The review by M.-R. Taskinen discusses the complex nature of diabetic dyslipidaemia, focusing on the heterogeneity of lipoprotein classes and the coordinated regulation of different lipoprotein species. The key findings include: 1. **Triglyceride-Rich Lipoproteins (TRLs)**: The increase in large VLDL 1 particles in Type 2 diabetes leads to the formation of atherogenic remnants, small dense LDL, and small dense HDL particles, collectively forming the atherogenic lipid triad. The increase in VLDL 1 particles is not fully captured by clinical lipid measures. 2. **VLDL Assembly and Secretion**: The mechanisms behind the increase in VLDL 1 particles are not fully understood. Key factors include low insulin signaling via PI-3 kinase, up-regulation of SREBP-1C, and excess availability of "polar molecules" in hepatocytes. These factors contribute to the overproduction of VLDL apo B and the inability of insulin to suppress VLDL 1 production in Type 2 diabetes. 3. **Apoproteins in TRLs**: Apo CIII and apo E play crucial roles in the metabolism and removal of TRLs. Apo CIII-containing TRLs are associated with increased CHD risk, while apo E enrichment of VLDL particles can reduce their catabolic rate, potentially exacerbating postprandial lipemia. 4. **Pathophysiology of VLDL Metabolism**: Insulin inhibits VLDL assembly and secretion, particularly of large VLDL 1 particles. In Type 2 diabetes, insulin fails to suppress VLDL 1 production, leading to inappropriate postprandial production and increased plasma triglyceride concentrations. 5. **Postprandial Lipemia**: Postprandial lipemia is a significant component of diabetic dyslipidaemia, with Type 2 diabetic patients showing exaggerated responses to fat loads. This is due to impaired lipolysis, reduced LPL activity, and impaired clearance of remnant particles. 6. **LDL Subclasses**: Small dense LDL particles are a common feature of diabetic dyslipidaemia, associated with increased risk of CHD. These particles are highly atherogenic due to their poor binding to LDL receptors and increased susceptibility to oxidation. 7. **HDL Subclasses**: Low HDL cholesterol is a dominant feature of diabetic dyslipidaemia. The lowering of HDL is driven by the exchange of core lipids between TRLs and HDL particles, leading to triglyceride-enriched HDL particles and reduced HDL size. 8. **Lipid Management**: The primary targets of lipid management in Type 2 diabetes should include small dense LDL, remnant particles, and low HDL concentration with unfavorable compositional alterations. Statins have been shown to reduce vascular events in people with diabetes, highlightingThe review by M.-R. Taskinen discusses the complex nature of diabetic dyslipidaemia, focusing on the heterogeneity of lipoprotein classes and the coordinated regulation of different lipoprotein species. The key findings include: 1. **Triglyceride-Rich Lipoproteins (TRLs)**: The increase in large VLDL 1 particles in Type 2 diabetes leads to the formation of atherogenic remnants, small dense LDL, and small dense HDL particles, collectively forming the atherogenic lipid triad. The increase in VLDL 1 particles is not fully captured by clinical lipid measures. 2. **VLDL Assembly and Secretion**: The mechanisms behind the increase in VLDL 1 particles are not fully understood. Key factors include low insulin signaling via PI-3 kinase, up-regulation of SREBP-1C, and excess availability of "polar molecules" in hepatocytes. These factors contribute to the overproduction of VLDL apo B and the inability of insulin to suppress VLDL 1 production in Type 2 diabetes. 3. **Apoproteins in TRLs**: Apo CIII and apo E play crucial roles in the metabolism and removal of TRLs. Apo CIII-containing TRLs are associated with increased CHD risk, while apo E enrichment of VLDL particles can reduce their catabolic rate, potentially exacerbating postprandial lipemia. 4. **Pathophysiology of VLDL Metabolism**: Insulin inhibits VLDL assembly and secretion, particularly of large VLDL 1 particles. In Type 2 diabetes, insulin fails to suppress VLDL 1 production, leading to inappropriate postprandial production and increased plasma triglyceride concentrations. 5. **Postprandial Lipemia**: Postprandial lipemia is a significant component of diabetic dyslipidaemia, with Type 2 diabetic patients showing exaggerated responses to fat loads. This is due to impaired lipolysis, reduced LPL activity, and impaired clearance of remnant particles. 6. **LDL Subclasses**: Small dense LDL particles are a common feature of diabetic dyslipidaemia, associated with increased risk of CHD. These particles are highly atherogenic due to their poor binding to LDL receptors and increased susceptibility to oxidation. 7. **HDL Subclasses**: Low HDL cholesterol is a dominant feature of diabetic dyslipidaemia. The lowering of HDL is driven by the exchange of core lipids between TRLs and HDL particles, leading to triglyceride-enriched HDL particles and reduced HDL size. 8. **Lipid Management**: The primary targets of lipid management in Type 2 diabetes should include small dense LDL, remnant particles, and low HDL concentration with unfavorable compositional alterations. Statins have been shown to reduce vascular events in people with diabetes, highlighting