The epidemic of type 2 diabetes (T2DM) is widely attributed to rising levels of obesity, which in turn are attributed to lifestyle issues (diet and exercise). So, at best, it’s society’s fault and, at worst, we get to blame each individual patient.
But surely there must be more to it that this? Every practicing clinician has patients with T2DM who are not overweight and, not only are the majority of people with so-called ‘morbid obesity’ non-diabetic, a significant proportion of them have normal insulin sensitivity (i.e. they don’t manifest insulin resistance, which is the way that obesity is meant to drive the increase in T2DM). Furthermore, the inexorable decline in beta-cell function, so clearly demonstrated by the UKPDS, seems to be reversible not only using glucagon-like peptide-1 (GLP-1) injectable therapies but more remarkably by malabsorptive bariatric surgical procedures. This has made various groups question the current thinking around the pathophysiology of T2DM, with a particular focus on the bowel.