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- Katsarou, Anastasia, et al.
(author)
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Type 1 diabetes mellitus
- 2017
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In: Nature Reviews Disease Primers. - : Springer Science and Business Media LLC. - 2056-676X. ; 3
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Journal article (peer-reviewed)abstract
- Type 1 diabetes mellitus (T1DM), also known as autoimmune diabetes, is a chronic disease characterized by insulin deficiency due to pancreatic beta-cell loss and leads to hyperglycaemia. Although the age of symptomatic onset is usually during childhood or adolescence, symptoms can sometimes develop much later. Although the aetiology of T1DM is not completely understood, the pathogenesis of the disease is thought to involve T cell-mediated destruction of beta-cells. Islet-targeting autoantibodies that target insulin, 65 kDa glutamic acid decarboxylase, insulinoma-associated protein 2 and zinc transporter 8 - all of which are proteins associated with secretory granules in beta-cells -are biomarkers of T1DM-associated autoimmunity that are found months to years before symptom onset, and can be used to identify and study individuals who are at risk of developing T1DM. The type of autoantibody that appears first depends on the environmental trigger and on genetic factors. The pathogenesis of T1DM can be divided into three stages depending on the absence or presence of hyperglycaemia and hyperglycaemia-associated symptoms (such as polyuria and thirst). A cure is not available, and patients depend on lifelong insulin injections; novel approaches to insulin treatment, such as insulin pumps, continuous glucose monitoring and hybrid closed-loop systems, are in development. Although intensive glycaemic control has reduced the incidence of microvascular and macrovascular complications, the majority of patients with T1DM are still developing these complications. Major research efforts are needed to achieve early diagnosis, prevent beta-cell loss and develop better treatment options to improve the quality of life and prognosis of those affected.
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| 2. |
- Shaat, Nael, et al.
(author)
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Glucose homeostasis, beta cell function, and insulin resistance in relation to vitamin D status after gestational diabetes mellitus
- 2017
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In: Acta Obstetricia et Gynecologica Scandinavica. - : Wiley. - 0001-6349. ; 96:7, s. 821-827
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Journal article (peer-reviewed)abstract
- Introduction: We wanted to determine vitamin D status after gestational diabetes mellitus (GDM) and to evaluate whether levels of 25-hydroxyvitamin D3 (25OHD3) are associated with beta cell function, insulin resistance or a diagnosis of diabetes after GDM. Material and methods: Glucose homeostasis was assessed during a 75-g oral glucose tolerance test one to two years after delivery in 376 women with previous GDM (287 European and 78 non-European, including 33 Arab and 35 Asian women). Insulin resistance was estimated using homeostasis model assessment of insulin resistance (HOMA-IR). The insulinogenic index (I/G30) and the disposition index [(I/G30)/HOMA-IR] were used to calculate insulin secretion. Concentrations of serum 25OHD3 were determined. Results: Mean (±SD) 25OHD3 concentration was 50.0 ± 22.3 nmol/L and differed significantly among subgroups of body mass index, ethnicity, and glucose tolerance status; 53% had 25OHD3 levels <50 nmol/L and 87% had 25OHD3 levels <75 nmol/L. There was a negative correlation between 25OHD3 concentration and HOMA-IR (p < 0.001) and a positive correlation between 25OHD3 and disposition index (p = 0.002) in univariable regression analysis. Correlations attenuated after adjustment for body mass index. In univariable regression analysis, 25OHD3 concentrations were significantly associated with diabetes after GDM (p = 0.004). However, in a multivariable model, non-European origin, HOMA-IR and insulinogenic index were significantly associated with postpartum diabetes, whereas 25OHD3 concentrations were not. Conclusion: Vitamin D deficiency/insufficiency in previous GDM cases appears to be associated with beta cell dysfunction and insulin resistance, but not with postpartum diabetes when factors well known to influence type-2 diabetes were adjusted for.
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