Type 1 diabetes occurs when the immune system mistakenly attacks and destroys pancreatic beta cells, resulting in absolute insulin deficiency.
Type 2 diabetes involves the body becoming insensitive to insulin (insulin resistance). In the early stage, the pancreas can still secrete insulin, but insulin production may become exhausted in the later stage. Type 2 diabetes is mainly related to insulin resistance and relative insulin insufficiency, and is often associated with obesity and unhealthy lifestyle. It can be controlled in the early stage with medication, diet, and exercise.
Type 1 diabetes usually develops suddenly in children or young, thin adults, with the classic symptoms of “three polys and one loss” (polyuria, polydipsia, polyphagia, and weight loss) and a rapid rise in blood glucose within days. Patients often seek medical attention for the first time due to diabetic ketoacidosis. In addition, it is strongly linked to specific genes (such as the HLA gene) and may be triggered by viral infections (e.g., Coxsackie virus).
Type 2 diabetes is more common in overweight adults, with an insidious onset. High blood sugar is often only detected during physical examinations, and there may be no obvious symptoms for years.
Patients with Type 1 diabetes must take insulin for life; missing even one injection may lead to ketoacidosis.
Patients with Type 2 diabetes are first managed with weight loss and oral medications. Some may also need insulin after several years, but stopping it does not immediately cause ketoacidosis.
In Type 1 diabetes, fasting C‑peptide is extremely low, and pancreatic autoantibodies are positive.
In Type 2 diabetes, C‑peptide is normal or high, autoantibodies are negative, and it is often accompanied by hypertension and fatty liver.