In-depth analysis of diabetes: its subtypes, causes, metabolic mechanisms, and physiological homeostasis of blood glucose regulation.

2026-04-02

Diabetes mellitus is a clinical syndrome characterized by a series of metabolic disorders caused by an absolute or relative deficiency of insulin in the body, or by insulin resistance in tissue cells. It is closely related to genetics. The World Health Organization classifies diabetes into: type 1 diabetes, type 2 diabetes, gestational diabetes, and other types of diabetes. All types of diabetes result in the pancreas's beta cells failing to produce sufficient insulin, or in cases of insulin receptor dysfunction or post-receptor dysfunction (or decreased insulin receptor function), to lower blood glucose levels, leading to hyperglycemia.

Although the symptoms of each type of diabetes are similar or identical, the causes of the disease differ. Type 1 diabetes is generally caused by a disorder of the autoimmune system leading to dysfunction of the beta cells that produce insulin; type 2 diabetes is caused by insulin resistance in tissue cells, beta cell dysfunction, or a variety of other reasons. The typical symptoms of diabetes that we usually refer to as "the three highs and one low" (i.e., polydipsia, polyphagia, polyuria, and weight loss) mainly appear in patients with type 1 diabetes.

Because type 1 diabetes patients lose a large amount of glucose in their urine, their bodies are in a state of semi-starvation, leading to energy deficiency, increased appetite, and increased food intake. Polyuria and osmotic diuresis cause excessive water loss, resulting in intracellular dehydration, which stimulates the thirst center, leading to excessive thirst and frequent drinking. After replenishing fluids, the frequency of urination also increases significantly. Furthermore, due to insufficient insulin, the body cannot fully utilize glucose and can only accelerate the breakdown of fat and protein to supplement energy and calories.

This results in a significant depletion of carbohydrates, fats, and proteins in the body, coupled with water loss, leading to weight loss, emaciation, fatigue, and lethargy. Therefore, patients with type 1 diabetes experience a marked decrease in weight after onset. The distinction between type 1 and type 2 diabetes is actually unrelated to body shape; both obese and underweight patients can have type 2 diabetes, and the two types often differ significantly in their pathogenesis and treatment.

Obesity is one of the most important contributing factors to type 2 diabetes. Obese patients with type 2 diabetes may have only a slightly reduced or normal pancreatic function; some obese patients even have stronger insulin secretion than normal individuals, yet their blood sugar remains uncontrolled. This is because obese patients have fewer insulin receptors and reduced sensitivity to insulin, resulting in insulin resistance. In other words, although they can secrete insulin, the secreted insulin is insufficient to lower blood sugar.

Weight gain coupled with lack of exercise creates a vicious cycle, leading to obesity, which in turn causes overeating and elevated blood glucose levels. This necessitates more insulin to convert glucose into energy, and the increased insulin demand inevitably leads to increased insulin secretion from pancreatic beta cells. However, type 2 diabetic patients who are underweight may not have severe insulin resistance, but rather only reduced pancreatic cell secretion function, resulting in the typical diabetic symptoms of polyuria, polydipsia, polyphagia, and weight loss.

Currently, the main method for distinguishing between type 1 and type 2 diabetes relies on testing for "glutamate decarboxylase (GAD) antibodies." A positive GAD antibody result indicates type 1 diabetes, while a negative result indicates type 2 diabetes. Diabetes classification cannot be determined solely by a patient's body shape. The human body contains polysaccharides, disaccharides, and monosaccharides. Blood glucose refers only to glucose in the blood and does not include monosaccharides such as fructose and galactose. In healthy individuals, blood glucose levels are in dynamic equilibrium, meaning they fluctuate within a certain range.

Most people have fasting blood glucose levels between 3.3 and 6.1 mmol/L, and postprandial blood glucose levels (30 minutes and 1 hour after a meal) do not exceed 11.11 mmol/L. Blood glucose originates from food digestion and absorption, breakdown of glycogen stored in the liver, and gluconeogenesis from fats and proteins. Blood glucose is disposed of through oxidation for energy; conversion into glycogen stored in the liver, kidneys, and muscles; and conversion into other nutrients such as fats and proteins for storage. The relatively constant blood glucose level in the human body is a result of regulation by the neuroendocrine system.

After ingestion, starchy foods are broken down into glucose by digestive enzymes, which is absorbed into the bloodstream, raising blood glucose levels. This stimulates pancreatic β-cells to secrete insulin, which promotes the transport of glucose into cells. Glycogen is synthesized in liver cells and muscle cells, and finally, it is broken down and utilized by tissue cells to produce energy. When the body is in a state of hunger, blood glucose levels drop, which excites the hunger center in the feeding center, generating a desire to eat and leading to food consumption.

On the other hand, if food cannot be ingested in time, the endocrine system can secrete hormones such as glucagon and adrenal medullary hormones that promote the breakdown of liver glycogen. The breakdown of liver glycogen releases glucose into the bloodstream, maintaining a relatively constant blood glucose concentration. Some human tissues and cells do not store glycogen themselves, such as brain cells and red blood cells; these cells constantly absorb glucose from the blood. If blood glucose drops to a certain level, the energy source for these tissues and cells is impaired, and their function can be affected. Therefore, the relative stability of blood glucose is an important factor in maintaining normal bodily functions.

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