Diabetes Mellitus Type 2 and Metabolic Syndrome

Type 2 diabetes mellitus (T2DM) is characterised by progressive insulin resistance in peripheral tissues (muscle, liver, adipose) combined with relative insulin insufficiency as beta-cell secretory capacity fails to compensate. Unlike T1DM, there is no absolute insulin deficiency initially, and autoimmunity is not the primary driver.

Insulin resistance is the state in which a normal amount of insulin produces a subnormal biological response. The HOMA-IR index (Homeostatic Model Assessment of Insulin Resistance) estimates insulin resistance from fasting glucose and fasting insulin: HOMA-IR = (fasting glucose [mmol/L] × fasting insulin [mU/L]) / 22.5. Values > 2.5–3.0 suggest significant insulin resistance.

Metabolic syndrome is a cluster of cardiometabolic risk factors. The International Diabetes Federation (IDF) criteria require central obesity (waist circumference ≥ 94 cm in European men, ≥ 80 cm in women; lower thresholds for Asian and Pacific people) plus any two of: triglycerides ≥ 1.7 mmol/L, HDL < 1.03 mmol/L (men) or < 1.29 mmol/L (women), blood pressure ≥ 130/85 mmHg, fasting plasma glucose ≥ 5.6 mmol/L. Metabolic syndrome substantially increases the risk of T2DM and cardiovascular disease.

The stepwise management of T2DM begins with lifestyle modification (diet and physical activity) — even a 5–7% weight loss can substantially improve insulin sensitivity. Metformin remains first-line pharmacotherapy: it reduces hepatic glucose production (AMPK pathway), is weight-neutral, inexpensive, and has cardiovascular safety evidence. Second-line agents are chosen based on co-morbidities: SGLT2 inhibitors (empagliflozin, dapagliflozin) are preferred if cardiovascular disease or heart failure is present (proven cardiovascular and renal outcome benefits); GLP-1 receptor agonists (semaglutide, liraglutide) if obesity or cardiovascular disease predominates. If HbA1c targets are not met, insulin (basal, then basal-bolus) is initiated.

In New Zealand, T2DM prevalence is approximately 6–7% of the total population but is 3–4 times higher in Māori and Pacific populations, driven by upstream social determinants (diet, poverty, housing, access to primary care), higher rates of abdominal obesity, and genetic predisposition. This disparity contributes substantially to inequitable cardiovascular and renal disease burden.

Diabetes complications screening is essential: HbA1c target is typically < 53 mmol/mol (7%) for most patients (individualised). Annual urinary albumin-to-creatinine ratio (ACR) and eGFR screen for diabetic nephropathy. Annual dilated retinal photography screens for diabetic retinopathy. Annual foot examination assesses peripheral neuropathy (10 g monofilament, vibration) and peripheral vascular disease. Statin therapy is indicated for most people with diabetes given their elevated cardiovascular risk.