Type 2 diabetes (T2D) and obesity are characterized by insulin resistance (IR) in skeletal muscle, liver, and adipose tissue, but the exact molecular mechanisms underlying IR are not fully understood. Mitochondria are dynamic organelles that continuously undergo fusion and fission to maintain a healthy mitochondrial population.
Proper function of β-cells is essential for maintaining glucose homeostasis. A significant reduction in both β-cell mass and function is observed in individuals with type 2 diabetes. Recently, it has been questioned whether β-cells actually are lost in type 2 diabetes or rather are dedifferentiating into less mature cells resulting in reduced functional β-cell mass.
Glucagon-like peptide 1 (GLP-1) analogues are currently successfully used to treat type 2 diabetes and obesity. However, the molecular mechanisms behind these effects of GLP-1 analogue treatment on glucose and energy metabolism remain largely unknown.
The number of people suffering from obesity and obesity-related disorders such as Type 2 Diabetes (T2DM) is increasing worldwide. To break this escalation new therapeutic options are needed. Brown adipose tissue (BAT), also known as brown fat, possesses the ability to “burn” calories by uncoupling the oxidative phosphorylation pathway in the mitochondria.
Type 2 diabetes and the constituents of the metabolic syndrome are associated with low and dysfunctional high-density lipoprotein (HDL). The main protein component of HDL, apolipoprotein A-I (apoA-I), was recently assigned to a glucose controlling function, since administration of apoA-I to cell cultures and in an insulin-resistant mouse model revealed an increase in glucose uptake and glucose tolerance, respectively.
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.
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