233 resultados para Diabetes Insípida


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AIMS: Smoking cessation has been suggested to increase the short-term risk of type 2 diabetes mellitus (T2DM). This study aimed at assessing the association between smoking cessation and incidence of T2DM and impaired fasting glucose (IFG). METHODS: Data from participants in the CoLaus study, Switzerland, aged 35-75 at baseline and followed for 5.5years were used. Participants were classified as smokers, recent (≤5years), long-term (>5years) quitters, and non-smokers at baseline. Outcomes were IFG (fasting serum glucose (FSG) 5.6-6.99mmol/l) and T2DM (FSG ≥7.0mmol/l and/or treatment) at follow up. RESULTS: 3,166 participants (63% women) had normal baseline FSG, of whom 26.7% were smokers, 6.5% recent quitters, and 23.5% long-term quitters. During follow-up 1,311 participants (41.4%) developed IFG (33.6% women, 54.7% men) and 47 (1.5%) developed T2DM (1.1% women, 2.1% men). Former smokers did not have statistically significant increased odds of IFG compared with smokers after adjustment for age, education, physical activity, hypercholesterolemia, hypertension and alcohol intake, with OR of 1.29 [95% confidence interval 0.94-1.76] for recent quitters and 1.03 [0.84-1.27] for long-term quitters. Former smokers did not have significant increased odds of T2DM compared with smokers with multivariable-adjusted OR of 1.53 [0.58-4.00] for recent quitters and 0.64 [0.27-1.48] for long-term quitters. Adjustment for body-mass index and waist circumference attenuated the association between recent quitting and IFG (OR 1.07 [0.78-1.48]) and T2DM (OR 1.28 [0.48-3.40]. CONCLUSION: In this middle-aged population, smoking cessation was not associated with an increased risk of IFG or T2DM.

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Elevated concentrations of albumin in the urine, albuminuria, are a hallmark of diabetic kidney disease and are associated with an increased risk for end-stage renal disease and cardiovascular events. To gain insight into the pathophysiological mechanisms underlying albuminuria, we conducted meta-analyses of genome-wide association studies and independent replication in up to 5,825 individuals of European ancestry with diabetes and up to 46,061 without diabetes, followed by functional studies. Known associations of variants in CUBN, encoding cubilin, with the urinary albumin-to-creatinine ratio (UACR) were confirmed in the overall sample (P = 2.4 × 10(-10)). Gene-by-diabetes interactions were detected and confirmed for variants in HS6ST1 and near RAB38/CTSC. Single nucleotide polymorphisms at these loci demonstrated a genetic effect on UACR in individuals with but not without diabetes. The change in the average UACR per minor allele was 21% for HS6ST1 (P = 6.3 × 10(-7)) and 13% for RAB38/CTSC (P = 5.8 × 10(-7)). Experiments using streptozotocin-induced diabetic Rab38 knockout and control rats showed higher urinary albumin concentrations and reduced amounts of megalin and cubilin at the proximal tubule cell surface in Rab38 knockout versus control rats. Relative expression of RAB38 was higher in tubuli of patients with diabetic kidney disease compared with control subjects. The loci identified here confirm known pathways and highlight novel pathways influencing albuminuria.

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Le tabagisme est associé à un risque augmenté de développer un diabète de type 2. Arrêter de fumer devrait donc diminuer le risqué de diabète. Seulement, les études concernant le risque métabolique à l'arrêt du tabac sont discordantes. Par ailleurs, les effets métaboliques du tabac et de l'arrêt du tabac diffèrent probablement selon le sexe, avec notamment un effet différent du tabac sur la santé des femmes, et une prise pondérale plus importante à l'arrêt que chez les hommes. Notre étude vise à évaluer le risque métabolique à l'arrêt du tabac, chez les femmes et les homes séparément. Nous avons utilisé les données de l'étude de cohorte prospective CoLaus, qui évalue différents facteurs de risque cardiovasculaire chez des sujets choisis de manière aléatoire, dans la population Lausannoise entre 35 et 75 ans, suivis sur 5.5 ans en moyenne. Parmi ceux avec une glycémie à jeun normale au départ, nous avons divisé les participants en quatre groupes selon leur statut tabagique : non fumeurs, personnes ayant arrêté de fumer depuis plus de 5 ans, celles ayant arrêté depuis moins de 5 ans, et fumeurs actifs. Nous avons mesuré les incidences de glycémie à jeun altérée (5.6-6.99 mmol/l) et de diabète (glycémie à jeun ≥ 7 mmol/l et/ou traitement pour le diabète) durant le période de suivi, stratifiées par sexe. Puis le risque d'incidence de glycémie altérée et de diabète a été calculé avec trois niveaux d'ajustement pour les facteurs confondants pour un risque métabolique. Nous avons inclus 3166 participants, dont 63% de femmes. Au total, 26.3% étaient fumeurs, 6.5% ex-fumeurs depuis moins de 5 ans et 23.5% ex-fumeurs depuis plus de 5 ans. Durant le suivi, 1311 (41.4%) personnes ont développé une glycémie à jeun altérée (33.6% des femmes, 54.7% des homes), et 47 (1.5%) ont développé un diabète (1.1% des femmes, 2.1% des hommes). Les personnes ayant arrêté de fumer n'avait pas de risque significativement plus élevé de développer une glycémie à jeun altérée ou un diabète que les fumeurs, après ajustement pour l'âge, l'éducation, l'hypercholestérolémie, la prise d'alcool, l'activité physique, la prise de poids, le BMI initial et le BMI d'arrivée dans les différents modèles d'ajustement. L'analyse de l'interaction du sexe avec ces résultats est également négative. Les analyses de sensibilité ont montré que l'exclusion des personnes ayant changé de statut tabagique durant le suivi ne changeait pas ces résultats. Nous avons refait les analyses en incluant les participants ayant une glycémie altérée au début du suivi, mais le risque d'incidence de diabète n'est pas plus élevé chez les ex-fumeurs que chez les fumeurs non plus dans cette population. Sur demande d'un reviewer, nous avons également refait les analyses avec la glycémie en continue (valeurs de base et valeurs à 5.5 ans), et la glycémie moyenne n'était pas différente par groupe de tabagisme. En conclusion, dans cette population européenne d'âge moyen, avec une prévalence basse d'obésité et une prise de poids modérée durant le suivi, nous n'avons pas trouvé de risque significativement plus élevé de développer un diabète en arrêtant de fumer, et ce pour les deux sexes. L'arrêt du tabac doit donc être encouragé chez toutes les fumeuses et tous les fumeurs.

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One of the global targets for non-communicable diseases is to halt, by 2025, the rise in the age-standardised adult prevalence of diabetes at its 2010 levels. We aimed to estimate worldwide trends in diabetes, how likely it is for countries to achieve the global target, and how changes in prevalence, together with population growth and ageing, are affecting the number of adults with diabetes. We pooled data from population-based studies that had collected data on diabetes through measurement of its biomarkers. We used a Bayesian hierarchical model to estimate trends in diabetes prevalence-defined as fasting plasma glucose of 7.0 mmol/L or higher, or history of diagnosis with diabetes, or use of insulin or oral hypoglycaemic drugs-in 200 countries and territories in 21 regions, by sex and from 1980 to 2014. We also calculated the posterior probability of meeting the global diabetes target if post-2000 trends continue. We used data from 751 studies including 4,372,000 adults from 146 of the 200 countries we make estimates for. Global age-standardised diabetes prevalence increased from 4.3% (95% credible interval 2.4-7.0) in 1980 to 9.0% (7.2-11.1) in 2014 in men, and from 5.0% (2.9-7.9) to 7.9% (6.4-9.7) in women. The number of adults with diabetes in the world increased from 108 million in 1980 to 422 million in 2014 (28.5% due to the rise in prevalence, 39.7% due to population growth and ageing, and 31.8% due to interaction of these two factors). Age-standardised adult diabetes prevalence in 2014 was lowest in northwestern Europe, and highest in Polynesia and Micronesia, at nearly 25%, followed by Melanesia and the Middle East and north Africa. Between 1980 and 2014 there was little change in age-standardised diabetes prevalence in adult women in continental western Europe, although crude prevalence rose because of ageing of the population. By contrast, age-standardised adult prevalence rose by 15 percentage points in men and women in Polynesia and Micronesia. In 2014, American Samoa had the highest national prevalence of diabetes (>30% in both sexes), with age-standardised adult prevalence also higher than 25% in some other islands in Polynesia and Micronesia. If post-2000 trends continue, the probability of meeting the global target of halting the rise in the prevalence of diabetes by 2025 at the 2010 level worldwide is lower than 1% for men and is 1% for women. Only nine countries for men and 29 countries for women, mostly in western Europe, have a 50% or higher probability of meeting the global target. Since 1980, age-standardised diabetes prevalence in adults has increased, or at best remained unchanged, in every country. Together with population growth and ageing, this rise has led to a near quadrupling of the number of adults with diabetes worldwide. The burden of diabetes, both in terms of prevalence and number of adults affected, has increased faster in low-income and middle-income countries than in high-income countries. Wellcome Trust.

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We examined the association between lifecourse socioeconomic status (SES) and the risk of type 2 diabetes at older ages, ascertaining the extent to which adult lifestyle factors and systemic inflammation explain this relationship. Data were drawn from the English Longitudinal Study of Ageing (ELSA) which, established in 2002, is a representative cohort study of ≥50-year olds individuals living in England. SES indicators were paternal social class, participants' education, participants' wealth, and a lifecourse socioeconomic index. Inflammatory markers (C-reactive protein and fibrinogen) and lifestyle factors were measured repeatedly; diabetes incidence (new cases) was monitored over 7.5 years of follow-up. Of the 6218 individuals free from diabetes at baseline (44% women, mean aged 66 years), 423 developed diabetes during follow-up. Relative to the most advantaged people, those in the lowest lifecourse SES group experienced more than double the risk of diabetes (hazard ratio 2.59; 95% Confidence Interval (CI) = 1.81-3.71). Lifestyle factors explained 52% (95%CI:30-85) and inflammatory markers 22% (95%CI:13-37) of this gradient. Similar results were apparent with the separate SES indicators. In a general population sample, socioeconomic inequalities in the risk of type 2 diabetes extend to older ages and appear to partially originate from socioeconomic variations in modifiable factors which include lifestyle and inflammation.