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- Adiels, Martin, 1976, et al.
(författare)
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Fatty liver, insulin resistance, and dyslipidemia.
- 2008
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Ingår i: Current diabetes reports. - : Springer Science and Business Media LLC. - 1539-0829 .- 1534-4827. ; 8:1, s. 60-4
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Forskningsöversikt (refereegranskat)abstract
- After recently being recognized as a feature of the metabolic syndrome, fatty liver has evolved as a key player in the pathogenesis of dyslipidemia. Development of nonalcoholic fatty liver disease comes from an imbalance between the influx and production of fatty acids and the use of fatty acids for oxidation or secretion as very low density lipoprotein (VLDL) triglycerides. Previously, we have shown a strong relationship between increased liver fat and overproduction of large VLDL particles. We observed recently that in patients with high liver fat, insulin was unable to regulate VLDL production. The result is increased concentrations of VLDL particles in the circulation. Consequently, changes are seen in the metabolism of other lipoproteins that interact with VLDL particles, the net result being decreased high-density lipoprotein cholesterol and increased formation of small, dense low-density lipoprotein. In this article, we review recent findings on the development of fatty liver and its role in the diabetic dyslipidemia pathogenesis.
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| 2. |
- Ahrén, Bo
(författare)
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Are Sulfonylureas Less Desirable Than DPP-4 Inhibitors as Add-on to Metformin in the Treatment of Type 2 Diabetes?
- 2011
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Ingår i: Current Diabetes Reports. - : Springer Science and Business Media LLC. - 1539-0829 .- 1534-4827. ; 11, s. 83-90
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Tidskriftsartikel (refereegranskat)abstract
- Sulfonylureas (SUs) are commonly used as add-on to metformin in treatment of type 2 diabetes in patients who are insufficiently controlled by metformin alone. They have good efficacy and have been shown to prevent microvascular complications. However, treatment with SUs is also associated with a high frequency of hypoglycemia, increased body weight, and a high risk of secondary failure. During recent years, dipeptidyl peptidase-4 (DPP-4) inhibitors have emerged as alternatives to SUs. They show similar efficacy as SUs but with lower risk of hypoglycemia, and reduction or no change in body weight, and if confirmed in humans, they may preserve islet function and thereby minimize the risk for secondary failure. Their limitation at present is the lack of long-term (>5 years) experience on durability and safety. Overall, therefore, the conclusion emerges that SUs are less desirable than DPP-4 inhibitors in management of hyperglycemia in type 2 diabetes.
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| 3. |
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| 4. |
- Akhtar, Simeen, et al.
(författare)
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A Review of the Eurodiale Studies: What Lessons for Diabetic Foot Care?
- 2011
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Ingår i: Current Diabetes Reports. - : Springer Science and Business Media LLC. - 1539-0829 .- 1534-4827. ; 11:4, s. 302-309
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Tidskriftsartikel (refereegranskat)abstract
- The prevalence of diabetes has been increasing at an alarming rate worldwide. Treatment of diabetes-related complications adds a huge financial burden on our health services, made worse in the current financial climate. The Eurodiale (European Study Group on Diabetes and the Lower Extremity) study was a prospective observational study conducted in 14 European centers in 2003 to 2004 and included data on characteristics of diabetic patients with foot ulcers, diagnostic and management procedures, health care organization, quality of life, and resource use. This was the first large multicenter study, included 1232 patients, and used an integrated approach for a multiorgan disease. The study has provided new insights into the intricacies involved in managing diabetic foot ulcers and how care can be improved. It has shown the differences in quality of care provided in different centers and also highlighted the need for more specific guidance related to diabetic foot disease.
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| 6. |
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| 7. |
- Carlsson, Per-Ola, et al.
(författare)
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Mesenchymal Stromal Cells to Halt the Progression of Type 1 Diabetes?
- 2015
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Ingår i: Current Diabetes Reports. - : Springer Science and Business Media LLC. - 1534-4827 .- 1539-0829. ; 15:7
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Tidskriftsartikel (refereegranskat)abstract
- No treatment to halt the progressive loss of insulin-producing beta-cells in type 1 diabetes mellitus has yet been clinically introduced. Strategies tested have at best only transiently preserved beta-cell function and in many cases with obvious side effects of drugs used. Several studies have suggested that mesenchymal stromal cells exert strong immunomodulatory properties with the capability to prevent or halt diabetes development in animal models of type 1 diabetes. A multitude of mechanisms has been forwarded to exert this effect. Recently, we translated this strategy into a first clinical phase I/IIa trial and observed no side effects, and preserved or even increased C-peptide responses to a mixed meal tolerance test during the first year after treatment. Future blinded, larger studies, with extended follow-up, are clearly of interest to investigate this treatment concept.
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| 8. |
- Docherty, N. G., et al.
(författare)
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Weight Loss Interventions and Progression of Diabetic Kidney Disease
- 2015
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Ingår i: Current Diabetes Reports. - : Springer Science and Business Media LLC. - 1534-4827 .- 1539-0829. ; 15:8
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Tidskriftsartikel (refereegranskat)abstract
- Progressive renal impairment (diabetic kidney disease (DKD)) occurs in upwards of 40 % of patients with obesity and type 2 diabetes mellitus (T2DM) and is a cause of significant morbidity and mortality. Means of attenuating the progression of DKD focus on amelioration of risk factors. Visceral obesity is implicated as a causative agent in impaired metabolic and cardiovascular control in T2DM, and various approaches primarily targeting weight have been examined for their impact on markers of renal injury and dysfunction in DKD. The current report summarises the evidence base for the impact of surgical, lifestyle and pharmacological approaches to weight loss on renal end points in DKD. The potential for a threshold of weight loss more readily achievable by surgical intervention to be a prerequisite for renal improvement is highlighted. Comparing efficacious nonsurgical weight loss strategies with surgical strategies in appropriately powered and controlled prospective studies is a priority for the field.
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| 9. |
- Eriksson, Olof
(författare)
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GPR44 as a Target for Imaging Pancreatic Beta-Cell Mass
- 2019
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Ingår i: Current Diabetes Reports. - : Springer. - 1534-4827 .- 1539-0829. ; 19:8
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Forskningsöversikt (refereegranskat)abstract
- Purpose of Review Quantitative markers for beta-cell mass (BCM) in human pancreas are currently lacking. Medical imaging using positron emission tomography (PET) markers for beta-cell restricted targets may provide an accurate and non-invasive measurement of BCM, to assist diagnosis and treatment of metabolic disease. GPR44 was recently discovered as a putative marker for beta cells and this review summarizes the developments so far. Recent Findings Several small molecule binders targeting GPR44 have been radiolabeled for PET imaging and evaluated in vitro and in small and large animal models. C-11-AZ12204657 and C-11-MK-7246 displayed a dose-dependent and GPR44-mediated binding to beta cells both in vitro and in vivo, with negligible uptake in exocrine pancreas. Summary GPR44 represents an attractive target for visualization of BCM. Further progress in radioligand development including clinical testing is expected to clarify the role of GPR44 as a surrogate marker for BCM in humans.
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| 10. |
- Espes, Daniel, et al.
(författare)
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Betatrophin in Diabetes Mellitus : the Epidemiological Evidence in Humans
- 2015
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Ingår i: Current Diabetes Reports. - : Springer Science and Business Media LLC. - 1534-4827 .- 1539-0829. ; 15:12
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Forskningsöversikt (refereegranskat)abstract
- The prevalence of type 2 diabetes is increasing worldwide, and while numerous treatments exist, none of the current pharmacologic therapies is curative. Pharmacologic approaches that increase beta cell mass may present an avenue for actual cure. There have been numerous reports on factors that can induce beta cell proliferation in rodents, whereas there are still very limited data on the occurrence of beta cell proliferation in humans. The recent discovery of the hormone betatrophin, which in mice counteracted glucose intolerance induced by insulin resistance by potently stimulating beta cell proliferation, has boosted the hope for a new target for drug development for the treatment of diabetes mellitus in humans. With the encouraging preclinical findings as a background, this review presents the available clinical data on betatrophin and discusses its possible role in humans.
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