Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Scientific interest in conjugated linoleic acid (CLA) started in 1987 when Michael Pariza's team of Wisconsin University observed its inhibitory effects on chemically induced skin tumors in mice. Numerous studies have since examined CLA's role in cancer, immune function, oxidative stress, atherosclerosis, lipid and fatty acids metabolism, bone formation and composition, obesity, and diabetes. Still it's not clear yet either through which mechanisms CLA produces its numerous metabolic effects. We now know that CLA contents in cow milk fat can be enriched through dry fractionation, but this knowledge doesn't allow sufficient certainty to qualify this nutrient, as a functional food, capable of increasing well being and reducing the risk of disease.
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PMID:Conjugated linoleic acid: a functional food? 1461 23

Progress in the development of antisense drugs over the last decade has led to the approval of the first such drug--Vitravene for AIDS-related CMV retinitis--and the development of a large number of antisense drugs in clinical trials. Antisense drugs are now being studied in Phase 3 trials for patients with cancer and inflammatory bowel disease. Other antisense drugs are in development for rheumatoid arthritis, other inflammatory conditions, and hepatitis C. Still other antisense drugs are entering clinical trials for treatment of metabolic conditions such as diabetes and hyperlipidemia. These latter applications provide the potential for target effects to be more directly measured in the clinic. Improved antisense chemistry, which will enhance the feasibility of subcutaneous and oral administration of antisense drugs and offer the potential of less frequent dosing, is expected to further expand the opportunities for antisense drug development.
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PMID:Applying antisense technology: Affinitak and other antisense oligonucleotides in clinical development. 1475 39

Haemoglobin A(1)c (HbA(1)c) or glycohaemoglobin is one of the most important parameters in the management of patients with diabetes mellitus, but to date there is no international standard for determining HbA(1)c. Most of the routine HbA(1)c assays are standardised against one of the local standardisation schemes like the NGSP (USA) and other schemes (Japan, Sweden). Still, results of HbA(1)c tests diverge considerably, as do the accompanying clinical decision limits. The IFCC Working Group on HbA(1)c Standardisation has developed a reference method and also set up a reference system for HbA(1)c, in which the analyte is defined as beta-N-glycated haemoglobin. This reference system consists of a network of reference laboratories that uses the reference methods and certified reference materials for optimal measurement of HbA(1)c in human blood. The main task of the network is to assign values to secondary reference materials, to be used by manufacturers of routine HbA(1)c assays to calibrate their assays. The high specificity of the reference method results in lower HbA(1)c values in blood samples, since the unspecific components falsely identified as HbA(1)c in routine methods are not measured by the reference method. The reference range for the new reference method was determined as 3 to 4% and the clinical decision limits were translated from existing guidelines: goal of treatment 5% HbA(1)c, change of therapy advised at HbA(1)c greater than 6%. Despite these lower values, worldwide implementation of the IFCC reference system for HbA(1)c is recommended, in order to end the great divergence in HbA(1)c results, with which physicians and patients are confronted today.
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PMID:Towards worldwide standardisation of HbA1c determination. 1524 96

The most severe adverse event of juvenile diabetes is death. Still these days it happens that children with diabetes die from diabetes before having received any treatment at all, sometimes probably undiagnosed. We have to improve the awareness and knowledge, both in the general population and also among health care staff and physicians. Retarded growth and development was seen earlier, but is now rare. But long-term complications affecting primarily blood vessels and nerves are still a real threat and may develop already after a few years. Unless diabetes is well treated, the disease is as dangerous as ever before. We know that a good metabolic control prevents complications, but not how to reach such control in many patients. Severe hypoglycemia has been feared to limit our possibilities to reach good metabolic balance. However, near-normal HbA1c must not be accompanied by increasing incidence of severe hypoglycemia. Too many patients are never offered an insulin treatment as physiological as possible. Adequate use of basal and bolus insulin is a prerequisite. Continuous adjustments should be monitored on the basis of glucose profiles, but without effective education and psychosocial support the treatment tends to fail. Intense treatment of diabetes may become a heavy burden, an "adverse event" in itself, for the patient and the parents of a diabetic child. Psychosocial support is often needed. Realistic information already from the onset of the disease is important, together with optimism, encouragement and not only criticism. Short-term goals and realistic agreements may help the patient to accept the disease. Independence and capacity to manage the treatment successfully contribute to a good metabolic control and also improves quality of life. Children with diabetes cannot expect a "normal" life, but they should be able to expect a long, active, exciting and happy life.
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PMID:Prevention of adverse events in juvenile diabetes. 1525 77

Cerebrovascular risk represents a progressive and evolving concept owing to the particular distribution of risk factors in patients with ischemic stroke and in light of the newest stroke subtype classifications that account for pathophysiological, instrumental, and clinical criteria. Age represents the strongest nonmodifiable risk factor associated with ischemic stroke, while hypertension constitutes the most important modifiable cerebrovascular risk factor, confirmed by a host of epidemiological data and by more recent intervention trials of primary (HOT, Syst-Eur, LIFE) and secondary (PROGRESS) prevention of stroke in hypertensive patients. To be sure, a curious relationship exists between stroke and diabetes. Although the Framingham Study, The Honolulu Heart Program, and a series of Finnish studies reported a linear relationship between improved glucose metabolism and cerebral ischemia, the clinical and prognostic profile of diabetic patients with ischemic stroke remains to be fully understood. Our group, on the basis of TOAST classification--a diagnostic classification of ischemic stroke developed in 1993 that distinguishes five different clinical subtypes of ischemic stroke: large-artery atherosclerosis (LAAS), cardioembolic infarct (CEI), lacunar infarct (LAC), stroke of other determined origin (ODE), and stroke of undetermined origin (UDE), and now extensively used in clinical and scientific context--analysed the prevalence of cerebrovascular risk factors and the distribution of TOAST subtypes in more 300 patients with acute ischemic stroke in two consecutives studies that reported the significant association between diabetes and the lacunar subtype and a better clinical outcome for diabetic patients, most likely related to the higher prevalence of the lacunar subtype. Well-confirmed are the roles of cigarette smoking, atrial fibrillation, and asymptomatic carotid stenosis as cerebrovascular risk factors. Particularly interesting seems to be the function of inflammation markers (CRP, TNF-alpha, IL-1 beta, ISPs) as potential risk factors. Still elusive remains the association between cholesterol serum levels and stroke, on the basis of the epidemiological data regarding this causative relationship, confirmed only by the results of intervention trials (4S, LIPID, CARE, HPS, ASCOT). Ultimately, cerebrovascular risk appears peculiar owing to the unique relationship between some modifiable risk factors (mainly diabetes and cholesterol) and the possible preferential association with stroke subtypes and specific cerebrovascular risks.
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PMID:Cerebrovascular risk factors and clinical classification of strokes. 1563 Jun 37

A critical challenge faced by clinical nephrologists today is the escalating number of patients developing end stage renal disease, a major proportion of which is attributed to diabetic nephropathy (DN). The need for new measures to prevent and treat this disease cannot be overemphasized. To this end, modern genetic approaches provide powerful tools to investigate the etiology of DN. Human studies have already established the importance of genetic susceptibility for DN. Several major susceptibility loci have been identified using linkage studies. In addition, linkage studies in rodents have pinpointed promising chromosomal segments that influence renal traits. Besides augmenting our understanding of disease pathogenesis, these animal studies may facilitate the cloning of disease susceptibility genes in man through the identification of homologous regions that contribute to renal disease. In human diabetes, various genes have been evaluated for their risk contribution to DN. This widespread strategy has been propelled by our knowledge of the glucose-activated pathways underlying DN. Evidence has emerged that a true association does indeed exist for some candidate genes. Furthermore, the in vivo manipulation of gene expression has shown that these genes can modify features of DN in transgenic and knockout rodent models, thus corroborating the findings from human association studies. Still, the exact molecular mechanisms involving these genes remain to be fully elucidated. This formidable task may be accomplished by continuing to harness the synergy between human and experimental genetic approaches. In this respect, our review provides a first synthesis of the current literature to facilitate this challenging effort.
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PMID:Molecular genetic approaches for studying the etiology of diabetic nephropathy. 1610 80

Still there are no effective methods to predict or cure type 1 diabetes (T1D) in humans. Soluble, dimeric MHC class II-peptide (DEF) chimeras have potential for both early diagnosis and immunospecific therapy. DEF chimeras prevent and reverse diabetes in mice by stimulating antigen-specific type 1 T regulatory cell (Tr1)-like cells. We also showed that diabetes could be predicted by changes in the phenotype of autoreactive CD4 T cells in peripheral blood. Herein, we demonstrated that human DEF (HLA-DR*0401/Fcgamma1) chimeras expressing peptides of beta-cell antigens stimulate Tr1-like cells in blood of patients with T1D, non-diabetic relatives, and controls. Furthermore, the specific and stable binding of DEF chimeras to cognate TCR and CD4 coreceptor allowed quantification and phenotyping of autoreactive CD4 T cells in non-stimulated blood by FACS. Our results indicate that (1) autoreactive CD4 T cells to GAD65 autoantigen are commonly present in humans expressing diabetes-susceptible HLA-DR*0401 molecules; (2) these autoreactive T cells undergo avidity maturation upon encountering the self antigen early in life; (3) the disease is associated with an imbalance between autoreactive CD4+CD25+ and CD4+CD69+ T cells specific for GAD65. Based on this, we propose a model to explain the kinetics of autoreactive CD4 T cells in blood during the natural history of T1D.
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PMID:Soluble, dimeric HLA DR4-peptide chimeras: an approach for detection and immunoregulation of human type-1 diabetes. 1610 71

Stem bark extracts of Terminalia superba Engl. and Diels and Canarium schweinfurthii Engl. are used in Africa for the treatment of various ailments, including diabetes mellitus. The anti-diabetic effects of the methanol/methylene chloride extracts of the stem barks on streptozotocin (STZ)-induced diabetes were evaluated on male rats. Through the subcutaneous route, diabetes was induced using 60 mg/mL of streptozotocin. After 2 days, the rats received, by gavage, 150 mg/kg and 300 mg/kg of extract daily for 14 days. At 300 mg/kg, the two extracts (Terminalia superba and Canarium schweinfurthii), significantly showed at least 67.1% and 69.9% reduction in blood glucose level, respectively, while insulin (three units) given subcutaneously and once daily, had 76.8% reduction compared to diabetic untreated control rats. Similarly, the weight gains were 6.6% and 4.9%, respectively, and were comparable to the normal rats, whereas, diabetic untreated rats lost 14.1% body weight. Still with the same dose, there was 68.5% and 58.5% (p < 0.001) significant decrease in food consumption and 79.7% and 64.0% (p < 0.001) in fluid intake by diabetic rats treated with the respective plant extracts. The insulin-treated rats showed 56.4% and 75.8% decrease in food and fluid intake compared to an augmentation for diabetic control rats, 43.0% and 383.8%, respectively, at the end of the second week of experimentation. These results showed that the plant extracts can reverse hyperglycemia, polyphagia and polydipsia provoked by streptozotocin, and thus, they have anti-diabetic properties.
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PMID:Anti-diabetic activity of methanol/methylene chloride stem bark extracts of Terminalia superba and Canarium schweinfurthii on streptozotocin-induced diabetic rats. 1627 36

Metabolic syndrome (MetS) is a complicated clinicopathological entity with clustering of cardiovascular and metabolic risk factors, which includes central obesity, hypertension, dyslipidemia and glucose intolerance. There were many studies investigating a wide variety of clinical and pathophysiological aspects of this syndrome. However, the cutoffs of the components of MetS are not yet being evaluated by measured the insulin resistance (IR) directly. In this study, we enrolled 564 (male/female: 250/314) middle-aged healthy subjects. Each of the male and the female group was further divided into four subgroups (group 1 to group 4). Group 4 had the top 25 percentile of most severe IR determined by insulin suppression test. We then obtain the mean values of each component of the MetS in group 4 and compared them with the definitions of World Health Organization, National Cholesterol Education Program Adult Treatment Panel III, European Study Group of Insulin Resistance and International Diabetes Federation. The means of the blood pressure (BP) (male, 125/81; female, 125/80 mmHg) and the triglyceride (TG) (male, 1.6; female, 1.4 mmol/l) in group 4 were lower, and the fasting plasma glucose (6.2 mmol/l) was higher than the cutoffs of the other four sets of the criteria. The means of the high-density lipoprotein cholesterol (male, 0.9; female, 1.03 mmol/l) and the body mass index (male, 26.9; female 26.1 kg/m(2)) in group 4 were consistent with the cutoffs of other four groups and also the Taiwan Health Department criteria. In conclusion, we suggest to lower the cutoffs of the BP from 140/90 to 125/80 mmHg, TG from 1.7 to 1.6 mmol/l for males and 1.4 mmol/l for females for MetS definition, at least in Taiwan. This may help to early detect subjects under high risk of future coronary heart disease and diabetes. Still, these newly proposed cutoffs need larger-scale epidemiological studies to confirm.
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PMID:The relationships between insulin resistance and components of metabolic syndrome in Taiwanese Asians. 1635 72

As the average lifespan in Western countries continues to expand, health care for the aged has become an increasingly important research focus. While clinicians and vertebrate researchers have frequently concentrated on specific age-related diseases, particularly neurodegenerative diseases such as Alzheimer's and Parkinson's Diseases, researchers working with invertebrate genetic model systems have gained important insights into global mechanisms of lifespan determination. Still others have employed biochemical and molecular approaches to elucidate processes contributing to common diseases of the elderly, such as cancer and diabetes. In between the broad focus on organismal aging and the more narrow focus on cellular dysfunction is the study of aging at the level of individual organ function. This review will attempt to highlight recent advances in the area of age-related deterioration of organ function provided by the use of transgenic model organisms, with a view toward incorporating these observations into a framework provided by both broader theories of the aging process and studies of cellular function during aging.
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PMID:Age-related cardiac deterioration: insights from Drosophila. 1712 82


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