Immune cells: Actors in pancreas development and regeneration that fail to fulfill their role and lead to diabetes?

ABSTRACT

Extract Epidemiologists have estimated that, by the year 2025, 250-300 million individuals worldwide will have diabetes mellitus, which consists of variable degrees of insulin-producing beta-cell dysfunction that is responsible for hyperglycemia (high level of sugar in the blood). The predominant form is type 2 diabetes (T2D), also called noninsulin-dependent diabetes mellitus (NIDDM), which is associated with insulin resistance (cells stop responding to insulin) and mainly affects obesity-prone mature adults. By contrast, type 1 diabetes (T1D) or insulin-dependent diabetes mellitus (IDDM), the less common form (characterized by a lack of insulin), also described as autoimmune diabetes, is predominantly observed in children and young adults. However, for several years, the clinical features of diabetes have been changing, as demonstrated by the late appearance of autoimmune signs that are characteristic of T1D, in adults initially diagnosed as having T2D (called latent autoimmune diabetes of adults or LADA), and of T2D in children or young adults. Intriguingly, accumulating evidence indicates that T2D and related obesity are linked to inflammation.