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Objectives: Serum markers of iron storage have been linked to type 2 diabetes; however, the mechanism underlying this association is unclear. In pregnancy, increased serum ferritin has been reported in women with gestational diabetes (GDM), a patient population at high risk of future type 2 diabetes. However, in the years after pregnancy, it is not known if ferritin relates to their diabetes risk or the pathophysiologic determinants thereof (insulin sensitivity and beta-cell function). Therefore, we sought to characterize the relationship between ferritin and glucose homeostasis in the early postpartum years in women with and without recent GDM., Methods: At both 1 and 3 years postpartum, 340 women (105 with recent GDM) underwent serum ferritin measurement and an oral glucose tolerance test that enabled assessment of insulin sensitivity and/or resistance (Matsuda index and Homeostasis Model Assessment [HOMA-IR]), beta-cell function (Insulin Secretion-Sensitivity Index-2 and insulinogenic index/HOMA-IR) and glucose tolerance., Results: Serum ferritin did not differ between women who had GDM and their peers at either 1 or 3 years postpartum. Baseline-adjusted change in ferritin between 1 and 3 years correlated with the concomitant change in C-reactive protein (r=0.21, p=0.0002) but was not associated with measures of insulin sensitivity and/or resistance, beta-cell function or glycemia. On adjusted analyses, neither baseline ferritin nor its change from 1 to 3 years was independently associated with any of the following metabolic outcomes at 3-years postpartum: Matsuda index, HOMA-IR, Insulin Secretion-Sensitivity Index-2, insulinogenic index/HOMA-IR, fasting glucose, 2-h glucose or glucose intolerance., Conclusions: Serum ferritin is not associated with glucose homeostasis in the early years after a GDM pregnancy., (Copyright © 2019 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.)

Background: Type 2 diabetes mellitus is a growing concern worldwide, particularly in Indigenous communities, which have undergone a marked nutrition transition characterized by reduced intakes of traditional foods and increased intakes of market foods. Few studies have assessed the relationships between differing dietary patterns and risk for type 2 diabetes in Indigenous communities in Canada. The objective of the study was to characterize dietary patterns using factor analysis (FA) and to relate these patterns to the incidence of type 2 diabetes after 10 years of follow up in a First Nations community in Ontario, Canada., Methods: We conducted a prospective analysis of 492 participants in the SLHDP who did not have diabetes at baseline (1993 to 1995) and were followed for 10 years. A food-frequency questionnaire was administered, and FA was used to identify patterns of food consumption. Multivariate logistic regression analyses determined associations of food patterns with incident type 2 diabetes, adjusting for sociodemographic and lifestyle confounders., Results: At follow up, 86 participants had developed incident type 2 diabetes. FA revealed 3 prominent dietary patterns: Balanced Market Foods, Beef and Processed Foods and Traditional Foods. After adjustment for age, sex, waist circumference, interleukin-6 and adiponectin, the Beef and Processed Foods pattern was associated with increased risk for incident type 2 diabetes (OR=1.38; 95% CI 1.02, 1.86). In contrast, the Balanced Market Foods and Traditional Foods Patterns were not significantly associated with type 2 diabetes., Conclusions: Dietary interventions should encourage reduced consumption of unhealthful market foods, in combination with improvements in local food environments so as to increase access to healthful foods and reduce food insecurity in Indigenous communities., (Copyright © 2016 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.)

Objective: With the expanding armamentarium of noninsulin therapies for type 2 diabetes mellitus, the use of insulin with various oral agents is becoming more common. In this study, we assessed the efficacy and cardiovascular (CV) safety of the dipeptidyl peptidase-4 inhibitor linagliptin as add-on to insulin in patients with type 2 diabetes., Methods: In this post hoc analysis, data for patients receiving basal or basal-bolus insulin were pooled from 4 randomized, double-blind, phase 3 clinical trials of linagliptin 5 mg once daily or placebo given as add-on to background glucose-lowering treatment. Changes in glycated hemoglobin (A1C) and CV risk factors were assessed from baseline to end of trial. The primary CV endpoint was a composite of CV death, nonfatal myocardial infarction, nonfatal stroke and hospitalization due to unstable angina., Results: The number of patients receiving basal or basal-bolus insulin as background therapy was 1613 (linagliptin: n=811; placebo: n=802). The placebo-adjusted mean (SE) change from baseline in A1C was -0.41 (0.05)% (95% CI -0.50, -0.32; p<0.0001). Treatment with linagliptin provided a relative weight benefit and reduced insulin requirements without affecting blood pressure, heart rate or lipids. The incidence of hypoglycemia with linagliptin was similar to that for placebo (38.7% vs. 39.4%, respectively). The hazard ratio (HR) for the primary endpoint showed that treatment with linagliptin was not associated with an increased CV risk (HR 1.07 [95% CI 0.62, 1.85])., Conclusions: Linagliptin, when added to ongoing insulin treatment in patients with type 2 diabetes, improves glycemic control and has a neutral impact on major adverse CV events., (Copyright © 2015 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.)

Glucagon-like peptide-1 receptor (GLP-1) agonists and dipeptidyl-peptidase-4 (DPP-4) inhibitors are therapies that are used to treat hyperglycemia in patients with type 2 diabetes mellitus. Although both of these medication types primarily lower prandial and fasting blood glucose levels by enhanced GLP-1 receptor signalling, they have distinct mechanisms of action. Whereas DPP-4 inhibitors boost patient levels of endogenously produced GLP-1 (and glucose-dependent insulinotropic peptide) by preventing its metabolism by DPP-4 enzymatic activity, GLP-1 receptor agonists are either synthetic analogues of human GLP-1 or exendin-4 based molecules. They are tailored to resist hydrolysis by DPP-4 activity and to provide longer durability in the circulation compared with native GLP-1. Several roles for incretin-based diabetes therapies beyond the endocrine pancreas and their glycemic-lowering properties have now been described, including attenuation of cardiac myocyte injury and reduction in post-ischemic infarction size after cardiovascular insult. Favourable outcomes have also been observed on systolic blood pressure reduction, postprandial intestinal lipoprotein metabolism, endothelial cell function, modulation of innate immune-mediated inflammation and surrogate markers of renal function. As hypertension is an independent risk factor for premature death in patients with type 2 diabetes, potential favourable extrapancreatic actions, particularly within the heart, blood vessels and kidney, for this drug class are of considerable clinical interest. Herein, we highlight and provide critical appraisal of the clinical data supporting the antihypertensive effects of GLP-1 receptor agonists and DPP-4 inhibitors and link possible mechanisms of action to clinical outcomes reported for this drug class., (Copyright © 2014 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.)