Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Diabetes

  • adolescent diabetes
  • adult-onset diabetes
  • alloxan-induced diabetes
  • autoimmune diabetes
  • childhood diabetes
  • childhood onset type 1 diabetes
  • controlled diabetes
  • dependent diabetes
  • diagnosed diabetes
  • diagnosed type 2 diabetes
  • experimental diabetes
  • gestational diabetes
  • human type 1 diabetes
  • i diabetes
  • ii diabetes
  • induced diabetes
  • insulin dependent diabetes
  • insulin-dependent diabetes
  • insulin-treated diabetes
  • latent autoimmune diabetes
  • maternal diabetes
  • maturity-onset diabetes
  • mitochondrial diabetes
  • monogenic diabetes
  • neonatal diabetes
  • new onset diabetes
  • new-onset diabetes
  • non-insulin-dependent diabetes
  • onset diabetes
  • onset type 1 diabetes
  • overt diabetes
  • pre-existing diabetes
  • pregestational diabetes
  • pretransplant diabetes
  • self-reported diabetes
  • streptozotocin-induced diabetes
  • type 1 diabetes
  • type 2 diabetes
  • type i diabetes
  • type ii diabetes
  • type-ii diabetes
  • uncontrolled diabetes
  • undiagnosed diabetes

  • Terms modified by Diabetes

  • diabetes Mellitu
  • diabetes association
  • diabetes care
  • diabetes center
  • diabetes centre
  • diabetes clinic
  • diabetes complications
  • diabetes control
  • diabetes development
  • diabetes diagnosis
  • diabetes duration
  • diabetes education
  • diabetes education programme
  • diabetes federation
  • diabetes federation criterioN
  • diabetes group
  • diabetes incidence
  • diabetes induction
  • diabetes intervention
  • diabetes management
  • diabetes medication
  • diabetes mellitu
  • diabetes mellitu patient
  • diabetes model
  • diabetes onset
  • diabetes pathogenesis
  • diabetes patient
  • diabetes population
  • diabetes prevalence
  • diabetes prevention
  • diabetes prevention program
  • diabetes quality
  • diabetes register
  • diabetes research
  • diabetes risk
  • diabetes risk factor
  • diabetes screening
  • diabetes self-care
  • diabetes self-management
  • diabetes service
  • diabetes services
  • diabetes specialist nurse
  • diabetes status
  • diabetes study
  • diabetes subject
  • diabetes team
  • diabetes therapy
  • diabetes treatment
  • diabetes treatment satisfaction questionnaire

  • Selected Abstracts


    ABSTRACT Red currants (Ribes rubrum L.), black currants (Ribes nigrum L.), red and green gooseberries (Ribes uva-crispa) were evaluated for the total phenolics, antioxidant capacity based on 2, 2-diphenyl-1-picrylhydrazyl radical scavenging assay and functionality such as in vitro inhibition of ,-amylase, ,-glucosidase and angiotensin I-converting enzyme (ACE) relevant for potential management of hyperglycemia and hypertension. The total phenolics content ranged from 3.2 (green gooseberries) to 13.5 (black currants) mg/g fruit fresh weight. No correlation was found between total phenolics and antioxidant activity. The major phenolic compounds were quercetin derivatives (black currants and green gooseberries) and chlorogenic acid (red currants and red gooseberries). Red currants had the highest ,-glucosidase, ,-amylase and ACE inhibitory activities. Therefore red currants could be good dietary sources with potential antidiabetes and antihypertension functionality to compliment overall dietary management of early stages of type 2 diabetes. [source]


    ABSTRACT The rationale for this investigation is that phenolic content in light-modulated pea seedlings could be enhanced by exogenous elicitors with antioxidant potential such as folic acid and vitamin C. Such phenolic-enriched extracts may have health benefits to consumers. The antioxidant-linked functional attributes of the phenolic-enriched extracts were evaluated for potential health-related benefits. Specifically, effectiveness in inhibiting ,-amylase and ,-glucosidase in relation to hyperglycemia (linked to diabetes management), as well as inhibiting angiotensin-converting enzyme I (ACE I), in relation to hypertension, was evaluated. The results show that phenolic-enriched extracts had the ability to inhibit ,-amylase and ,-glucosidase activity. On the day with the highest total phenolic content, day 8, inhibition of ,-amylase and ,-glucosidase was most prominent. Further, the same extracts showed positive benefits for potential hypertension management reflected in the inhibition of ACE I. These results taken together indicated that light-sprouted pea seedling extracts when incorporated into the diet could contribute to potential management of hyperglycemia linked to diabetes and hypertension related to cardiovascular risk. PRACTICAL APPLICATIONS In this in vitro study results show the positive effect of the different phenolic-enriched pea sprouts on hyperglycemia risk factors. It is clear that phenolic-enriched pea sprouts have high antioxidant activity, ACE 1 inhibitory activity and also good inhibitory activity on carbohydrate-modulating enzyme such as alpha-glucosidase related to glucose absorption in the intestine. The potential for managing both glucose absorption and cellular redox dysfunction for preventing postprandial hyperglycemia linked to type 2 diabetes and hyperglycemia-induced vascular complications leading to hypertension can be designed in part through food systems and therefore provides the rationale basis for further clinical studies. This strategy can be further extended to enhance phenolic-linked health benefits of a wide variety of legumes, fruits and vegetables and therefore can be the basis for food ingredient design for functional food applications. [source]


    ABSTRACT Natural ,-amylase and ,-glucosidase inhibitors from food-grade plants offer an attractive strategy to manage postprandial hyperglycemia for type 2 diabetes management via control of starch breakdown and intestinal glucose absorption. In this study, four random sources of red and white wines as well as four types of teas were investigated for ,-amylase and ,-glucosidase inhibitory potential. Water extracts of black tea had the highest ,-glucosidase inhibitory activity, followed by white tea and oolong tea. All the randomly selected red wines had significant ,-glucosidase inhibitory activity compared to white wine. The ,-glucosidase inhibitory activity of the tea and wines correlated to the phenolic content, antioxidant activity and phenolic profile of the extracts. Further, these extracts had less or no ,-amylase inhibitory activity, indicating potential to overcome the side effects of undigested starch. This research has relevance for managing hyperglycemia and related oxidation-linked dysfunction and concurrently reducing problems of undigested starch. PRACTICAL APPLICATIONS In this study anti-diabetic-relevant potential of wines and teas were confirmed in four types of red and white wines as well as four types of commonly available teas using in vitro enzyme assays for alpha-glucosidase and alpha-amylase inhibitory activities. In vitro inhibitory activities of these enzymes provide a strong biochemical rationale for further in vivo studies and dietary management strategy for type 2 diabetes through the control of glucose absorption. Further this phenolic antioxidant-enriched dietary strategy using specific beverage combinations can generate a whole food profile that has the potential to reduce hyperglycemia-induced pathogenesis and also associated complications linked to cellular oxidation stress. [source]


    Fiona Symes BSc (Hons)
    SUMMARY Increased collaboration between the vascular specialities is clearly leading to increased understanding of the interrelationships between the different disease states and how each impacts and influences the other. This advantage will be reflected in improved patient care if the practical outputs of this growing knowledge are carefully implemented at service level. This article outlines how the aspects of diet and lifestyle associated with vascular-related disease complement, contrast and in some cases contradict each other. It gives information and guidelines as to how the expertise of dietitians working in the different specialist areas might usefully be shared to be of maximum advantage to all patients. [source]


    AI Vinik
    OBJECTIVE: To review evidence for a relationship between dermal neurovascular dysfunction and other components of the metabolic syndrome of type 2 diabetes. RESEARCH DESIGN AND METHODS: We review and present data supporting concepts relating dermal neurovascular function to prediabetes and the metabolic syndrome. Skin blood flow can be easily measured by laser Doppler techniques. RESULTS: Heat and gravity have been shown to have specific neural, nitrergic, and independent mediators to regulate skin blood flow. We describe data showing that this new tool identifies dermal neurovascular dysfunction in the majority of type 2 diabetic patients. The defect in skin vasodilation is detectable before the development of diabetes and is partially correctable with insulin sensitizers. This defect is associated with C-fiber dysfunction (i.e., the dermal neurovascular unit) and coexists with variables of the insulin resistance syndrome. The defect most likely results from an imbalance among the endogenous vasodilator compound nitric oxide, the vasodilator neuropeptides substance P and calcitonin gene-related peptide, and the vasoconstrictors angiotensin 11 and endothelin. Hypertension per se increases skin vasodilation and does not impair the responses to gravity, which is opposite to that of diabetes, suggesting that the effects of diabetes override and counteract those of hypertension. CONCLUSIONS: These observations suggest that dermal neurovascular function is largely regulated by peripheral C-fiber neurons and that dysregulation may be a component of the metabolic syndrome associated with type 2 diabetes. [source]


    GH TeschArticle first published online: 15 AUG 200
    SUMMARY 1Macrophage accumulation is a feature of Type 2 diabetes and is associated with the development of diabetic complications (nephropathy, atherosclerosis, neuropathy and retinopathy). The present article reviews the current evidence that macrophages contribute to the complications of Type 2 diabetes. 2Macrophage-depletion studies in rodent models have demonstrated a causal role for macrophages in the development of diabetic complications. 3Components of the diabetic milieu (high glucose, advanced glycation end-products and oxidized low-density lipoprotein) promote macrophage accumulation (via induction of chemokines and adhesion molecules) and macrophage activation within diabetic tissues. 4Macrophages mediate diabetic injury through a variety of mechanisms, including production of reactive oxygen species, cytokines and proteases, which result in tissue damage leading to sclerosis. 5A number of existing and experimental therapies can indirectly reduce macrophage-mediated injury in diabetic complications. The present article discusses the use of these therapies, given alone and in combination, in suppressing macrophage accumulation and activity. 6In conclusion, current evidence supports a critical role for macrophages in the evolution of diabetic complications. Present therapies are limited in slowing the progression of macrophage-mediated injury. Novel strategies that are more specific at targeting macrophages may provide better protection against the development of Type 2 diabetic complications. [source]


    Susumu Ogawa
    SUMMARY 1Over the course of treatment with angiotensin-converting enzyme inhibitor (ACEI), plasma levels of aldosterone have been shown to increase and this increase would blunt the effectiveness of the ACEI (aldosterone escape phenomenon). 2In the present study, we assessed a potential renal benefit of additional aldosterone blockade with spironolactone in hypertensive diabetic patients treated with ACEI showing the phase of aldosterone escape. 3The present clinical study was a randomized prospective study to assess difference between the clinical effects of spironolactone and furosemide. Thirty hypertensive type II diabetics (DM2) with a urinary alubumin : creatinine ratio (ACR) above 30 mg/g creatinine (showing albuminuria) and plasma B-type natriuretic peptide (BNP) levels above 100 pg/mL (showing mild heart failure) were treated with an ACEI (imidapril 5 mg/day) for 1 year and then randomly divided into two groups, one group receiving additional spironolactone (25 mg/day) treatment and the other receiving furosemide (20 mg/day) treatment. Blood pressure, ACR and plasma BNP levels were monitored in both groups. 4Treatment with the ACEI reduced ACR initially but, in 1 year, ACR tended to increase. Additional spironolactone treatment progressively reduced ACR, whereas furosemide treatment did not show any effect. Plasma BNP levels were reduced by ACEI and were further reduced by additional spironolactone treatment, but not furosemide treatment. Blood pressure levels in both groups were comparable. 5In conclusion, additional therapy with spironolactone in ACEI treatment exerts a renoprotective, as well as cardioprotective, effect in hypertensive diabetes. [source]

    Diabetic embryopathy: Studies using a rat embryo culture system and an animal model

    Shoichi Akazawa
    ABSTRACT The mechanism of diabetic embryopathy was investigated using in vitro experiments in a rat embryo culture system and in streptozotocin-induced diabetic pregnant rats. The energy metabolism in embryos during early organogenesis was characterized by a high rate of glucose utilization and lactic acid production (anaerobic glycolysis). Embryos uninterruptedly underwent glycolysis. When embryos were cultured with hypoglycemic serum, such embryos showed malformations in association with a significant reduction in glycolysis. In a diabetic environment, hyperglycemia caused an increased glucose flux into embryonic cells without a down-regulation of GLUT1 and an increased metabolic overload on mitochondria, leading to an increased formation of reactive oxygen species (ROS). Activation of the hexamine pathway, subsequently occurring with increased protein carbonylation and increased lipid peroxidation, also contributed to the increased generation of ROS. Hyperglycemia also caused a myo-inositol deficiency with a competitive inhibition of ambient glucose, which might have been associated with a diminished phosphoinositide signal transduction. In the presence of low activity of the mitochondrial oxidative glucose metabolism, the ROS scavenging system in the embryo was not sufficiently developed. Diabetes further weakened the antioxidant system, especially, the enzyme for GSH synthesis, ,-GCS, thereby reducing the GSH concentration. GSH depletion also disturbed prostaglandin biosynthesis. An increased formation of ROS in a diminished GSH-dependent antioxidant system may, therefore, play an important role in the development of embryonic malformations in diabetes. [source]

    Admission Hyperglycemia and Length of Hospital Stay in Patients With Diabetes and Heart Failure: A Prospective Cohort Study

    Yohannes Gebreegziabher MD
    The authors assessed the relationship between glycemia and length of hospital stay (LOS) in a prospective cohort study of patients with diabetes mellitus and heart failure (HF). Of 212 patients with acute HF exacerbation, 119 (56%) also had diabetes. The mean age of the cohort was 63±0.87 years, and the mean body mass index was 29.3 kg/m2. Diabetic patients had significantly longer LOS compared with the nondiabetics (5.0±0.29 vs 3.4±0.19; P<.001). In patients with diabetes, the mean glycated hemoglobin A1c was 8.3%, admission blood glucose (BG) was 169±7.7 mg/dL, and average BG was 196±8.1 mg/dL. After adjusting for age, sex, weight, hypertension, renal function, and anemia, LOS was significantly correlated with admission BG (r=0.31; P<.001) and average BG (r=0.34; P=.001). In patients with acute HF exacerbation, diabetes significantly prolonged LOS. Hyperglycemia correlated with LOS. [source]

    Heart Failure and Diabetes: Collateral Benefit of Chronic Disease Management

    Molly G. Ware MD
    To test the hypothesis that a focus on heart failure (HF) care may be associated with inadequate diabetes care, the authors screened 78 patients (aged 64±11 years; 69% male) with diabetes enrolled in an HF disease management program for diabetes care as recommended by the American Diabetes Association (ADA). Ninety-five percent of patients had hemoglobin A1c levels measured within 12 months, and 71% monitored their glucose at least once daily. Most patients received counseling regarding diabetic diet and exercise, and approximately 80% reported receiving regular eye and foot examinations. Mean hemoglobin A1c level was 7.8±1.9%. There was no relationship between hemoglobin A1c levels and New York Heart Association class or history of HF hospitalizations. Contrary to the authors' hypothesis, patients in an HF disease management program demonstrated levels of diabetic care close to ADA goals. "Collateral benefit" of HF disease management may contribute to improved patient outcomes in diabetic patients with HF. [source]

    Expressional changes of ganglioside GM3 during ovarian maturation and early embryonic development in db/db mice

    Dong Hoon Kwak
    Diabetes and obesity cause abnormal development of reproductive processes in a variety of species, but the mechanisms that underlie this effect have not been fully elucidated. This study examined the expressional changes of ganglioside GM3 during ovarian maturation, in vitro fertilization (IVF) and early embryonic development in diabetic/obese db/db mice. In high-performance thin-layer chromatography studies, GM3 expression was conspicuously low in the ovaries of db/db mice compared to non-diabetic db/+ mice. Signal detected by anti-GM3 monoclonal antibody was greatly reduced in the primary, secondary and graffian follicles of db/db mice compared to control mice. Results from IVF with ova and sperm from db/db mice showed that GM3 expression during early embryonic development was obviously decreased compared to db/+ mice. This study also elucidated the effects of high glucose (20 and 30 mm) on early embryonic development in ICR strain mice. High glucose caused a decrease in GM3 expression during early embryonic development. Taken together, the results of this study indicate decreased GM3 expression during ovarian maturation and embryonic development of db/db mice, suggesting that alteration of ganglioside expression induced by the diabetic condition may be implicated in the abnormal follicular embryonic development. [source]

    The unfolded protein response is required to maintain the integrity of the endoplasmic reticulum, prevent oxidative stress and preserve differentiation in , -cells

    R. J. Kaufman
    Diabetes is an epidemic of worldwide proportions caused by , -cell failure. Nutrient fluctuations and insulin resistance drive , -cells to synthesize insulin beyond their capacity for protein folding and secretion and thereby activate the unfolded protein response (UPR), an adaptive signalling pathway to promote cell survival upon accumulation of unfolded protein in the endoplasmic reticulum (ER). Protein kinase-like endoplasmic reticulum kinase (PERK) signals one component of the UPR through phosphorylation of eukaryotic initiation factor 2 on the , -subunit (eIF2,) to attenuate protein synthesis, thereby reducing the biosynthetic burden. , -Cells uniquely require PERK-mediated phosphorylation of eIF2, to preserve cell function. Unabated protein synthesis in , -cells is sufficient to initiate a cascade of events, including oxidative stress, that are characteristic of , -cell failure observed in type 2 diabetes. In contrast to acute adaptive UPR activation, chronic activation increases expression of the proapoptotic transcription factor CAAT/enhancer-binding protein homologous protein (CHOP). Chop deletion in insulin-resistant mice profoundly increases , -cell mass and prevents , -cell failure to forestall the progression of diabetes. The findings suggest an unprecedented link by which protein synthesis and/or misfolding in the ER causes oxidative stress and should encourage the development of novel strategies to treat diabetes. [source]

    Interpreting clinical trials of diabetic dyslipidaemia: new insights

    A. S. Wierzbicki
    Current treatment guidelines highlight the importance of aggressive lipid-modifying therapy in reducing cardiovascular risk in patients with type 2 diabetes. Statins are established as the cornerstone of dyslipidaemia management in diabetic patients, based on their efficacy in lowering levels of low-density lipoprotein cholesterol (LDL-C). However, statins fail to address the high residual cardiovascular risk in treated patients, some of which may be attributable to low HDL cholesterol (HDL-C) and elevated triglycerides and to a preponderance of small, dense LDL particles, indicating the need for further intervention. Fibrates are effective against all components of atherogenic dyslipidaemia associated with type 2 diabetes. Clinical studies, most notably the Fenofibrate Intervention and Event Lowering in Diabetes, indicate that fibrates, most likely in combination with a statin, have a secondary role in reducing cardiovascular risk in patients with type 2 diabetes, particularly in those without prior cardiovascular disease or patients with low HDL-C. Results are awaited from the ongoing Action to Control Cardiovascular Risk in Diabetes trial to fully evaluate the outcome benefits of this combination strategy. [source]

    Combination statin,fibrate therapy: safety aspects

    R. Franssen
    Patients with type 2 diabetes or metabolic syndrome remain at high residual risk of cardiovascular events even after intensive statin therapy. While treatment guidelines recommend the addition of a fibrate to statin therapy in this setting, concerns about the potential for myopathy may limit the use of this combination in clinical practice. These concerns are certainly justified for gemfibrozil, which interferes with statin glucuronidation, leading to elevation in statin plasma concentrations and an increased risk of myotoxicity in combination with a range of commonly prescribed statins. However, the available evidence refutes suggestions that this is a class effect for fibrates. Fenofibrate does not adversely influence the metabolism or pharmacokinetics of any of the commonly prescribed statins. This in turn translates to a reduced potential for myotoxicity in combination with a statin. Data are awaited from the ongoing Action to Control Cardiovascular Risk in Diabetes (ACCORD) study to evaluate the efficacy and safety of fenofibrate plus simvastatin combination therapy in type 2 diabetes patients. [source]

    The usage of a simplified self-titration dosing guideline (303 Algorithm) for insulin detemir in patients with type 2 diabetes , results of the randomized, controlled PREDICTIVEÔ 303 study

    L. Meneghini
    The Predictable Results and Experience in Diabetes through Intensification and Control to Target: An International Variability Evaluation 303 (PREDICTIVEÔ 303) Study (n = 5604) evaluated the effectiveness of insulin detemir, a long-acting basal insulin analogue, using a simplified patient self-adjusted dosing algorithm (303 Algorithm group) compared with standard-of-care physician-driven adjustments (Standard-of-care group) in a predominantly primary care setting, over a period of 6 months. Insulin detemir was to be started once-daily as add-on therapy to any other glucose-lowering regimens or as a replacement of prestudy basal insulin in patients with type 2 diabetes. Investigator sites rather than individual patients were randomized to either the 303 Algorithm group or the Standard-of-care group. Patients from the 303 Algorithm group sites were instructed to adjust their insulin detemir dose every 3 days based on the mean of three ,adjusted' fasting plasma glucose (aFPG) values (capillary blood glucose calibrated to equivalent plasma glucose values) using a simple algorithm: mean aFPG < 80 mg/dl (<4.4 mmol/l), reduce dose by 3 U; aFPG between 80 and 110 mg/dl (4.4,6.1 mmol/l), no change; and aFPG > 110 mg/dl (>1.1 mmol/l), increase dose by 3 U. The insulin detemir dose for patients in the Standard-of-care group was adjusted by the investigator according to the standard of care. Mean A1C decreased from 8.5% at baseline to 7.9% at 26 weeks for the 303 Algorithm group and from 8.5 to 8.0% for the Standard-of-care group (p = 0.0106 for difference in A1C reduction between the two groups). Mean FPG values decreased from 175 mg/dl (9.7 mmol/l) at baseline to 141 mg/dl (7.8 mmol/l) for the 303 Algorithm group and decreased from 174 mg/dl (9.7 mmol/l) to 152 mg/dl (8.4 mmol/l) for the Standard-of-care group (p < 0.0001 for difference in FPG reduction between the two groups). Mean body weight remained the same at 26 weeks in both groups (change from baseline 0.1 and ,0.2 kg for the 303 Algorithm group and the Standard-of-care group respectively). At 26 weeks, 91% of the patients in the 303 Algorithm group and 85% of the patients in the Standard-of-care group remained on once-daily insulin detemir administration. The rates of overall hypoglycaemia (events/patient/year) decreased significantly from baseline in both groups [from 9.05 to 6.44 for the 303 Algorithm group (p = 0.0039) and from 9.53 to 4.95 for the Standard-of-care group (p < 0.0001)]. Major hypoglycaemic events were rare in both groups (0.26 events/patient/year for the 303 Algorithm group and 0.20 events/patient/year for the Standard-of-care group; p = 0.2395). In conclusion, patients in the 303 Algorithm group achieved comparable glycaemic control with higher rate of hypoglycaemia as compared with patients in the Standard-of-care group, possibly because of more aggressive insulin dose adjustments. The vast majority of the patients in both groups were effectively treated with once-daily insulin detemir therapy. The use of insulin detemir in this predominantly primary care setting achieved significant improvements in glycaemic control with minimal risk of hypoglycaemia and no weight gain. [source]

    Cataracts in experimentally diabetic mouse: morphological and apoptotic changes

    K. R. Hegde
    Aim:, The objective of these investigations was to extend our earlier study on the induction of cataracts in diabetic mice, a low aldose reductase (AR) animal model at morphological level. Previous studies were done primarily at biochemical level. Methods:, Diabetes was induced by intraperitoneal administration of streptozotocin. The lenses isolated after the establishment of diabetes were then subjected to histologic and electron microscopic studies. Results:, Morphological alterations were characterized by shrinkage, elongation and lobulization of the nuclei of the epithelial cells. This was associated with chromatin condensation and its margination. Similar structural aberrations were also observed in a significant number of the subepithelial fibre cells representing defect in fibre maturation. More interestingly, unlike that in other common animal models of diabetic cataract, such abnormally nucleated cells were also found to be prevalent in the posterior subcapsular region, a finding common in human diabetics also. Conclusion:, The present studies further affirm the suitability of the mouse model for a study of cataractogenesis induced by diabetes. Because of the findings reported herein, as well as the known biochemical similarity between the lenses of the mice and humans in respect of AR deficiency, contrary to the rat model where it is very high, use of this species is considered more useful towards understanding the basic aetiology as well as for evaluating the efficacy of various referred nutritional and metabolic antioxidants against such cataracts. [source]

    Diabetes and cardiovascular disease

    Andrew Neil
    First page of article [source]

    The impact of diabetes and obesity on liver histology in patients with hepatitis C

    F. Friedenberg
    Aim:, An association between diabetes mellitus and HCV has been recognized previously. No study has examined whether there is an independent association between the degree of hepatic fibrosis and the incidence of diabetes in HCV patients when controlling for other risk factors. Methods:, We reviewed the charts of 264 consecutive patients with chronic HCV infection at a referral liver centre from January 1991 to December 1999. Demographic background, medical history, laboratory and liver biopsy results were retrieved. Results:, The prevalence of diabetes was 16.3%. Gender, intravenous drug use, steatosis scores, aminotransferase levels and iron studies were similarly distributed in patients with and without diabetes (all p > 0.05). In contrast, mean age was greater in the diabetic group (49.8 vs. 44.3, p = 0.003). The prevalence of diabetes was substantially higher in African-Americans (p = 0.001) and those with BMI > 30 (p = 0.015). Although the fibrosis score was higher in diabetics (, = 0.14, p = 0.03), that association did not remain significant when controlling for diabetes risk factors (p > 0.3). The degree of steatosis and fibrosis both tended to increase with increasing BMI (, = 0.47, p < 0.001 and , = 0.13, p = 0.03, respectively). Even after controlling for diabetes, age, gender, race, and current alcohol use, those associations remained (both p < 0.001). Conclusions:, The prevalence of diabetes in our group of HCV patients was high, consistent with other studies. Diabetes is not an independent predictor of degree of fibrosis. Body mass index is an independent predictor of both fibrosis and steatosis in HCV patients. [source]

    Effects of aminoguanidine and tolrestat on the development of ocular and renal structural changes in experimental diabetic rats

    Ö. Azal
    Studies that researched the role of aminoguanidine and tolestat in the prevention of diabetic retinopathy and nephropathy resulted in conflicting data. We investigated the effects of these agents in the prevention of ocular and renal changes in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced by intravenous injection of STZ in 30 rats. Ten rats that were not given STZ served as non-diabetic control (Group 1). Ten STZ-diabetic rats that were not given any treatment served as diabetic control (Group 2). Groups 3 and 4 were composed of STZ-induced diabetic rats (10 each) that were given tolrestat and aminoguanidine respectively. Eyes and kidneys were examined at the 24th week under electronmicroscopy. Cataract was observed in all six of the surviving rats in Groups 2 and 4, and in one of 6 surviving rats in group 3. Cataract development was lower in Group 3 than Groups 2 and 4. All retinal samples obtained from group 2 demonstrated a number of structural abnormalities, whereas there were no significant ultrastructural changes in groups 3 and 4. Groups 2 and 3 demonstrated mesangial proliferation and expansion, diffuse glomerular basement membrane (GBM) thickening, and focal GBM thickening in the bulb form. Group 4 demonstrated a normally appearing mesangial space, minimal diffuse but no focal GBM thickening. The urinary albumin excretion (UAE) was lower in Group 4 than the other groups. In conclusion, our results suggest that aminoguanidine may be an important agent for the prevention of renal changes, whereas tolrestat may be effective for the prevention of ocular changes in diabetes mellitus. [source]

    Lipid-lowering therapy in patients with type 2 diabetes: the case for early intervention

    Armin Steinmetz
    Abstract Chronic complications of type 2 diabetes, in particular, macrovascular complications, confer substantial morbidity and mortality and adversely affect a patient's quality of life. Early intensive intervention to control cardiovascular risk factors is essential in clinical management. Atherogenic dyslipidaemia characterized by elevated triglycerides, a low level of high-density lipoprotein cholesterol (HDL-C), and an increase in the preponderance of small, dense low-density lipoprotein (LDL) particles, is a key modifiable risk factor for macrovascular diabetic complications. Lowering low-density lipoprotein cholesterol (LDL-C) with a statin (or the combination of statin and ezetimibe) is the main focus for reducing cardiovascular risk in patients with diabetes. However, statins fail to address the residual cardiovascular risk associated with low HDL-C. Fibrates are effective against all components of the atherogenic dyslipidaemia associated with type 2 diabetes. Secondary analyses of the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study suggest a role for early treatment with fenofibrate in improving cardiovascular risk reduction in type 2 diabetes and provide safety data supporting the use of fenofibrate in combination with a statin. Data from the FIELD study suggest that fenofibrate may also have potential to impact on microvascular diabetic complications associated with type 2 diabetes. Data are awaited from the ongoing Action to Control Cardiovascular Risk in Diabetes (ACCORD) study to evaluate the outcome benefits of combining fenofibrate with a statin in patients with type 2 diabetes. Finally, in view of divergent study results and outstanding data, assessment of the risk of the individual with type 2 diabetes is mandatory to assist clinical decision-making when initiating lipid therapy. Copyright © 2008 John Wiley & Sons, Ltd. [source]

    Role of histone and transcription factor acetylation in diabetes pathogenesis

    Steven G. Gray
    Abstract Globally, diabetes (and, in particular, type 2 diabetes) represents a major challenge to world health. Currently in the United States, the costs of treating diabetes and its associated complications exceed $100 billion annually, and this figure is expected to soar in the near future. Despite decades of intense research efforts, the genetic basis of the events involved in the pathogenesis of diabetes is still poorly understood. Diabetes is a complex multigenic syndrome primarily due to beta-cell dysfunction associated with a variable degree of insulin resistance. Recent advances have led to exciting new developments with regard to our understanding of the mechanisms that regulate insulin transcription. These include data that implicate chromatin as a critical regulator of this event. The ,Histone Code' is a widely accepted hypothesis, whereby sequential modifications to the histones in chromatin lead to regulated transcription of genes. One of the modifications used in the histone code is acetylation. This is probably the best characterized modification of histones, which is carried out under the control of histone acetyltransferases (HATs) and histone deacetylases (HDACs). These enzymes also regulate the activity of a number of transcription factors through acetylation. Increasing evidence links possible dysregulation of these mechanisms in the pathogenesis of diabetes, with important therapeutic implications. Copyright © 2005 John Wiley & Sons, Ltd. [source]

    Diabetes: insulin resistance and derangements in lipid metabolism.

    Cure through intervention in fat transport, storage
    Abstract We present multiple findings on derangements in lipid metabolism in type 2 diabetes. The increase in the intracellular deposition of triglycerides (TG) in muscles, liver and pancreas in subjects prone to diabetes is well documented and demonstrated to attenuate glucose metabolism by interfering with insulin signaling and insulin secretion. The obesity often associated with type 2 diabetes is mainly central, resulting in the overload of abdominal adipocytes with TG and reducing fat depot capacity to protect other tissues from utilizing a large proportion of dietary fat. In contrast to subcutaneous adipocytes, the central adipocytes exhibit a high rate of basal lipolysis and are highly sensitive to fat mobilizing hormones, but respond poorly to lipolysis restraining insulin. The enlarged visceral adipocytes are flooding the portal circulation with free fatty acids (FFA) at metabolically inappropriate time, when FFA should be oxidized, thus exposing nonadipose tissues to fat excess. This leads to ectopic TG accumulation in muscles, liver and pancreatic beta-cells, resulting in insulin resistance and beta-cell dysfunction. This situation, based on a large number of observations in humans and experimental animals, confirms that peripheral adipose tissue is closely regulated, performing a vital role of buffering fluxes of FFA in the circulation. The central adipose tissues tend to upset this balance by releasing large amounts of FFA. To reduce the excessive fat outflow from the abdominal depots and prevent the ectopic fat deposition it is important to decrease the volume of central fat stores or increase the peripheral fat stores. One possibility is to downregulate the activity of lipoprotein lipase, which is overexpressed in abdominal relatively to subcutaneous fat stores. This can be achieved by gastrointestinal bypass or gastroplasty, which decrease dietary fat absorption, or by direct means that include surgical removal of mesenteric fat. Indirect treatment consists of the compliant application of drastic lifestyle change comprising both diet and exercise and pharmacotherapy that reduces mesenteric fat mass and activity. The first step should be an attempt to effectively induce a lifestyle change. Next comes pharmacotherapy including acarbose, metformin, PPAR,, or PPAR,, agonists, statins and orlistat, estrogens in postmenopausal women or testosterone in men. Among surgical procedures, gastric bypass has been proven to produce beneficial results in advance of other surgical techniques, the evidence basis of which still needs strengthening. Copyright © 2004 John Wiley & Sons, Ltd. [source]

    Stroke in patients with diabetes mellitus

    Boris N. Mankovsky
    Abstract The article's objective is to review the key advances in the scientific literature related to the association of stroke with diabetes mellitus and to summarize the current approaches to stroke prevention in diabetic patients. The key findings from the literature regarding stroke incidence in patients with diabetes, specific and nonspecific risk factors of stroke in the diabetic population, such as arterial hypertension, dyslipidemia, hyperglycemia, diabetes duration, diabetic complications, insulin resistance/hyperinsulinemia, course and outcome of stroke in subjects with diabetes and/or hyperglycemia, and the peculiarities of type, site and size of stroke in diabetic patients are discussed. The results of recent clinical trials aimed at correcting hyperglycemia, hypertension, and dyslipidemia, to prevent stroke in people with diabetes, are reviewed. The medical database Medline along with original articles from peer-reviewed journals were used for analysis. There is convincing evidence suggesting that diabetes mellitus represents a strong independent risk factor of stroke. The contribution of hyperglycemia to increased stroke risk is not proven. Data suggest an association of the full cluster of the insulin resistance syndrome and stroke. Diabetes is a risk factor mainly for ischemic stroke, while its association with hemorrhagic stroke remains controversial. Hyperglycemia is common in stroke patients, but it is not known whether it independently influences the course and outcome of stroke or merely reflects stroke severity and location. Aggressive control of arterial hypertension and dyslipidemia allows to decrease the risk of stroke in diabetic patients substantially, while the importance of glucose control for stroke prevention remains unproven. Copyright © 2004 John Wiley & Sons, Ltd. [source]

    Neuropathic pain and diabetes

    Dilip Kapur
    Abstract Neuropathic pain is a common phenomenon resulting from injury to the central or peripheral nervous system. The means by which diabetes results in nerve injury is unclear but the effect is to cause injury at all levels of the nervous system from the level of the peripheral nerves to the brain. Nerve injury causes pain through a cascade of mechanisms resulting in altered processing of sensory input into the nervous system. This alteration occurs through chemical and anatomical changes in the nervous system that are similar to some of the processes seen in central sensitisation following acute pain. Following nerve injury, neuropathic pain occurs not only when these mechanisms are activated but also when sensitisation is maintained. Other processes occurring in neuropathic pain appear to be a loss of normal inhibitory controls as seen by a reduction in local GABA-ergic and descending monoaminergic influences. There are also important changes mediated via glial cells that can maintain neuropathic pain. Diabetes affects all areas of the nervous system and the contribution of higher levels of the nervous system is often overlooked. Neurophysiological and MRI evidence strongly suggest that these may contribute to the pain of diabetic neuropathy. Psychological dysfunction in diabetic patients is an important factor in increasing the suffering associated with all aspects of the disease, but treatment and control of pain can greatly improve the quality of life. Copyright © 2003 John Wiley & Sons, Ltd. [source]

    Editorial: Diabetes: costs and cost-effectiveness

    DIABETIC MEDICINE, Issue 9 2010
    A. M. Gray
    No abstract is available for this article. [source]

    Commentary: Diabetes in the UK: time for a reality check?

    DIABETIC MEDICINE, Issue 9 2010
    E. A. M. Gale
    First page of article [source]

    Diabetes and mental health; the problem of co-morbidity

    DIABETIC MEDICINE, Issue 8 2010
    C. E. Lloyd
    No abstract is available for this article. [source]

    Independent predictive roles of eotaxin Ala23Thr, paraoxonase 2 Ser311Cys and ,3 -adrenergic receptor Trp64Arg polymorphisms on cardiac disease in Type 2 Diabetes,an 8-year prospective cohort analysis of 1297 patients

    DIABETIC MEDICINE, Issue 4 2010
    Y. Wang
    Diabet. Med. 27, 376,383 (2010) Abstract Aims, To examine the independent and joint effects of multiple genetic variants on a cardiac end-point in an 8-year prospective study of a Chinese diabetic cohort. Methods, Seventy-seven single nucleotide polymorphisms (SNPs) of 53 candidate genes for inflammation, thrombosis, vascular tone regulation and lipid metabolism were genotyped in 1297 Chinese patients with no prior history of coronary heart disease (CHD) or heart failure at baseline. Cardiac end-point was defined by the occurrence of CHD and/or heart failure. Results, In Cox regression model, after adjustment for baseline confounding variables including age, sex, smoking status, duration of diabetes, glycaemic control, lipid levels, waist circumference, blood pressure, albuminuria and estimated glomerular filtration rate, genetic variants, including Ala/Ala of SCYA11 (eotaxin) Ala23Thr, Cys/Cys or Cys/Ser of PON2 (paraoxonase 2) Ser311Cys and Arg/Arg of ADRB3 (,3 -adrenergic receptor) Trp64Arg, were independently associated with incident cardiac end-point, with respective hazard ratios (95% confidence interval) of 1.70 (1.10,2.61, P = 0.037), 1.42 (1.08,1.88, P = 0.013) and 3.84 (1.18,12.50, P = 0.025). Analysis of the joint effect of the risk alleles showed significant increased risk of the cardiac end-point with increasing number of risk alleles (P < 0.001). The adjusted risk for the cardiac end-point was 4.11 (P = 0.002) for patients carrying four risk alleles compared with those carrying one or no risk allele. Conclusions, The independent risk conferred by genetic variants encoding pathways such as inflammation and lipid metabolism, not adequately reflected by conventional biomarkers, may identify high-risk individuals for intensified control of modifiable risk factors. [source]

    Ramadan Education and Awareness in Diabetes (READ) programme for Muslims with Type 2 diabetes who fast during Ramadan

    DIABETIC MEDICINE, Issue 3 2010
    V. Bravis
    Diabet. Med. 27, 327,331 (2010) Abstract Background and Aims, During Ramadan, Muslims fast from dawn to dusk for one lunar month. The majority of Muslim diabetic patients are unaware of complications such as hypoglycaemia during fasting. The safety of fasting has not been assessed in the UK Muslim population with diabetes. The aim of this study was to determine the impact of Ramadan-focused education on weight and hypoglycaemic episodes during Ramadan in a Type 2 diabetic Muslim population taking oral glucose-lowering agents. Methods, We retrospectively analysed two groups. Group A attended a structured education programme about physical activity, meal planning, glucose monitoring, hypoglycaemia, dosage and timing of medications. Group B did not. Hypoglycaemia was defined as home blood glucose < 3.5 mmol/l. Results, There was a mean weight loss of 0.7 kg after Ramadan in group A, compared with a 0.6-kg mean weight gain in group B (P < 0.001). The weight changes observed were independent of the class of glucose-lowering agents used. There was a significant decrease in the total number of hypoglycaemic events in group A, from nine to five, compared with an increase in group B from nine to 36 (P < 0.001). The majority were in patients treated with short-acting sulphonylureas (group A,100%, group B,94%). At 12 months after attending the programme, glycated haemoglobin (HbA1c) reduction were sustained in group A. Conclusions, Ramadan-focused education in diabetes can empower patients to change their lifestyle during Ramadan. It minimizes the risk of hypoglycaemic events and prevents weight gain during this festive period for Muslims, which potentially benefits metabolic control. [source]

    Not all roads lead to Rome,a review of quality of life measurement in adults with diabetes

    DIABETIC MEDICINE, Issue 4 2009
    J. Speight
    Abstract Aims Quality of life (QoL) is recognized widely as an important health outcome in diabetes, where the burden of self-management places great demands on the individual. However, the concept of QoL remains ambiguous and poorly defined. The aim of our review is to clarify the measurement of QoL in terms of conceptualization, terminology and psychometric properties, to review the instruments that have been used most frequently to assess QoL in diabetes research and make recommendations for how to select measures appropriately. Methods A systematic literature search was conducted to identify the ten measures most frequently used to assess QoL in diabetes research (including clinical trials) from 1995 to March 2008. Results Six thousand and eight-five abstracts were identified and screened for instrument names. Of the ten instruments most frequently used to assess ,QoL', only three actually do so [i.e. the generic World Health Organization Quality of Life (WHOQOL) and the diabetes-specific Diabetes Quality of Life (DQOL) and Audit of Diabetes-Dependent Quality of Life (ADDQoL)]. Seven instruments more accurately measure health status [Short-Form 36 (SF-36), EuroQoL 5-Dimension (EQ-5D)], treatment satisfaction [Diabetes Treatment Satisfaction Questionnaire (DTSQ)] and psychological well-being [Beck Depression Inventory (BDI), Hospital Anxiety and Depression Scale (HADS), Well-Being Questionnaire (W-BQ), Problem Areas in Diabetes (PAID)]. Conclusions No single measure can suit every purpose or application but, when measures are selected inappropriately and data misinterpreted, any conclusions drawn are fundamentally flawed. If we value QoL as a therapeutic goal, we must ensure that the instruments we use are both valid and reliable. QoL assessment has the proven potential to identify ways in which treatments can be tailored to reduce the burden of diabetes. With careful consideration, appropriate measures can be selected and truly robust assessments undertaken successfully. [source]