[Show abstract][Hide abstract] ABSTRACT: This review presents an analysis of clinical and experimental studies related to post-transplantation diabetes mellitus (PTDM) - a specific complication after solid organ transplantation. A search of the databases eLibrary, PubMed and Scopus using the keywords ≪posttransplantation diabetes mellitus≫, ≪new onset diabetes after transplantation≫, ≪transplantation≫ and ≪immunosuppression≫ yielded in 523 results, including four from Russian literature (one original research manuscript). The analysis included original research, reviews, meta-analyses and monographs published not before 2005 in Russian and English. A total of 60 relevant original researches and reviews were included in this review. Diagnostic criteria, disease risk factors and potential pathogenic mechanisms were all considered. The mechanisms of the diabetogenic effect of modern immunosuppressive drugs were analysed. The principles of pre- and post-transplantation screening for PTDM and optimal management strategies for patients with PTDM are presented. The current controversial issues concerning the various aspects of PTDM are discussed.
[Show abstract][Hide abstract] ABSTRACT: The program of renoprotection in patients with diabetes mellitus (DM) is based on a conceptual model of development and progression of diabetic kidney disease, which is the result of combined impact of genetically modulated metabolic and hemodynamic factors. Compensation of carbohydrate metabolism, which is crucial at the clinical debut of nephropathy, becomes problematic at the late stages of chronic kidney disease (CKD). ADA (American Diabetes Association) and EASD (European Association for the Study of Diabetes) recommendations formalized in a consensus on the treatment of patients with type 2 diabetes (T2D) should only be extrapolated to patients with CKD with great prudence. Incretin-based drugs gain reputation as promising and perspective therapy for metabolic control in patients with type 2 DM and CKD. There is an obvious need for large-scale, long-term studies involving patients with various severity of renal disease and related complications to assess the potential of this new diabetes therapy trend.
[Show abstract][Hide abstract] ABSTRACT: During latest decade, as threat of acute complications of diabetes mellitus was surmounted, cardiovascular complications became leading cause of death. Clinical manifestation of coronary, brachiocephalic and renal atherosclerosis is quite dramatic in diabetes mellitus, which determines extent of dissemination and intensity of lesions. Combination of these mutually confounding conditions is a characteristic problem of patients with diabetes mellitus. Presence of 2+ risk factors (one of which is diabetes mellitus in itself) requires active examination in order to rule out coronary, brachiocephalic, peripheral and renal artery lesions. Aggressive care is necessary in order to control progression of disease and administer adequate conservative and endovascular treatment with account of high risk of combination of lesions.
[Show abstract][Hide abstract] ABSTRACT: The second isoform of the PPARgamma2 is specific for adipose tissue. In adipocytes, this isoform is involved in the regulation of adipogenesis and lipid storage, insulin and glucose metabolism. Pro12Ala, a missense mutation in exon 2 of PPARG, reduces transcriptional activity of PPARgamma2 and is shown to be associated with increased insulin sensitivity and protection from T2D. Previously, this polymorphism has never been assessed in a Russian population for its relationship to T2D, insulin resistance, and diabetes-related metabolic traits. In this study, we tested 588 Russian T2D patients and 597 normoglycaemic controls. Carriers of the Pro12 allele and subjects homozygous for Pro/Pro had significantly increased risk of developing T2D (OR 1.43 and 2.04, respectively). In Pro/Pro homozygotes, adjustment for potential confounding risk factors resulted in reducing the OR value from 2.04 to 1.69, but the association remained significant (p=0.046).The Pro/Pro genotype also showed association with increased levels of fasting insulin (p=0.019) in non-diabetic controls and elevated serum triglycerides (p=0.019) in T2D patients. Compared with other genotypes, non-diabetic and diabetic subjects homozygous for Pro/Pro had a significantly higher HOMA-IR score and reduced ISI value. This observation strongly supports the implication of the PPARG Pro12Ala in insulin resistance and T2D in a Russian population.
[Show abstract][Hide abstract] ABSTRACT: AimsMarkers rs12255372 (G/T) of the transcription factor 7-like 2 (TCF7L2) and rs13266634 (R325W) of the solute carrier family 30 (zinc transporter) member 8 (SLC30A8) showed association with type 2 diabetes (T2D) in multiple ethnic groups. In this study, we evaluated whether these markers confer susceptibility to T2D in a Russian population.Methods
Using a direct DNA sequencing, we genotyped these markers in 588 unrelated Russian T2D patients and 597 normoglycemic non-diabetic controls at age 50 and older. Association between these markers and patients’ clinical and metabolic traits was assessed by the ANCOVA analysis, with adjustment for possible confounding risk factors.ResultsThe allele T of rs12255372 and allele R of rs13266634 showed significant association with a higher diabetes risk (Odds Ratio (OR) = 1.37 and 1.22, respectively). Adjustment for confounding risk factors strengthened the association increasing OR from 1.54 (p = 0.24) up to 1.89 (p = 0.046) in homozygotes T/T and from 1.29 (p = 0.035) up to 1.35 (p = 0.019) in homozygotes R/R. Compared to other genotypes, homozygous carriers of the risk variants of TCF7L2 and SLC30A8 (both diabetic and non-diabetic) had significantly lower levels of 2 h insulin and decreased values of the homeostasis model assessment of β-cell function (HOMA-β).ConclusionsTCF7L2 rs12255372 and SLC30A8 rs13266634 modulate risk of T2D in a Russian population through impaired function of β-cells.
Diabetes and Metabolic Syndrome Clinical Research and Reviews 12/2009; 3(4):219–223. DOI:10.1016/j.dsx.2009.07.005