Because many patients with Type 2 Diabetes are asymptomatic, the diagnosis of type 2 diabetes can be unexpected, occurring incidentally during a routine medical exam. In a space of a few minutes, the patient’s concept of himself or herself must undergo a radical change from an image of someone with good health to an image of someone with the chronic disease.
Type 2 diabetes tends to evolve over the years as a result of multiple factors. The evolution would be;
- Non-diabetic state
- Early abnormalities in deteriorating glucose homeostasis
- Type 2 diabetes
In our previous write-up, we have seen the normal glucose homeostasis in an healthy individual who is non-diabetic. This post will elaborate on the pathophysiologic evolution of type 2 diabetes.
Although still evolving, the following concepts are important in our scientific understanding of the complex and multifaceted pathogenesis of type 2 diabetes.
- Beta Cell failure. It is an early , progressive, and fundamental component in the pathophysiologic evolution of type 2 diabetes. The substantial amount of beta cell function has been lost by the time of diagnosis of diabetes. In long-standing diabetes, beta cell mass is decreased.
- Insulin resistance. It is another component in the pathogenesis of type 2 diabetes. The body’s need for insulin may vary over time such as insulin resistant states. Impaired beta cell function may not be able to keep up with increased demand for insulin secretion and hypoglycemia may result.
- Hepatic glucose production. The changes in glucagon secretion results in dysregulated hepatic glucose production. Suppression of glucagon secretion by glucose and insulin, both basal and postprandial, is altered in type 2 diabetes.
In our previous section, it is already explained with characteristics like;
- The beta cells are functioning normally, producing appropriate amounts of insulin.
- Sensitivity to insulin is normal, and insulin effectively facilitates transport of glucose into cells (e.g. muscle, fat, and liver cells).
- There is an adequate level of insulin production to meet the body’s needs.
- Glucose levels are normal, termed euglycemia.
- One of the early changes that occurs in the pathophysiology in the long evolution towards type 2 diabetes is that the muscle, fat, and liver cells become less sensitive and more resistant to the effects of insulin. This means that insulin is less effective at facilitating the transport of glucose into muscle, fat, and liver cells; insulin sensitivity begins to decrease.
- Because of the resistance, beta cells must produce a greater amount of insulin keep the blood glucose levels normal. Moreover, it results in hypeinsulinemia i.e. higher insulin levels. Clinically, this stage can be recognized as metabolic syndrome.
- The demand on beta cells pushes them to increase the production of insulin. Some degree of impairment of beta cell function or secretory reserve may be present.
- At this phase, the body successfully responds with increased amounts of insulin and is able to move an appropriate amount of glucose into the cells. Thus, blood glucose levels remain relatively normal.
The following progression occurs in this stage;
- Insulin sensitivity continues to worsen i.e. insulin sensitivity decreases and insulin resistance increases.
- The beta cells are incessantly called upon to produce more and more insulin, resulting in increasing hyperinsulinemia.
- However, the beta cells eventually cannot keep up with the increased demand for insulin production. The available insulin is insufficient to move enough glucose into the cells, and blood glucose levels start to rise above the normal range.
- Hepatic glucose production also increases, contributing to increased glucose levels. When glucose levels are higher than normal but not yet in the range for a diagnosis of diabetes, the individual can be described as having pre-diabetes. It is defined by impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT).
- Pre-diabetes becomes evident as beta cell dysfunction progresses. Beta cell dysfunction is considered fundamental to the eventual development of type 2 diabetes.
- Plasma glucose in the range of 100 to 125 mg/dL (Fasting plasma glucose)
- Plasma glucose in the range of 140 to 199 mg/dL (Oral glucose tolerance test)
- HbA1C – In the range of 5.7% to 6.4%
Type 2 Diabetes
As beta cell health further declines, less insulin is available than is required to maintain normal glucose homeostasis. This decline in insulin production reflects progressive beta cell failure. When the plasma glucose levels rise above the pre-diabetic range, type 2 diabetes is diagnosed.
- Progressive beta cell failure occurs over time.
- The insulin secretory capacity of the beta cell steadily declines.
- Loss of insulin sensitivity may get worse.
Read all the possible symptoms and risk factors of type 2 diabetes, Here. A patient is diagnosed type 2 diabetes when plasma glucose levels reaches;
- More than or equal to 200 mg/dL (Random plasma glucose)
- More than or equal to 126 mg/dL (Fasting plasma glucose)
- More than or equal to 200 mg/dL ( Oral glucose tolerance test)
- HbA1c – 6.5% or above
- Coupled with symptoms like Polyuria, Polydipsia, unexpected weight loss, etc.
Read our full-text article on reversing the diabetes.