Year in diabetes 2012: The diabetes tsunami

Abstract

Diabetes affects more than 300 million individuals globally, contributing to significant morbidity and mortality worldwide. As the incidence and prevalence of diabetes continue to escalate with the force of an approaching tsunami, it is imperative that we better define the biological mechanisms causing both obesity and diabetes and identify optimal prevention and treatment strategies that will enable a healthier environment and calmer waters. New guidelines from the American Diabetes Association/European Association of the Study of Diabetes and The Endocrine Society encourage individualized care for each patient with diabetes, both in the outpatient and inpatient setting. Recent data suggest that restoration of normal glucose metabolism in people with prediabetes may delay progression to type 2 diabetes (T2DM). However, several large clinical trials have underscored the limitations of current treatment options once T2DM has developed, particularly in obese children with the disease. Prospects for reversing new-onset type 1 diabetes also appear limited, although recent clinical trials indicate that immunotherapy can delay the loss of β-cell function, suggesting potential benefits if treatment is initiated earlier. Research demonstrating a role for the central nervous system in the development of obesity and T2DM, the identification of a new hormone that simulates some of the benefits of exercise, and the development of new β-cell imaging techniques may provide novel therapeutic targets and biomarkers of early diabetes detection for optimization of interventions. Today's message is that a diabetes tsunami is imminent, and the only way to minimize the damage is to create an early warning system and improve interventions to protect those in its path.

Fig. 1.

The ADA/ESAD 2012 Position Statement algorithm on antihyperglycemic therapy in T2DM (abbreviated figure). The guidelines emphasize taking a personalized approach to each patient; focusing initially on lifestyle changes in patients with mild diabetes, progressing to metformin, then other oral and injectable medications, and eventually to insulin to ensure glycemic control. DPP-4-I, DPP-4 inhibitor; GLP-1-RA, GLP-1 receptor agonist; SU, sulfonylurea; TZD, thiazolidinedione. [Adapted from S. E. Inzucchi et al.: Management of hyperglycemia in type 2 diabetes: a patient-centered approach: position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care 35:1364–1379, 2012 (6), with permission. © American Diabetes Association.]

Fig. 2.

Medical therapy vs. RYGB and sleeve gastrectomy. Marked improvement in HbA1c in the RYGB and sleeve gastrostomy treatment groups during the study period. P values are for the comparison between each surgical group and the medical-therapy group and were calculated from a repeated-measures model that considers data over time. [Reproduced from P. R. Schauer et al.: Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med 366:1567–1576, 2012 (15), with permission. © Massachusetts Medical Society.]

Fig. 3.

Delayed decline in C-peptide AUC with abatacept in young patients recently diagnosed with T1DM. Population mean of stimulated C-peptide 2-h AUC mean over time for each treatment group. The estimates are from the analysis of covariance model adjusting for age, sex, baseline value of C-peptide, and treatment assignment. Error bars show 95% confidence intervals. [Reproduced from T. Orban et al.: Co-stimulation modulation with abatacept in patients with recent-onset type 1 diabetes: a randomised, double-blind, placebo-controlled trial. Lancet 378:412–419, 2011 (21), with permission. © Elsevier.]