The Review of Diabetic Studies (Rev Diabet Stud)

Publisher: Society for Biomedical Diabetes Research

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ISSN 1614-0575
OCLC 150315954
Material type Series, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

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    ABSTRACT: Adipose tissue secretes an abundance of proteins. Some of these proteins are known as adipokines and adipose-derived hormones which have been linked with metabolic disorders, including type 2 diabetes, and even with cancer. Variance in serum adipokine concentration is often closely associated with an increase (obesity) or decrease (lipodystrophy) in fat tissue mass, and it is affected by age, gender, and localization of the adipose tissue. However, there may be genetic variants which, in consequence, influence the serum concentration of a certain adipokine, and thereby promote metabolic disturbances or, with regard to the "protective" allele, exert beneficial effects. This review focuses on the genetic determination of serum levels of the following adipokines: adiponectin, chemerin, leptin, progranulin, resistin, retinol binding protein 4, vaspin, adipsin, apelin, and omentin. The article reports on the latest findings from genome-wide association studies (GWAS) and candidate gene studies, showing variants located in/nearby the adipokine genes and other (non-receptor) genes. An extra chapter highlights adipokine-receptor variants. Epigenetic studies on adipokines are also addressed.
    No preview · Article · Feb 2016 · The Review of Diabetic Studies
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    ABSTRACT: Objectives: Studies in rodents suggest that metformin treatment during pregnancy may have harmful effects on testicular development in offspring. Our aim was to determine whether metformin treatment of gestational diabetes mellitus (GDM) affects testicular size in male offspring. Methods: We compared the testicular size in prepubertal boys born to mothers who participated in a randomized controlled trial (RCT) comparing metformin with insulin in the treatment of GDM. Twenty-five (42.4% of invited) and 27 (52.9% of invited) boys whose mothers had been treated with metformin or insulin, respectively, participated in the study. Testicular size was measured by a ruler, an orchidometer, and by ultrasonography at the age of 33 to 85 months. Results: The mean age of the boys was 60 months at the time of examination, and did not differ between the metformin and insulin group (p = 0.88). There was no difference in testicular size between the boys in the two groups (p always ≥ 0.40), and there were no significant differences in height, weight, BMI, BMI z-score, or waist-to-hip ratio (WHR) between the boys in the groups. Conclusions: Prepubertal testicular size did not differ between offspring born to metformin-treated mothers and those born to insulin-treated mothers.
    No preview · Article · Feb 2016 · The Review of Diabetic Studies
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    ABSTRACT: This article reviews the impact of diabetes and its treatment on vascular function with a focus on the reactivity of epineurial arterioles, blood vessels that provide circulation to the sciatic nerve. Another focus is the relationship between the dysregulation of neurovascular function and diabetic peripheral neuropathy. Diabetic peripheral neuropathy is a debilitating disorder that occurs in more than 50 percent of patients with diabetes. The etiology involves metabolic, vascular, and immunologic pathways besides neurohormonal growth factor deficiency and extracellular matrix remodeling. In the light of this complex etiology, an effective treatment for diabetic peripheral neuropathy has not yet been identified. Current opinion postulates that any effective treatment for diabetic peripheral neuropathy will require a combination of life style and therapeutic interventions. However, a more comprehensive understanding of the factors contributing to neurovascular and neural dysfunction in diabetes is needed before such a treatment strategy can be developed. After reading this review, the reader should have gained insight into the complex regulation of vascular function and blood flow to the sciatic nerve, and the impact of diabetes on numerous elements of vascular reactivity of epineurial arterioles of the sciatic nerve. © 2015, Society for Biomedical Diabetes Research. All rights reserved.
    No preview · Article · Dec 2015 · The Review of Diabetic Studies
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    ABSTRACT: Diabetic retinopathy is a common microvascular complication of diabetes mellitus. It affects a substantial proportion of US adults over age 40. The condition is a leading cause of visual loss. Much attention has been given to expanding the role of current treatments along with investigating various novel therapies and drug delivery methods. In the treatment of diabetic macular edema (DME), intravitreal pharmacotherapies, especially anti-vascular endothelial growth factor (anti-VEGF) agents, have gained popularity. Currently, anti-VEGF agents are often used as first-line agents in center-involved DME, with recent data suggesting that among these agents, aflibercept leads to better visual outcomes in patients with worse baseline visual acuities. While photocoagulation remains the standard treatment for proliferative diabetic retinopathy (PDR), recent FDA approvals of ranibizumab and aflibercept in the management of diabetic retinopathy associated with DME may suggest a potential for pharmacologic treatments of PDR as well. Novel therapies, including small interfering RNAs, chemokines, kallikrein-kinin inhibitors, and various anti-angiogenic agents, are currently being evaluated for the management of diabetic retinopathy and DME. In addition to these strategies, novel drug delivery methods such as sustained-release implants and refillable reservoir implants are either under active evaluation or have recently gained FDA approval. This review provides an update on the novel developments in the treatment of diabetic retinopathy. © 2015, Society for Biomedical Diabetes Research. All rights reserved.
    No preview · Article · Dec 2015 · The Review of Diabetic Studies
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    ABSTRACT: The term “diabetic kidney” has recently been proposed to encompass the various lesions, involving all kidney structures that characterize protean kidney damage in patients with diabetes. While glomerular diseases may follow the stepwise progression that was described several decades ago, the tenet that proteinuria identifies diabetic nephropathy is disputed today and should be limited to glomerular lesions. Improvements in glycemic control may have contributed to a decrease in the prevalence of glomerular lesions, initially described as hallmarks of diabetic nephropathy, and revealed other types of renal damage, mainly related to vasculature and interstitium, and these types usually present with little or no proteinuria. Whilst glomerular damage is the hallmark of microvascular lesions, ischemic nephropathies, renal infarction, and cholesterol emboli syndrome are the result of macrovascular involvement, and the presence of underlying renal damage sets the stage for acute infections and drug-induced kidney injuries. Impairment of the phagocytic response can cause severe and unusual forms of acute and chronic pyelonephritis. It is thus concluded that screening for albuminuria, which is useful for detecting “glomerular diabetic nephropathy”, does not identify all potential nephropathies in diabetes patients. As diabetes is a risk factor for all forms of kidney disease, diagnosis in diabetic patients should include the same combination of biochemical, clinical, and imaging tests as employed in non-diabetic subjects, but with the specific consideration that chronic kidney disease (CKD) may develop more rapidly and severely in diabetic patients. © 2015, Society for Biomedical Diabetes Research. All rights reserved.
    No preview · Article · Dec 2015 · The Review of Diabetic Studies
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    ABSTRACT: The burden of diabetes mellitus is relentlessly increasing. Diabetic nephropathy is the most common cause of end-stage renal disease (ESRD) worldwide and a major cause of morbidity and mortality in patients with diabetes. The current standard therapy of diabetic nephropathy involves intensive treatment of hyperglycemia and strict blood pressure control, mainly via blockade of the renin-angiotensin system (RAS). Attention has been drawn to additional beneficial effects of oral hypoglycemic drugs and fibrates on other aspects of diabetic nephropathy. On the other hand, antiproteinuric effects of RAS combination therapy do not seem to enhance the prevention of renal disease progression, and it has been associated with an increased rate of serious adverse events. Novel agents, such as bardoxolone methyl, pentoxifylline, inhibitors of protein kinase C (PKC), sulodexide, pirfenidone, endothelin receptor antagonists, vitamin D supplements, and phosphate binders have been associated with controversial outcomes or significant side effects. Although new insights into the pathogenetic mechanisms have opened new horizons towards novel interventions, there is still a long way to go in the field of DN research. The aim of this review is to highlight the recent progress made in the field of diabetes management based on the existing evidence. The article also discusses novel targets of therapy, with a special focus on the major pathophysiologic mechanisms implicated in the initiation and progression of diabetic nephropathy. © 2015, Society for Biomedical Diabetes Research. All rights reserved.
    No preview · Article · Dec 2015 · The Review of Diabetic Studies
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    ABSTRACT: Neurological complications of diabetes are common, affecting up to 50% of people with diabetes. In these patients, diabetic sensorimotor neuropathy (DSPN) is by far the most frequent complication. Detecting DSPN has traditionally been a clinical exercise that is based on signs and symptoms. However, the appearance of morphometric and neurophysiological techniques along with composite scoring systems and new screening tools has induced a paradigm change in the detection and stratification of DSPN and our understanding of its natural history and etiopathogenesis. These newer techniques have provided further evidence that changes in small nerve fiber structure and function precede large fiber changes in diabetes. Although useful, the challenge for the use of these new techniques will be their sensitivity and specificity when widely adopted and ultimately, their ability to demonstrate improvement when pathogenic mechanisms are corrected. Concurrently, we have also witnessed an emergence of simpler screening tools or methods that are mainly aimed at quicker detection of large fiber neuropathy in the outpatient setting. In this review, we have focused on techniques and tools that receive particular attention in the current literature, their use in research and potential use in the clinical environment. © 2015, Society for Biomedical Diabetes Research. All rights reserved.
    No preview · Article · Dec 2015 · The Review of Diabetic Studies
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    ABSTRACT: Aim: To find a potential simplification of the established Ewing's battery for the diagnosis of cardiovascular autonomic neuropathy (CAN) in type 2 diabetes (T2D). Methods: We included 152 patients (92 men) with mean age 64.51 ± 7.85 years and median diabetes duration of 12 years. Ewing's battery was used as the gold standard for the diagnosis of CAN. Against this, we compared the results from each test and their combinations. Results: The 30:15 ratio exhibited the best diagnostic performance (AUC = 0.817, 95% CI: 0.730-0.903, p < 0.001), with 96% sensitivity, 65% specificity, and 94% negative predictive value (NPV). The corresponding values for the Valsalva ratio (VR) were 62%, 92%, and 85%, respectively. The 30:15 ratio was the strongest independent predictor of neuropathy in multivariate regression analysis; low levels yielded an odds ratio (OR) of 21.14 for CAN. The rise in diastolic blood pressure and the expiration/inspiration/VR ratio (E/I/VR) were also identified as independent predictors of CAN, with 9.45 and 10.79 ORs, respectively. Conclusions: The 30:15 ratio has the best diagnostic accuracy, primarily in the exclusion of CAN, by virtue of its very high sensitivity and NPV. If this ratio is positive for CAN, the VR, the rise in diastolic blood pressure, and the E/I/VR may be useful to increase diagnostic accuracy. This procedure is a simplified diagnostic approach that merits further evaluation to enable wider screening for CAN.
    No preview · Article · Dec 2015 · The Review of Diabetic Studies
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    ABSTRACT: Distal symmetric sensorimotor polyneuropathy (DSPN) is the most common neurological manifestation in diabetes. Major risk factors of DSPN include diabetes duration, hyperglycemia, and age, followed by prediabetes, hypertension, dyslipidemia, and obesity. Height, smoking, insulin resistance, hypoinsulinemia, and others represent an additional risk. Importantly, hyperglycemia, hypertension, dyslipidemia, obesity, and smoking are modifiable. Stringent glycemic control has been shown to be effective in type 1, but not to the same extent in type 2 diabetes. Antilipidemic treatment, especially with fenofibrate, and multi-factorial intervention have produced encouraging results, but more experience is necessary. The major comorbidities of DSPN are depression, autonomic neuropathy, peripheral arterial disease, cardiovascular disease, nephropathy, retinopathy, and medial arterial calcification. Knowledge of risk factors and comorbidities has the potential to enrich the therapeutic strategy in clinical practice as part of the overall medical care for patients with neuropathy. This article provides an updated overview of DSPN risk factors and comorbidities. © 2015, Society for Biomedical Diabetes Research. All rights reserved.
    No preview · Article · Dec 2015 · The Review of Diabetic Studies
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    ABSTRACT: There is a global diabetes epidemic correlating with an increase in obesity. This coincidence may lead to a rise in the prevalence of type 2 diabetes. There is also an as yet unexplained increase in the incidence of type 1 diabetes, which is not related to adiposity. Whilst improved diabetes care has substantially improved diabetes outcomes, the disease remains a common cause of working age adult-onset blindness. Diabetic retinopathy is the most frequently occurring complication of diabetes; it is greatly feared by many diabetes patients. There are multiple risk factors and markers for the onset and progression of diabetic retinopathy, yet residual risk remains. Screening for diabetic retinopathy is recommended to facilitate early detection and treatment. Common biomarkers of diabetic retinopathy and its risk in clinical practice today relate to the visualization of the retinal vasculature and measures of glycemia, lipids, blood pressure, body weight, smoking, and pregnancy status. Greater knowledge of novel biomarkers and mediators of diabetic retinopathy, such as those related to inflammation and angiogenesis, has contributed to the development of additional therapeutics, in particular for late-stage retinopathy, including intra-ocular corticosteroids and intravitreal vascular endothelial growth factor inhibitors ('anti-VEGFs') agents. Unfortunately, in spite of a range of treatments (including laser photocoagulation, intraocular steroids, and anti-VEGF agents, and more recently oral fenofibrate, a PPAR-alpha agonist lipid-lowering drug), many patients with diabetic retinopathy do not respond well to current therapeutics. Therefore, more effective treatments for diabetic retinopathy are necessary. New analytical techniques, in particular those related to molecular markers, are accelerating progress in diabetic retinopathy research. Given the increasing incidence and prevalence of diabetes, and the limited capacity of healthcare systems to screen and treat diabetic retinopathy, there is need to reliably identify and triage people with diabetes. Biomarkers may facilitate a better understanding of diabetic retinopathy, and contribute to the development of novel treatments and new clinical strategies to prevent vision loss in people with diabetes. This article reviews key aspects related to biomarker research, and focuses on some specific biomarkers relevant to diabetic retinopathy.
    No preview · Article · Dec 2015 · The Review of Diabetic Studies
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    ABSTRACT: Aim: The main objective was to investigate the physiological effects of ancient wheat whole grain flour diets on the development and progression of type 2 diabetes in Zucker diabetic fatty (ZDF) rats, and specifically to look at the acute glycemic responses. Methods: An intervention study was conducted, involving 40 ZDF rats consuming one of 5 different diets (emmer, einkorn, spelt, rye and refined wheat) for 9 weeks. Refined wheat flour and whole grain rye flour were included as negative and positive controls, respectively. Results: After 9 weeks of intervention, a downregulation of the hepatic genes PPAR-α, GLUT2, and SREBP-1c was observed in the emmer group compared to the control wheat group. Likewise, expression of hepatic SREBP-2 was lower for emmer, einkorn, and rye compared with the control group. Furthermore, spelt and rye induced a low acute glycemic response. The wheat group had higher HDL- and total cholesterol levels. Conclusions: Ancient wheat diets caused a downregulation of key regulatory genes involved in glucose and fat metabolism, equivalent to a prevention or delay of diabetes development. Spelt and rye induced a low acute glycemic response compared to wheat.
    Preview · Article · Jul 2015 · The Review of Diabetic Studies
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    ABSTRACT: Glucagon-like peptide-1 (GLP-1) receptor agonists are a class of injective anti-diabetic drugs that improve glycemic control and many other atherosclerosis-related parameters in patients with type 2 diabetes (T2D). However, the use of this relatively new class of drugs may be associated with certain adverse effects. Concerns have been expressed regarding the effects of these drugs on pancreatic and thyroid tissue, since animal studies and analyses of drug databases indicate an association of GLP-1 receptor agonists with pancreatitis, pancreatic cancer, and thyroid cancer. However, several meta-analyses failed to confirm a cause-effect relation between GLP-1 receptor agonists and the development of these adverse effects. One benefit of GLP-1 receptor agonists is that they do not cause hypoglycemia when combined with metformin or thiazolidinediones, but the dose of concomitant sulphonylurea or insulin may have to be decreased to reduce the risk of hypoglycemic episodes. On the other hand, several case reports have linked the use of these drugs, mainly exenatide, with the occurrence of acute kidney injury, primarily through hemodynamic derangement due to nausea, vomiting, and diarrhea. The most common symptoms associated with the use of GLP-1 receptor agonists are gastrointestinal symptoms, mainly nausea. Other common adverse effects include injection site reactions, headache, and nasopharyngitis, but these effects do not usually result in discontinuation of the drug. Current evidence shows that GLP-1 receptor agonists have no negative effects on the cardiovascular risk of patients with T2D. Thus, GLP-1 receptor agonists appear to have a favorable safety profile, but ongoing trials will further assess their cardiovascular effects. The aim of this review is to analyze critically the available data regarding adverse events of GLP-1 receptor agonists in different anatomic systems published in Pubmed and Scopus. Whenever possible, certain differences between GLP-1 receptor agonists are described. The review also provides the reader with structured data that compare the rates of the most common adverse effects for each of the various GLP-1 receptor agonists.
    No preview · Article · Jul 2015 · The Review of Diabetic Studies
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    ABSTRACT: Both type 1 and type 2 diabetes mellitus can lead to the common microvascular complications of diabetic retinopathy, kidney disease, and neuropathy. Diabetic patients do not universally develop these complications. Long duration of diabetes and poor glycemic control explain a lot of the variability in the development of microvascular complications, but not all. Genetic factors account for some of the remaining variability because of the heritability and familial clustering of these complications. There have been a large number of investigations, including linkage studies, candidate gene studies, and genome-wide association studies, all of which have sought to identify the specific variants that increase susceptibility. For retinopathy, several genome-wide association studies have been performed in small or midsize samples, but no reproducible loci across the studies have been identified. For diabetic kidney disease, genome-wide association studies in larger samples have been performed, and loci for this complication are beginning to emerge. However, validation of the existing discoveries, and further novel discoveries in larger samples is ongoing. The amount of genetic research into diabetic neuropathy has been very limited, and much is dedicated to the understanding of genetic risk factors only. Collaborations that pool samples and aim to detect phenotype classifications more precisely are promising avenues for a better explanation of the genetics of diabetic microvascular complications. © 2015, Society for Biomedical Diabetes Research. All rights reserved.
    No preview · Article · Jan 2015 · The Review of Diabetic Studies
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    ABSTRACT: Diabetes mellitus results from a deficiency or failure to maintain normal glucose homeostasis. The most common form of the disease is type 2 diabetes (T2D), a progressive metabolic disorder characterized by elevated glucose levels that develops in response to either multi-organ insulin resistance or insufficient insulin secretion from pancreatic β-cells. Although the etiology of T2D is complex, many factors are known to contribute to defects of glucose homeostasis, including obesity, unhealthy lifestyle choices, genetic susceptibility, and environmental exposures. In addition to these factors, noncoding RNAs (ncRNAs) have also been recently implicated in the pathogenesis of T2D, playing roles in several of the pathophysiological mechanisms underlying the disease, particularly in insulin-sensitive tissues such as pancreatic β-cells, liver, muscle, and adipose tissue. A growing number of publications demonstrate that polymorphisms in ncRNAs or their target genes may represent a new class of genetic variation contributing to the development of T2D. This review summarizes both the current state of knowledge of ncRNAs, specifically microRNAs (miRNAs), involved in the regulation of β-cell function, insulin sensitivity, and insulin action in peripheral organs. The role of genetic variation in miRNAs or miRNA binding sites in the pathogenesis of T2D is also discussed. While far less is known about the impact of long ncRNAs (lncRNAs) in the development of T2D, emerging evidence suggests that these molecules may be able to contribute to β-cell dysfunction in response to hyperglycemia. This article provides an overview of the studies conducted to date in this field, focusing on lncRNAs that are dysregulated in human pancreatic islets. © 2015, Society for Biomedical Diabetes Research. All rights reserved.
    No preview · Article · Jan 2015 · The Review of Diabetic Studies
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    ABSTRACT: Objectives: Despite the fact that statins have been prescribed widely, cardiovascular disease (CVD) remains the leading cause of death in diabetic patients. The aim of this study was to reassess the benefits of statins for CVD prevention in patients with diabetes mellitus. Methods: Two independent investigators searched for prospective, randomized statin trials that investigated the power of reducing CVD in statin-treated patients. The search was performed using Pubmed, Web of Science, and CENTRAL databases. Data was extracted from eligible studies. Results: A total of 7061 articles were surveyed and 22 articles were identified as eligible articles. The meta-analyses of the 22 trials showed that statin treatment was positively associated with a lowered risk of CVD in the following groups: (i) total population with pooled odds ratios (OR) of 0.791 (95 % CI: 0.74-0.846, p < 0.001), (ii) diabetic population with OR 0.792 (95% CI: 0.721-0.872, p < 0.001), and (iii) non-diabetic population with OR 0.791 (95% CI: 0.730-0.857, p < 0.001). In diabetic patients, statins were also helpful in the primary and secondary prevention of CVD, with pooled ORs of 0.757 (95% CI: 0.676 to 0.847, p < 0.001) and 0.800 (95% CI: 0.712 to 0.898, p < 0.001), respectively. However, when trials that investigated only diabetic patients (i.e., CARDS, 4D, and ASPEN) were included in the analysis, statin treatment was not found to reduce CVD significantly (OR: 0.817, 95% CI: 0.649 to 1.029, p = 0.086). Furthermore, after performing subgroup analysis, no benefit of statin treatment was found in primary prevention (OR: 0.774, 95% CI: 0.506 to 1.186, p = 0.240) or secondary prevention (OR: 0.893, 95% CI: 0.734 to 1.088, p = 0.262) of CVD in diabetic patients. Conclusions: Although our study may be limited by unmeasured confounders and heterogeneity among the studies included, the results suggest that the effects of statins in the prevention of CVD in diabetic patients are not only beneficial. More informative data are needed to verify the benefits of statins in the protection against CVD in diabetic patients.
    Preview · Article · Dec 2013 · The Review of Diabetic Studies