood glucose concentration is controlled by a number of hormone and neurotransmitter signals, either increasing or reducing glucose levels in the case of hypoglycemia or hyperglycemia, respectively. The pancreatic beta-cell responds to an increase in circulating glucose levels by a cascade of metabolic and electrophysiological events leading to the secretion of insulin. Type 2 diabetes is a metabolic disorder characterized by chronic hyperglycemia; the progressive pancreatic beta-cell dysfunction, with altered insulin production and secretion, is a major pathophysiological determinant of the disease together with the resistance of insulin-sensitive tissues to the action of the hormone. Hence, drugs which stimulate or enhance insulin secretion will reduce plasma glucose concentrations; this lowering of hyperglycemia will, in turn, reduce the occurrence of long-term complications. K(ATP) channels play a critical role in insulin secretion and can be considered as transducers of glucose-induced metabolic changes into biophysical events leading to the exocytosis of insulin granules. All currently marketed insulin secretagogues, sulfonylureas and glinides, target the beta-cell K(ATP) channels and reduce their opening probability. They induce insulin release regardless of the plasma glucose concentration, thus favoring the occurrence of hypoglycemia in the fasting state. Despite the intensive use of current drugs, many patients suffering from type 2 diabetes still exhibit poor glycemic control, others fail to respond to the treatment, and some develop serious complications. Therefore, there is a real need for innovative compounds, either enhancing insulin secretion from the pancreas or improving insulin action on the hormone-sensitive tissues. Here, we overview the existing and novel approaches targeting the beta-cell to enhance the release of insulin, with special emphasis on new ways of amplifying insulin secretion in a glucose-dependent manner.
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PMID:Pharmacological interventions that directly stimulate or modulate insulin secretion from pancreatic beta-cell: implications for the treatment of type 2 diabetes. 1631 76

Charcot-Marie-Tooth (CMT) disease is a hereditary demyelinating peripheral neuropathy, and CMT Type 1A is the most common form. In most cases, CMT1A is usually caused by duplication at chromosome 17p11.2-12. Type 2 diabetes mellitus (Type 2 DM) is a common metabolic disorder, characterized by chronic hyperglycemia that can be associated with micro- and/or macrovascular complications. Only a few studies reported CMT1A duplication in association with Type 2 DM. This article explores the characteristics of a large family of 69 members with respect to CMT1A and Type 2 DM. CMT1A was detected in 28 of them. Molecular genetic study was performed in 22, and duplication was detected in all of them. Six of the 22 members with CMT1A also had Type 2 DM based on the American Diabetes Association diagnostic criteria. Association of these two conditions may be coincidental; however, the occurrence of these two diseases in this large family may also suggest a genetic basis. More extensive reports and further investigations of such families having this combination will certainly provide a better understanding of this link.
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PMID:A large family with Charcot-Marie-Tooth Type 1a and Type 2 diabetes mellitus. 1639 77

Gestational diabetes mellitus (GDM) is a transient metabolic disorder that is a strong predictor of type 2 diabetes and cardiovascular disease. Previously, GDM was associated with reduced red cell long-chain omega-6 and omega-3 fatty acids in population (British) with high intake of total and saturated fat. The aim of the study was to examine blood fatty acids status of GDM patients (n=12) and normoglycaemic women (control, n=12) from South Korea where typical diet retains high omega-3 fat with low total fat intake. Subjects were matched for BMI and gestation week. Blood obtained at delivery were analyzed for plasma triacylglycerols (TG), phosphatidylcholine (PC), sphingomyelin (SM), and red cell PC, phosphatidylethanolamine (PE) and SM fatty acids. GDM patients had lower total saturated fatty acids (SFA) in the plasma TG (p<0.05) and PC (p<0.0001), and higher omega-6 and omega-3 metabolites in the plasma PC (p<0.05) than the controls. Conversely, the red cell PC and PE of the GDM contained higher proportions of palmitic (p<0.05) and SFA (p<0.05) but lower arachidonic (p<0.05) and docosahexaenoic (p>0.05) acids compared with the controls. Interestingly, red cell PC arachidonic acid level was comparable between Korean and British women whereas docosahexaenoic acid level decreased in the order of Korean control (5.5+/-0.9)>Korean GDM (3.5+/-2.1)=British control (3.9+/-2.9)>British GDM (2.8+/-2.3) (p<0.05). The similarity in the plasma and red cell fatty acids profile between Korean and British cohort suggests that the reduced membrane arachidonic and docosahexaenoic acids in GDM might be attributed to the effect of the disease itself regardless of ethnicity, obesity, or diet.
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PMID:A distinctive fatty acid profile in circulating lipids of Korean gestational diabetics: a pilot study. 1645 50

Diabetes mellitus is a complex metabolic disorder, caused by defects in insulin action and/or insulin production and is defined as a fasting hyperglycaemia of >126 mg/dl, with normoglycaemia being > or = 70 and < or = 110 mg/dl. There are two main types of diabetes. Type 1 diabetes (around 10% of cases) is an autoimmune disease, usually of early onset, in which pancreatic islet beta cells that secrete insulin are destroyed. Type 2 diabetes (around 85% of cases) is characterised principally by insulin resistance and impaired insulin secretion. Heredity and obesity are major risk factors for Type 2 diabetes. Diabetes is associated with potentially life-threatening microvascular and macrovascular complications caused by elevated serum glucose levels. Treatment of diabetes aims at restoring glycaemic control. In Type 1 diabetes, this can be achieved by injecting insulin. Oral hypoglycaemic medications that stimulate insulin secretion and/or modify glucose metabolism can be used as a first-line treatment in Type 2 diabetes mellitus. However, insulin is usually necessary in later phases of the disease. Lifestyle changes, such as diet and exercise, are also important. Glycaemic control can be measured by fasting blood glucose levels and also by glycosylated haemoglobin levels. The latter measure gives an indication of glycaemic control over a period of three months, and a reduction in glycosylated haemoglobin is the most appropriate treatment goal in the management of diabetes.
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PMID:What a psychiatrist needs to know about diabetes. 1645 46

Untreated anemia can caused significant cardiac and kidney damage. The aim of this study was to investigate the efficiency of anemia and hyperglycemia treatment in type 2 diabetes and their impact on kidney and heart impairment. The study is clinical retrospective and prospective and it was conducted in Clinic of Endocrinology, Diabetes Mellitus and Metabolic Diseases, University Clinical Center of Sarajevo. Prior to the study all patients were taking oral hypoglycemic drugs included sulfonylureas and biguanides. These subjects were put on 2 times daily fix mix insulin and biguanides after lunch. Each day, subjects received Iron tab 1 x 100 mg/ day, and C vitamin 1 x 100 mg/day. The results of our study are showing that effective treatment of glycaemia and anemia in patients with diabetes, reduces blood pressure, urine albumin secretion and pulse rate, diminishing cardiovascular damage and improving kidney function.
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PMID:Effects of hyperglycemia and iron deficiency on kidney and heart function in type 2 diabetes disease. 1653 86

Type 2 diabetes is a complex polygenic metabolic disorder of epidemic proportions. This review provides a brief overview of the susceptibility genes in type 2 diabetes that primarily affect pancreatic 3 cells, with emphasis on their function and most relevant polymorphisms. We focus on calpain 10, the only susceptibility gene identified thus far through a positional cloning approach in subjects with diabetes.
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PMID:Genes of type 2 diabetes in beta cells. 1663 98

Diabetic dyslipoproteinemia is considered to be an integral component of type 2 diabetes mellitus and the metabolic syndrome. Major pathogenetic factors include abdominal obesity, insulin resistance and hyperglycemia with increased hepatic secretion of triglyceride-rich lipoproteins. Elevated concentrations of triglycerides and cholesterol, together with decreased HDL cholesterol are therefore found. LDL cholesterol is either normal or only slightly increased, but at the same time, the composition of the LDL particles is altered. This metabolic disorder contributes considerably to the clearly elevated cardiovascular risk. Dyslipoproteinemia, usually in the form of hypertriglyceridemia, may also occur in type 1 diabetes mellitus. Since general measures and good blood sugar control often fail to achieve the desired lipid levels, many patients require medication, initially usually statins, but, where necessary, combination treatment. In patients with isolated hypertriglyceridemia, treatment with fibrates may also be considered.
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PMID:[Diabetic dyslipoproteinemia]. 1666 77

Obesity is a metabolic disorder often associated with type 2 diabetes, insulin resistance, and hepatic steatosis. Leptin-deficient (ob/ob) mice are a well-characterized mouse model of obesity in which increased hepatic lipogenesis is thought to be responsible for the phenotype of insulin resistance. We have recently demonstrated that carbohydrate responsive element-binding protein (ChREBP) plays a key role in the control of lipogenesis through the transcriptional regulation of lipogenic genes, including acetyl-CoA carboxylase and fatty acid synthase. The present study reveals that ChREBP gene expression and ChREBP nuclear protein content are significantly increased in liver of ob/ob mice. To explore the involvement of ChREBP in the physiopathology of hepatic steatosis and insulin resistance, we have developed an adenovirus-mediated RNA interference technique in which short hairpin RNAs (shRNAs) were used to inhibit ChREBP expression in vivo. Liver-specific inhibition of ChREBP in ob/ob mice markedly improved hepatic steatosis by specifically decreasing lipogenic rates. Correction of hepatic steatosis also led to decreased levels of plasma triglycerides and nonesterified fatty acids. As a consequence, insulin signaling was improved in liver, skeletal muscles, and white adipose tissue, and overall glucose tolerance and insulin sensitivity were restored in ob/ob mice after a 7-day treatment with the recombinant adenovirus expressing shRNA against ChREBP. Taken together, our results demonstrate that ChREBP is central for the regulation of lipogenesis in vivo and plays a determinant role in the development of the hepatic steatosis and of insulin resistance in ob/ob mice.
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PMID:Liver-specific inhibition of ChREBP improves hepatic steatosis and insulin resistance in ob/ob mice. 1687 78

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of liver disease whose hallmark is the accumulation of large-droplet fat in hepatocytes. This metabolic disorder occurs mainly in overweight or obese individuals. The disease mechanism involves hyperinsulinemia and hepatic insulin resistance, not ethanol abuse. NAFLD may be the hepatic manifestation of the "metabolic syndrome" classically associated with type 2 diabetes mellitus and cardiovascular disease. NAFLD ranges from simple steatosis, which is the least rapidly progressing disorder, to nonalcoholic steatohepatitis to cirrhosis, which can evolve to chronic liver failure. The high prevalence of NAFLD in children has been recognized only in the past 5 to 10 years, as rates of childhood obesity have soared. Accordingly, the best strategies for diagnosis and treatment of childhood NAFLD are a work in progress and remain controversial. Weight reduction through a healthy diet and regular medium-intensity exercise is the mainstay of current treatment. Few research data are available to guide pharmacologic therapy. Certain points regarding management of childhood NAFLD require emphasis: It is a serious liver disease that requires detailed clinical investigation. Other liver diseases causing fatty liver and/or abnormal liver tests, notably Wilson disease and chronic viral hepatitis, need to be excluded. Liver biopsy can provide critical diagnostic and staging information. Associated genetic or endocrine disorders need to be identified. Treatment should begin with a low-glycemic index diet that provides adequate nutrients but is low in harmful fats and eliminates foods causing postprandial hyperglycemia. Initially, this can target two to three problem foods so that it is easy for the adolescent to follow. Regular exercise suited to the capabilities and interests of the teenager should be added to the daily routine. Where possible, a team approach, including a dietician and psychologist, should be utilized, as adolescents do better in a supportive atmosphere. Optimal drug treatment requires further research: current front-runners are vitamin E and metformin. The roles of drugs that alter appetite and bariatric surgery for adolescents with NAFLD have not been determined.
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PMID:Nonalcoholic Fatty Liver Disease (NAFLD): Approach in the Adolescent Patient. 1694 68

Type 2 diabetes mellitus (DM2) is a common metabolic disorder. DM2 is associated with cognitive impairments, and with depressive symptoms, which occur in about one third of patients. In the current study we compared the cognitive profile and psychological well-being of 119 patients with DM2 (mean age: 66 +/- 6; mean duration: 9 +/- 6 years) with 55 age and education matched-control participants. Groups were compared on cognitive performance in five major cognitive domains, psychological wellbeing [assessed by Symptom Checklist (SCL)-90-R and the Beck Depression Inventory (BDI-II)] and abnormalities on brain MRI. We hypothesized an interrelationship between cognition, MRI abnormalities, and psychological well-being. DM2 patients performed significantly worse than controls on cognitive tasks, especially on tasks that required more mental efficiency, although the differences were modest (effect sizes Cohen d < .6). We speculate that DM2 patients have a diminished ability to efficiently process unstructured information. Patients with DM2 had significantly higher scores on the SCL-90-R (p < .001) and on the BDI-II (p < .001) and worse MRI ratings than controls, but psychological distress did not correlate with cognition, MRI ratings or biomedical characteristics. Contrary to our hypothesis, cognitive disturbances and psychological distress thus seem independent symptoms of the same disease.
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PMID:A detailed profile of cognitive dysfunction and its relation to psychological distress in patients with type 2 diabetes mellitus. 1728 86


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