Patients with type 2 diabetes mellitus (T2D) have an increased risk of fracture of up to 1.7 in spite of a normal to elevated bone mineral density (BMD). There is currently a gap in our understanding linking the pathophysiological changes at the tissue level with the epidemiological observations of the increased fracture risk in patients with T2D.
Around 3-10% of patients clinically diagnosed with type 2 diabetes (T2D) have circulating autoantibodies as seen in type 1 diabetes (T1D). This diabetic subtype is termed latent autoimmune diabetes in adults (LADA), and it is the second most common type of diabetes only exceeded in numbers by T2D. Despite the prevalence, LADA is far less studied than its more renowned counterparts T1D and T2D.
Modern living is associated with an epidemic of type 2 diabetes mellitus. Many studies have shown that pre- and postnatal environmental factors exert major influences on the disease risk. Sleep disturbances are strong independent risk factors for incident diabetes with a magnitude of effect comparable to a family history of diabetes.
Studies suggest differences in gestational diabetes mellitus (GDM) prevalence among different ethnic groups, with Caucasians generally having the lowest risk. Furthermore, studies from high income countries generally report an inverse relationship between GDM risk and socio-economic position.
Insulin resistance is a central feature of T2DM and is the primary target for therapy. Nevertheless, the pathological consequences of T2DM predominantly relate to cerebro- and cardiovascular disease (CVD), representing the leading cause of morbidity and mortality in T2DM. Up to 60% of all deaths in T2DM are directly related to CVD, whilst patients with T2DM develop microvascular complications (e.g. retinopathy, nephropathy and neuropathy).
During the last years a great scientific focus has been on the potential implications of exposure to hyperglycemia during pregnancy for long-term adiposity and cardio-metabolic outcomes in the offspring.
Age is a major risk factor for insulin resistance, and thus, type 2 diabetes. The development of insulin resistance has been associated with metabolic inflexibility (MI), yet the underlying mechanisms are complex and not well understood. MI is defined and observed as an inability to favor lipid metabolism during fasting and exercise, and conversely, to suppress lipid oxidation and increase glucose uptake, storage, and oxidation under insulin-stimulated conditions (feeding).
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