Diabetes: Definition, Etiology, Clinical Manifestations, Diagnosis, and Treatment Essentials

Diabetes is a group of metabolic diseases characterized by chronic hyperglycemia resulting from insufficient insulin secretion or impaired insulin action. This article integrates both Traditional Chinese Medicine and Western medical understandings of etiology, summarizes typical clinical manifestations and WHO diagnostic criteria, and provides an overview of common treatment and differential diagnostic points. After reading, one can quickly grasp the diagnostic thresholds and basic treatment approach.

Terminology and Definition

Diabetes mellitus (DM) is a metabolic disease characterized by elevated blood glucose levels caused by absolute or relative insulin deficiency (impaired insulin secretion) and decreased sensitivity of target tissues or organs to insulin (impaired insulin action), often accompanied by lipid abnormalities. In Traditional Chinese Medicine, it is classified within categories such as “Pi Zhang” and “Xiao Ke”.

Etiological Factors

Middle-aged person sitting sedentarily in the living room eating high-calorie takeout, representing unhealthy diet and sedentary lifestyle

Traditional Chinese Medicine Etiology and Pathogenesis

  • Dietary factors: Overconsumption of rich, sweet, and greasy foods or changes in diet structure and quality are major causes. “Excessive eating damages the stomach and intestine.” “Fatty foods induce internal heat, sweet foods cause fullness.” Excessive intake leads to gastric and spleen stagnation, blockage of the middle burner, impaired ascending and descending functions, faulty transformation and transportation, accumulation of dampness, turbid phlegm generation, gradually heat injuring body fluids, causing the disease.
  • Sedentary lifestyle: Reduced activity leads to spleen Qi stagnation and disrupted transformation functions; depletion of spleen Qi injures stomach Qi, both become weak; failure of spleen to disperse essence causes misdirection of refined substances into dampness and phlegm, which over time transform to heat and cause the disease.
  • Emotional disturbances: Liver Qi stagnation disrupts Qi flow in the middle burner, leading to liver-spleen Qi stagnation or liver-stomach Qi stagnation; abnormal spleen and stomach function causes food accumulation producing heat and phlegm, which transforms into the disease.

Western Medicine Etiology and Pathogenesis

  • Type 1 Diabetes Mellitus (T1DM): Related to genetics, environment, and autoimmunity. The HLA gene located on chromosome 6p21 is the major susceptibility gene, with at least 16 gene loci associated with T1DM onset. Both humoral and cellular immunity participate in the pathology, leading to autoimmune insulitis and selective pancreatic beta-cell damage. Viruses (such as mumps virus, Coxsackie B4 virus, rubella virus), chemicals (e.g., streptozotocin, alloxan), and food proteins (e.g., cow’s milk protein) may trigger autoimmune islet damage; autoimmune beta-cell apoptosis leads to T1DM.
  • Type 2 Diabetes Mellitus (T2DM): A complex disease involving both genetic and environmental factors. Multiple genes (e.g., TCF7L2, PPAR-gamma, KCNJ11) are implicated; different patients carry different susceptibility genes affecting various glucose metabolism pathways. Obesity, improper diet, insufficient physical activity, low birth weight, and GLP-1 deficiency can trigger T2DM. Insulin resistance is central, including decreased insulin sensitivity and response due to receptor defects (pre-receptor, receptor, and post-receptor defects). Genetic factors, high sugar/fat diets, amyloid toxicity, and GLP-1 deficiency can impair beta-cell function, resulting in insufficient insulin secretion, defective secretion, disrupted pulsatile secretion, and increased proinsulin levels.

Clinical Manifestations

Middle-aged person tiredly holding a large bottle of water in the kitchen, representing typical symptoms of polydipsia and fatigue

Typical signs of diabetes include polydipsia, polyphagia, polyuria, and weight loss. Approximately 50% of T2DM patients are asymptomatic; about 80% present first with symptoms such as pruritus of skin or external genitalia, suppurative skin infections, or blurred vision.

Symptoms

  • Main symptoms: increased thirst, frequent urination, irritability with thirst, preference for cold drinks; frequent urination with visible foam or sweet odor. Polyphagia and increased appetite are common.
  • Other symptoms: fatigue, tiredness, irritability, insomnia with vivid dreams, forgetfulness, soreness and weakness in the lower back and knees; women may experience increased vaginal discharge and menstrual irregularities.

Signs

Early stages often lack obvious signs; related complications may manifest corresponding signs, such as hyperactive tendon reflexes in early diabetic neuropathy, which may disappear in later stages.

Diagnostic Criteria for Diabetes

Close-up of outpatient nurse performing venous blood sampling for a patient, illustrating the blood glucose testing process needed for diabetes diagnosis

According to the 1999 WHO Expert Consultation on the definition, classification, and diagnostic criteria of DM:

Test Item Condition Description Diagnostic Threshold
Random Plasma Glucose (VPG) With symptoms such as polyuria, polydipsia, unexplained weight loss ≥ 11.1 mmol/L (200 mg/dL)
Fasting Plasma Glucose (FPG) Fasting ≥ 8 hours ≥ 7.0 mmol/L (126 mg/dL)
Oral Glucose Tolerance Test (OGTT) 2-hour glucose 75 g anhydrous glucose ≥ 11.1 mmol/L (200 mg/dL)

Note: In the absence of acute metabolic decompensation, repeat any test on another day to confirm diagnosis; a third OGTT is not routinely recommended.

Differential Diagnosis

Non-glucose glycosuria

Lactosuria occurs in lactating women, pregnant women, and infants; fructose and pentose glycosuria may be seen after consuming large amounts of fruit or in rare congenital disorders.

Non-diabetic glucosuria

  • Transient glucosuria may occur after excessive hunger followed by intake of large amounts of sugar.
  • A few healthy individuals may develop temporary nutritional glucosuria after large sugar intake or rapid absorption.
  • Gastrectomy or hyperthyroidism can cause temporary glucosuria and hypoglycemic symptoms; nephritis and nephropathy can cause renal glycosuria due to impaired tubular reabsorption.
  • Reducing substances like uric acid, vitamin C, glucuronic acid, or drugs excreted in urine such as isoniazid, penicillin, cardiac glycosides, and thiazide diuretics may cause false positive glucosuria.

Hyperthyroidism

Manifests as increased appetite, easy hunger, dry mouth and thirst, heat intolerance with sweating, irritability and agitation, accompanied by elevated blood thyroid hormone levels. Eye protrusion and anterior neck thyroid enlargement differ from diabetes, and classic diabetic symptoms of polydipsia, polyuria, and sweet-smelling urine are absent.

Treatment

Close-up of insulin pen injection in a home environment, with visible healthy diet and exercise equipment in the background, representing comprehensive treatment and self-management

Western Medicine Treatment Principles

Type 1 Diabetes Mellitus (T1DM)

  • Early initiation of intensive insulin therapy with highly individualized dosing and adjustments to minimize hypoglycemia risk.
  • Other treatments may include pancreas and islet transplantation, stem cell therapy, and combined oral hypoglycemic agents; islet transplantation is mostly used in brittle diabetes with complete loss of islet function, often combined with kidney transplant.
  • Stem cell therapy remains in preclinical research and observational stages.
  • Oral hypoglycemic agents are generally not recommended for routine T1DM treatment.

Type 2 Diabetes Mellitus (T2DM) Simplified Glycemic Treatment Pathway

  • Foundation is lifestyle intervention.
  • Initiate pharmacotherapy when glycemic control is inadequate (HbA1c ≥ 7.0%).
  • First-line therapy is metformin monotherapy.
  • If insufficient efficacy, add other oral or injectable agents to metformin: insulin secretagogues, alpha-glucosidase inhibitors, dipeptidyl peptidase-4 (DPP-4) inhibitors, thiazolidinediones, sodium-glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, or insulin.
  • If dual therapy fails, switch to triple therapy with agents having different mechanisms.
  • If glycemic control remains poor, initiate insulin therapy promptly.
  • Options include basal insulin combined with prandial insulin or multiple daily premixed insulin injections.
  • Continue metformin as adjunct when initiating insulin if necessary.
  • Emphasize individualized, stepwise glycemic goals and treatment plans.

Traditional Chinese Medicine Treatment Principles

Chinese patent medicines are mainly used for T2DM (non-insulin-dependent diabetes) and should be prescribed based on syndrome differentiation. Long-term medication requires periodic monitoring of blood glucose and liver and kidney function; if blood glucose does not improve, combination or alternative therapies are recommended.

Note: Chinese-Western compound preparations (such as Xiaoke pills, Xiaotangling capsules, Shiwei hypoglycemic granules, Tangwei capsules) contain western medicine ingredient glibenclamide, an insulin secretagogue with strong hypoglycemic effect. Usage must consider indications, contraindications, and potential hypoglycemic reactions; caution is advised especially when combined with western medications.

Diagnosis of diabetes requires a combination of clinical symptoms and laboratory blood glucose measurements, with repeat testing in different circumstances to confirm. Treatment should be based on lifestyle modifications combined with individualized medication or insulin regimens. When appropriate, Traditional Chinese Medicine syndrome differentiation and integrative approaches may be considered under professional guidance. Long-term management emphasizes screening for complications and dynamic monitoring of blood glucose and liver and kidney function to ensure safety.