Fear of Falling, Lower Extremity Strength, and Physical and Balance Performance in Older Adults with Diabetes MellitusRead the full article
Journal of Diabetes Research publishes articles related to type 1 and type 2 diabetes. Topics include etiology, pathogenesis, management, and prevention of diabetes, as well as associated complications such as nephropathy.
Chief Editor Dr Mark Yorek, from the University of Iowa, is currently researching vascular and neural disease related to obesity and diabetes. His active research studies focus on etiology, treatment and prevention of nerve damage.
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The Epidemiology of Depression and Diabetes Distress in Type 2 Diabetes in Kuwait
This study is aimed at describing the prevalence of and risk factors for depression and diabetes distress in people with type 2 diabetes and whether depression and distress are independently associated with worse biomedical outcomes. The study was of cross-sectional design. The setting was the Dasman Diabetes Institute, Kuwait. The Patient Health Questionnaire-9 (PHQ-9) was used to measure the prevalence of depression, defined as a (depression caseness). The Problem Areas in Diabetes (PAID) was used to measure diabetes-related distress. Data on biomedical outcomes, lifestyle factors, and sociodemographic information were collected. The prevalence of depression and diabetes distress caseness was 29% and 14%, respectively. Depression caseness patients were more likely to be female (60%; ), have Kuwaiti nationality (68%, ), were on insulin (67%, ), have higher body mass index (), were less physically active (78%; ), have a higher PAID score (), and have hypertension (74%, ). After adjustment of sociodemographics (age, gender, and marital status) and body mass index, the prevalence of depression was associated with higher HbA1c (, 95% confidence interval 0.01 to 0.60), while diabetes distress had a weak association with HbA1c (, 95% confidence interval 0.04 to 0.22). In conclusion, people with type 2 diabetes in Kuwait have a high prevalence of depression but lower diabetes distress and this was associated with worse glycaemic control.
Effects of Exenatide and Humalog Mix25 on Fat Distribution, Insulin Sensitivity, and β-Cell Function in Normal BMI Patients with Type 2 Diabetes and Visceral Adiposity
In China, most normal BMI (body mass index of ≥18.5 to <25 kg/m2) adults with type 2 diabetes (T2DM) exhibit visceral adiposity. This study compared the effects of exenatide and humalog Mix25 on normal BMI patients with T2DM and visceral adiposity. A total of 95 patients were randomized to receive either exenatide or humalog Mix25 treatment for 24 weeks. Subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were quantified by magnetic resonance imaging (MRI) and liver fat content (LFC) by liver proton magnetic resonance spectroscopy (1H MRS). Each patient’s weight, waist circumference, BMI, blood glucose, insulin sensitivity, pancreatic β-cell function, and fibroblast growth factor 21 (FGF-21) levels were measured. Data from 81 patients who completed the study (40 and 41 in the exenatide and humalog Mix25 groups, respectively) were analysed. The change in 2 h plasma blood glucose was greater in the exenatide group (). HOMA-IR and MBCI improved significantly after exenatide therapy (, ). VAT and LFC decreased in both groups ( for all) but to a greater extent in the exenatide group, while SAT only decreased with exenatide therapy (). FGF-21 levels declined more in the exenatide group (), but were positively correlated with VAT in the entire cohort before (, ) and after (, ) the intervention. The effects of exenatide on glycaemic metabolism, insulin resistance, pancreatic β-cell function, and fat deposition support its administration to normal BMI patients with T2DM and visceral adiposity.
Sitagliptin and the Blood-Retina Barrier: Effects on Retinal Endothelial Cells Manifested Only after Prolonged Exposure
Inhibitors of dipeptidyl peptidase-4 (DPP-4) are widely used to treat diabetes mellitus, but data concerning their effects on the barrier stability of retinal endothelial cells (REC) in vivo and in vitro are inconsistent. Therefore, we studied whether the barrier properties of immortalized endothelial cells of the bovine retina (iBREC) were affected by the inhibitors of DPP-4 sitagliptin (10-1000 nM) and diprotin A (1-25 μM). Their effects were also investigated in the presence of VEGF-A165 because diabetic patients often develop macular edema caused by VEGF-A-induced permeability of REC. To detect even transient or subtle changes of paracellular and transcellular flow as well as adhesion of the cells to the extracellular matrix, we continuously monitored the cell index (CI) of confluent iBREC grown on gold electrodes. Initially, the CI remained stable but started to decline significantly and persistently at 40 h or 55 h after addition of sitagliptin or diprotin A, respectively. Both inhibitors did not modulate, prevent, or revert the persistent VEGF-A165-induced reduction of the CI. Interestingly, sitagliptin and diprotin A increased the expression of the tight-junction protein claudin-1 which is an important component of a functional barrier formed by iBREC. In contrast, expressions of CD29—a subunit of the fibronectin receptor—or of the tetraspanin CD9 were lower after extended treatment with the DPP-4 inhibitors; less of the CD9 was seen at the plasma membrane after prolonged exposure to sitagliptin. Because both associated proteins are important for adhesion of iBREC to the extracellular matrix, the observed low CI might be caused by weakened attachment of the cells. From our results, we conclude that extended inhibition of DPP-4 destabilizes the barrier formed by microvascular REC and that DPP-4 inhibitors like sitagliptin do not counteract or enhance a VEGF-A165-induced barrier dysfunction as frequently observed in DME.
Function of Adenosine 2A Receptor in High-Fat Diet-Induced Peripheral Neuropathy
Peripheral diabetic neuropathy (DPN) is a complication observed in up to half of all patients with type 2 diabetes. DPN has also been shown to be associated with obesity. High-fat diet (HFD) affects glucose metabolism, and the impaired glucose tolerance can lead to type 2 diabetes. There is evidence to suggest a role of adenosine 2A receptors (A2ARs) and semaphorin 3A (Sema3a) signaling in DPN. The link between the expression of Sema3a and A2AR in DPN was hypothesized, but the underlying mechanisms remain poorly understood. In this study, we investigated the regulation of Sema3a by A2AR in the spinal cord and the functional implications thereof in DPN. We examined the expression of A2ARs and Sema3a, as well as Neuropilin 1 and Plexin A, the coreceptors of Sema3a, in the dorsal horn of the lumbar spinal cord of an animal model with HFD-induced diabetes. Our results demonstrate that HFD dysregulates the A2AR-mediated Sema3a expression, with functional implications for the type 2 diabetes-induced peripheral neuropathy. These observations could stimulate clinical studies to improve our understanding on the subject.
Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility
Individuals with type 2 diabetes mellitus (T2DM) have an increased risk of bone fragility fractures compared to nondiabetic subjects. This increased fracture risk may occur despite normal or even increased values of bone mineral density (BMD), and poor bone quality is suggested to contribute to skeletal fragility in this population. These concepts explain why the only evaluation of BMD could not be considered an adequate tool for evaluating the risk of fracture in the individual T2DM patient. Unfortunately, nowadays, the bone quality could not be reliably evaluated in the routine clinical practice. On the other hand, getting further insight on the pathogenesis of T2DM-related bone fragility could consent to ameliorate both the detection of the patients at risk for fracture and their appropriate treatment. The pathophysiological mechanisms underlying the increased risk of fragility fractures in a T2DM population are complex. Indeed, in T2DM, bone health is negatively affected by several factors, such as inflammatory cytokines, muscle-derived hormones, incretins, hydrogen sulfide (H2S) production and cortisol secretion, peripheral activation, and sensitivity. All these factors may alter bone formation and resorption, collagen formation, and bone marrow adiposity, ultimately leading to reduced bone strength. Additional factors such as hypoglycemia and the consequent increased propensity for falls and the direct effects on bone and mineral metabolism of certain antidiabetic medications may contribute to the increased fracture risk in this population. The purpose of this review is to summarize the literature evidence that faces the pathophysiological mechanisms underlying bone fragility in T2DM patients.
The 7-Year Change in the Prevalence of Insulin Resistance, Inflammatory Biomarkers, and Their Determinants in an Urban South African Population
Background. Insulin resistance (IR) and subclinical inflammation are involved in pathological pathways leading to the development of biological cardiovascular risk factors and subsequent cardiovascular events. Therefore, monitoring these processes can provide advanced information on the trajectory of cardiovascular risk profile of a population and inform prevention and control strategies. We investigated changes in IR and subclinical inflammation in a population from Cape Town, South Africa, between 2008/09 and 2014/16. Methods. In a total of 2503 (, 2008/09) and (, 2014/16) participants, IR was calculated using five indices, i.e., insulin fasting, HOMA-IR, QUICKI, McAuley, and Matsuda while subclinical inflammation was measured using usCRP and gamma GT. Linear and logistic regression analyses and interaction tests were conducted. Results. The mean age of participants was 53.2 (2008/09) and 48.2 (2014/16), respectively. In females, IR prevalence significantly decreased between 2008/09 and 2014/2016 by all indices (), while subclinical inflammation prevalence increased from 54.7% (2008/09) to 57.1% (2014/16) based on usCRP and 29.6% to 33.4% based on gamma GT. In a multivariate analysis adjusted for the year of study, age, and gender, prominent factors associated with increased IR or subclinical inflammation were obesity levels measured using waist circumference, glycated haemoglobin, and fasting insulin levels. Conclusions. Over the 7-year period, subclinical inflammation increased and this was associated with IR and the metabolic syndrome components, both of which are strong predictors of CVDs. The decrease in IR over the year period reflects in part the much younger age in the second survey.