Type 1 diabetes mellitus (T1DM) is an autoimmune disease, making up <5% of all diabetes diagnoses.  There is somewhat of a genetic component to T1DM as research has demonstrated that certain genes are recognized to increase susceptibility to the development of T1DM. Similarly, current research suggests that environmental triggers also play a role in development of T1DM alongside genetics: colder climates, preceding viral infection, and dietary patterns during infancy.

T1DM involves loss of beta cells from the pancreas resulting in no insulin production. T1DM patients have insulin receptors. A combination of genetics and environmental triggers causes the body’s immune system to recognize beta cells as foreign and, as a result, the body eliminates the beta cells. This is a progressive condition, which culminates in lack of beta cells and consequently lack of insulin production. T1DM usually manifests in childhood or early adulthood, earning the alternate name “juvenille diabetes”. However, adults can develop T1DM. Thus the current name “Type 1: insulin-dependent diabetes” is more accurate.

Pathology of T1DM –  Upper panel: the immune system attacks the beta cells leading to a lack of insulin production.  Lower panel:  there is no insulin (purple triangles) circulating in blood.  Images created by Sarah Perkins under a CC BY NC license

Revisit this link , from the “Anatomy and histology of the endocrine pancreas and glucose homeostasis” chapter to view an animation describing the role of insulin and the pancreas in diabetes mellitus.

Manifestations of Type 1 Diabetes

The clinical consequences are due to the lack of insulin in the blood circulation and eventually the lack of glucose uptake by the cells. The most common manifestations of T1DM are hunger, excessive urination, and thirst. This is also known as the 3P’s of diabetes: polyphagia, polyuria, & polydipsia. Normally, kidneys reabsorb all of the sugar that escapes into the filtrate (see AKI chapter for review). However, in hyperglycemia, there is too much glucose in the blood already so excess glucose stays in the filtrate. Excess glucose in the filtrate will retain water in the urine:  as a result a person with T1DM urinates an abnormally large and frequent quantity of ‘sweet’ urine. Since there is a loss of large quantities of fluid, the body becomes dehydrated and so thirst is unusually and continually present. Similarly, people with T1DM may also experience persistent hunger because the body cells are unable to access the glucose in the bloodstream due to lack of insulin (recall that the tissue’s insulin receptors are present and working appropriately). This may force tissues to use fat metabolism and gluconeogenesis to meet its energy needs. As a consequence, dangerous byproducts (e.g. acidic ketones) will increase in blood and tissues.