By the end of this section, you will be able to:
- Identify some risk factors of developing type 1 diabetes mellitus
- Identify the manifestations of type 1 diabetes mellitus
- Briefly describe the management of type 1 diabetes mellitus
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 increased susceptibility to the development of diabetes. Similarly, current research suggests that environmental triggers also play a role in development of T1DM along with genetics: colder climates, preceding viral infection, and diet during infancy.
T1DM involves loss of beta cells from the pancreas resulting in no insulin production. T1DM have insulin receptors on all tissues and these receptors work fine. A combination of genetics and environmental triggers causes the body’s immune system to recognize beta cells as a pathogen and, as a result, the body eliminates the beta cells. Because of this progression, 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.
Figure 7.4 Pathology of T1DM – Upper panel: the immune system attacks the beta cells leading to a loss 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
T1DM causes hyperglycemia – Since there is no circulating insulin (purple triangles), the insulin receptors (blue) on tissues are not stimulated. Thus there is nothing to stimulate glucose receptors (green) to allow glucose (gold hexagons) to enter the tissues. As a result, the cells are deprived of glucose and glucose stays in the blood causing hyperglycemia. Images created by Sarah Perkins under a CC BY NC license
Histologically, pancreatic tissue will be affected in Type I diabetes. Immunological destruction of beta cells in the islets will result in hyaline tissue being laid down to replace the missing beta cells. However, all other tissues will look normal as both the insulin and glucose receptors are unaffected.
DHPLC Specimen PATH 425-125 – hyalinization of the islets of Langherhans; pancreatic tissue with H&E staining. Created by Jennifer Kong licensed under All rights reserved.
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 most common manifestations of diabetes are hunger and excessive urination and thirst. This is also known as the 3P’s of diabetes: polyphagia, polyuria, & polydipsia. These manifestations demonstrate how high blood sugar (hyperglycemia) affect kidney function. Normally, kidneys reabsorb all of the sugar that escape into the filtrate (see AKI chapter for review). However, in hyperglycemia, there is too much glucose in the blood already so that glucose stays in the filtrate. Glucose in the filtrate will retain water in the urine: as a result the diabetic urinates an abnormally large quantity of ‘sweet’ urine manifesting in frequent urination. Since there is a loss of large quantities of fluid, the body becomes dehydrated and so the diabetic becomes unusually and continually thirsty. Similarly, the diabetic 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).
Management of Type I Diabetes
T1DM diabetics do not have beta cells, thus they can not produce insulin; thus, synthetic insulin must be administered by injection or infusion to help regulate glucose homeostasis throughout the day.
Regardless of the cause, T1DM results in the loss of beta cells in the pancreatic islet tissue. Thus there is no insulin release to be delivered to tissues. At the tissue level, there is no stimulation of the glucose receptor (normally, it would respond to insulin receptor binding and activation) so the glucose receptor does not open to allow glucose to enter the cell for metabolism. The glucose stays in the blood leading to hyperglycemia. Hyperglycemia will affect all tissues in that it:
- forces 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
- hyperglycemia causes an osmotic imbalance resulting in both glucose and excessive water to be lost in urine (i.e. polyuria). As a consequence, thirst and dehydration will occur.
- as insulin is needed to build tissues, there is no opportunity to gain tissue mass. In a child, this would appear as “failure to thrive” and a slow growth rate.