Unraveling Pancreatic Islet Function Tests: Answering Essential Questions & Demystifying the Process

The impact of high glucose toxicity on islet cell function can be mitigated by a period of intensive insulin treatment. According to Professor Weng's research, after two weeks of such treatment, including one week where blood sugar reaches the target and another week for stabilization at a better level, it is possible to detect and potentially restore the reversible part of the pancreatic islet cells' function. Typically, in clinical practice, insulin is used for one month to control blood sugar before conducting an islet cell function test, which helps to rule out the impact of high glucose toxicity on islet cell function.

The necessity to stop insulin or secretagogues during islet cell function tests depends on the blood sugar control level. If the fasting blood sugar is below 5mmol/L, it may be necessary to discontinue the medication due to the low stimulation threshold for endogenous insulin. If the fasting blood sugar is around 8 or 9mmol/L, basal insulin does not need to be stopped. To prevent postprandial hypoglycemia, which could otherwise stimulate endogenous insulin, insulin may be omitted during a meal before the test. The same applies to secretagogues.

There is no definitive cutoff for hyperinsulinemia, but it is categorized into absolute and relative conditions. Absolute hyperinsulinemia indicates insulin levels above the normal range, which, if accompanied by uncontrolled blood sugar, may suggest insulin resistance. Relative hyperinsulinemia refers to insulin levels above the median normal value, nearing the upper limit, even though blood sugar remains high, indicating the presence of insulin resistance.

For new-onset diabetic patients, it is theoretically easier to reach a honeymoon phase with the use of GLP-1 receptor agonists or DPP-4 inhibitors. This is supported by basic research showing that these drugs may reduce islet cell apoptosis and increase the number of beta cells.

The pathogenesis differs between diabetic patients with metabolic syndrome and elderly patients without it. In young patients with T2DM and metabolic syndrome, the onset is often due to insulin resistance induced by environmental factors, while in elderly patients with new-onset T2DM, it is usually due to reduced endogenous pancreatic islet function. This highlights that age is a significant risk factor for T2DM, as pancreatic beta cell function naturally declines with age, whereas insulin resistance does not necessarily increase with age.