Type 2 Diabetes Mellitus: Beyond the Beta Cell

Type 2 diabetes mellitus (T2DM) currently affects >8% of the world population. It is the leading cause of blindness, end-stage kidney disease, and neuropathy, and doubles the risk of developing cardiovascular disease. Until recently, the treatment of diabetes had broadly emphasised the management of hyperglycaemia as the key diagnostic criterion for T2DM. The pathophysiology of T2DM however is now understood to be rooted in the associated metabolic syndrome including intra-abdominal fat deposition, lipid abnormalities, high blood pressure, hypercoagulability, and macrovascular complications occurring in parallel with glucose dysregulation. Accordingly, closer attention to the medical management of these conditions is at the forefront of diabetologists’ treatment rationale in an attempt to prevent and mitigate both micro and macrovascular complications, especially in light of the recent positive data from cardiovascular outcome trials with both sodium-glucose co-transporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists. This symposium included a discussion of the evolution of treatment for T2DM and presented the rationale for the use of novel agents and combination therapies for patients according to their individual disease progression. Several newer drug classes were highlighted, including GLP-1 receptor agonists, dipeptidyl-peptidase-4 inhibitors (DPP-4 inhibitors), and SGLT2 inhibitors. Finally, an overview of the exciting new fields of prevention and treatment for T2DM were discussed; including stem cell proliferation into pancreatic beta cells, the reprogramming of white adipose tissue into brown fat, mimicking physiological effects of bariatric surgery pharmacologically, and other approaches to make the treatment more targeted and personalised.