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Pancreatic beta-cell failure is the common characteristic of type 1 and type 2 diabetes. Type 1 diabetes is induced by pancreatic beta-cell destruction, which is mediated by an autoimmune mechanism and consequent inflammatory proc...
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Pancreatic beta-cell failure is the common characteristic of type 1 and type 2 diabetes. Type 1 diabetes is induced by pancreatic beta-cell destruction, which is mediated by an autoimmune mechanism and consequent inflammatory process. Various inflammatory cytokines and oxidative stress produced by islet-infiltrating immune cells have been proposed to play an important role in mediating the destruction of beta cells. The JNK pathway is also activated by such cytokines and oxidative stress and is involved in beta-cell destruction. Type 2 diabetes is the most prevalent and serious metabolic disease affecting people all over the world. Pancreatic beta-cell dysfunction and insulin resistance are the hallmark of type 2 diabetes. Once hyperglycemia becomes apparent, beta-cell function gradually deteriorates, and insulin resistance is aggravated. This process is called "glucose toxicity." Under such conditions, oxidative stress is provoked, and the JNK pathway is activated, which is likely involved in pancreatic beta-cell dysfunction and insulin resistance. In addition, oxidative stress and activation of the JNK pathway are involved in the progression of atherosclerosis, which is often observed under diabetic conditions. Taken together, it is likely that oxidative stress and subsequent activation of the JNK pathway are involved in the pathogenesis of type 1 and type 2 diabetes.
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Until recently, diabetes in children was virtually synonymous with type 1 diabetes mellitus, whereas type 2 diabetes was a disease of middle age and the elderly. Over the past 10-20 years, an alarming increase in the prevalence of...
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Until recently, diabetes in children was virtually synonymous with type 1 diabetes mellitus, whereas type 2 diabetes was a disease of middle age and the elderly. Over the past 10-20 years, an alarming increase in the prevalence of type 2 diabetes has been reported from pediatric diabetes centers in North America and elsewhere in the world. Lifestyle factors responsible for the worldwide epidemic of overweight and obesity are responsible for the increase in the prevalence of type 2 diabetes in adults and children. This article briefly discusses the diagnosis and major types of diabetes in children but focuses on aspects of type 2 diabetes in children and adolescents, including demographics, pathophysiology, clinical presentation, screening, prevention and treatment. The identification of children at risk for type 2 diabetes and the implementation of community-wide preventive programs will be essential to reverse the tide. The availability of calorie dense "fast foods," candy, and sugared soft drinks must be restricted in schools and other venues frequented by children. Parents must limit the amount of time their children spend watching television and playing computer games. After-school programs that promote physical activity should be a priority of local and central governmental agencies. Prevention will only succeed if governments and local communities recognize that childhood obesity is an important public health problem and provide an environment that promotes changes in lifestyle that prevent and reverse obesity.
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Maturity-onset diabetes of the young (MODY) is a type of non-insulin-dependent diabetes mellitus caused by rare autosomal-dominant mutations. MODY genes play key biochemical roles in the pancreatic beta cell; therefore, common var...
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Maturity-onset diabetes of the young (MODY) is a type of non-insulin-dependent diabetes mellitus caused by rare autosomal-dominant mutations. MODY genes play key biochemical roles in the pancreatic beta cell; therefore, common variants of MODY genes are excellent candidate genes for type 2 diabetes. We review recent studies that suggest that common MODY gene variation contributes modestly to the heritability of type 2 diabetes.
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OBJECTIVE: To describe the characteristics of youth-onset noninsulin-dependent diabetes mellitus (NIDDM) at diagnosis and compare them with youths with insulin-dependent diabetes mellitus (IDDM) when matched for age, sex, and geog...
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OBJECTIVE: To describe the characteristics of youth-onset noninsulin-dependent diabetes mellitus (NIDDM) at diagnosis and compare them with youths with insulin-dependent diabetes mellitus (IDDM) when matched for age, sex, and geographic region of residence. STUDY DESIGN: Medical records of youths referred for evaluation of diabetes to a pediatric tertiary care center from 1988 to 1995 were reviewed to identify youths diagnosed with NIDDM. Patients selected for study met National Diabetes Data Group criteria for type of diabetes. RESULTS: Fifty patients with NIDDM were reviewed and compared with similar IDDM patients. The NIDDM female:male ratio was 1.6:1 and 74% were African-American. Only 18% of the IDDM patients were African-American. The mean body mass index +/- standard error at diagnosis of NIDDM patients was 35 +/- 1.1 kg/m in contrast to IDDM, 20 +/- .8 kg/m. Ninety-six percent of NIDDM and 24% of IDDM youths had a body mass index >/=85th percentile. More then 30% of NIDDM youths presented with hypertension. Diabetic ketoacidosis was present in >25% of NIDDM patients. Acanthosis nigricans was documented in 86% of NIDDM and 0% of IDDM patients. CONCLUSIONS: In Arkansas, youths with NIDDM are characterized by significant obesity in contrast to youths with IDDM. Physical characteristics such as obesity, acanthosis nigricans, and hypertension on examination of any youth with new-onset diabetes should raise suspicion of NIDDM.
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The study was conducted to investigate the effect of diabetes mellitus upon female sexual function, and to detect possible risk factors that might predict sexual dysfunction. The study consisted of 127 married women: 21 women with...
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The study was conducted to investigate the effect of diabetes mellitus upon female sexual function, and to detect possible risk factors that might predict sexual dysfunction. The study consisted of 127 married women: 21 women with type 1 diabetes, 50 women with type 2 diabetes and 56 healthy women as a control. Female sexual functions were evaluated with a questionnaire to assess sexual desire, arousal, lubrication, orgasm, satisfaction and pain. The prevalence of sexual dysfunction was 71% in the type 1 diabetic group, 42% in the type 2 diabetic group and 37% in the control subjects. The scores for sexual desire, arousal and lubrication were significantly lower in the type 1 diabetes group than in the control subjects (p < 0.05). The scores of orgasm, satisfaction, dyspareunia and total sexual function were slightly lower in the type 1 diabetic group than in the other groups. No factor predicted sexual dysfunction in the diabetic women while further age, poor education, absence of occupation and menopause predicted sexual dysfunction in the control subjects. The prevalence of sexual dysfunction was significantly higher in the type 1 diabetic women than in the type 2 diabetics and control subjects. However, no risk factors that might cause sexual dysfunction could be predicted in diabetic women.
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BACKGROUND AND AIMS: Following recent reports of increased numbers of adolescents being diagnosed with the adult or type 2 form of diabetes we aimed to describe the prevalence of both type 2 and other forms of diabetes in an urban...
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BACKGROUND AND AIMS: Following recent reports of increased numbers of adolescents being diagnosed with the adult or type 2 form of diabetes we aimed to describe the prevalence of both type 2 and other forms of diabetes in an urban population of children and young people in northern England. METHODS: A hospital based cross sectional study was performed in patients aged < or =30 years attending diabetic clinics in Leeds during the year 2000. RESULTS: A total of 677 subjects were identified, of whom 621 (92%) and 37 (5%) had type 1 and type 2 diabetes respectively. Four patients had confirmed maturity onset diabetes of the young, while the cause was uncertain for four. Median age of all patients was 22 years, with 396 (58%) aged 20-30; 32/37 patients with type 2 diabetes were aged 20-30. The prevalence of type 2 diabetes was 0.13 per 1000 overall, compared to 2.2 per 1000 for patients with type 1 diabetes. Of all type 2 diabetes patients, 24% were south Asian compared to 5% of the background population; 87% were categorised into the two least affluent tertiles of the Townsend score. This link with deprivation was not explained by the proportion of Asian patients across tertiles (approximately 25%). CONCLUSIONS: This study shows extremely low prevalence of type 2 diabetes in 10-19 year olds, but will provide a baseline for future comparisons. Overall, type 2 diabetes is seen more commonly in south Asians, and an association with deprivation is suggested.
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Illness can have a number of effects on diabetes, which require changes in management based on the individual patient's needs. Common effects of illness are discussed, together with strategies for regaining control. Where there is...
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Illness can have a number of effects on diabetes, which require changes in management based on the individual patient's needs. Common effects of illness are discussed, together with strategies for regaining control. Where there is any doubt about the patient's condition or the dosage change, specialist advice should be sought
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In summary, the significant rise in types 1 and 2 diabetes mellitus is poised to impart grave consequences on health and lifespan of the world's population if left unchecked. Recent publications in ATVB highlight progress toward t...
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In summary, the significant rise in types 1 and 2 diabetes mellitus is poised to impart grave consequences on health and lifespan of the world's population if left unchecked. Recent publications in ATVB highlight progress toward the identification of the fundamental mechanisms, and their interplay, that contribute to derangements in endothelial function, oxidative and inflammatory stresses in diabetes mellitus to mediate complications. Studies reported from primary cells contribute to elucidation of the key signaling mechanisms underlying complications and are buttressed by hypothesis-driven research in animal models. Using genetic modulation strategies, modulators of miRs, pharmacological agents and siRNA knockdown strategies, observations and associations progress to causality in diabetes mellitus. In large animal models of diabetes mellitus and atherosclerosis, efforts to improve imaging and diagnostic capabilities with respect to atherosclerotic plaques hold promise for extrapolation to human subjects, given the similarity between the 2 species in vessel size and anatomic characteristics. The messages from these studies are brought home to the human subject in multiple papers that both suggest means to reduce diabetes mellitus risk and to mitigate the complications. Surely, we are getting closer to identifying fundamental causative pathways in complications-the challenge is to develop therapeutic strategies for rigorous testing in human subjects. ATVB will continue to track the promise of basic, translational, and clinical research in diabetes mellitus and its complications.
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A 30year-old Hispanic male who presented with transient neonatal diabetes mellitus at 4 months has been intensively studied with 12 islet-cell secretagogues from 4 months to 24 years. He was both ICA- and GAD-65-negative, but at 2...
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A 30year-old Hispanic male who presented with transient neonatal diabetes mellitus at 4 months has been intensively studied with 12 islet-cell secretagogues from 4 months to 24 years. He was both ICA- and GAD-65-negative, but at 28 years was diagnosed with hypothyroidism due to positive thyroperoxidase antibodies. The course of his disease(s) and the various presentations of hyperglycemia are documented and illustrated by the responses in islet cell hormone secretion, namely, insulin, glucagon, and C-peptide. Insulin secretion gradually fell over 24 years, glucagon secretion persisted from infancy to 24 years but was only minimal during i.v. glucose at 24 years, and C-peptide secretion remained normal, although modest, throughout the 24 years. These data suggest that, despite changing presentations of diabetes mellitus over time, the islets continued to process proinsulin, although the patient required insulin therapy.
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The present study was performed to evaluate pregnancy outcomes in women with type 1 and type 2 diabetes mellitus (DM) in Japan. This multi-institutional retrospective study was conducted in 40 general hospitals in Japan during 200...
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The present study was performed to evaluate pregnancy outcomes in women with type 1 and type 2 diabetes mellitus (DM) in Japan. This multi-institutional retrospective study was conducted in 40 general hospitals in Japan during 2003-2009. We evaluated 369 and 579 pregnant women with type 1 and type 2 DM, respectively, and compared pregnancy outcomes between the two groups. Glycosylated hemoglobin levels in the first trimester did not differ significantly between the studied groups. Gestational weight gain was lower in type 2 DM than in type 1 DM. Although there were no significant differences in perinatal outcomes between the groups, the primary cesarean section rate was higher in type 2 DM than in type 1 DM. Multiple logistic regression analysis revealed that primigravida status, pre-gestational body mass index (BMI), gestational weight gain, chronic hypertension, and microvascular disease including diabetic retinopathy or nephropathy were associated with onset of pregnancy-induced hypertension. Further, pre-gestational BMI was associated with the need for primary cesarean section. This study demonstrated that no differences were observed in the rates of perinatal mortality and congenital malformation between pregnant women with type 1 DM and type 2 DM; however, women with type 2 DM displayed a higher risk of primary cesarean section.
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