Key result
Hypertriglyceridemia linked to ~40% higher risk of diabetic peripheral neuropathy in obese T2D patients.
Why the study?
Are lipid metabolism disturbances and lipidomic alterations associated with the development and progression of diabetic peripheral neuropathy in patients with obesity and type 2 diabetes?
Systematic Review
Are lipid metabolism disturbances and lipidomic alterations associated with the development and progression of diabetic peripheral neuropathy in patients with obesity and type 2 diabetes?
Effect estimate: 40% increased risk
Hypertriglyceridemia and specific lipidomic alterations are associated with an increased risk of diabetic peripheral neuropathy in patients with obesity and type 2 diabetes, suggesting potential future biomarkers and therapeutic targets.
Background and Objectives: Diabetic peripheral neuropathy (DPN) is a common and debilitating complication of obesity and type 2 diabetes (T2D) affecting up to 50% of patients with long-standing disease. While chronic hyperglycemia plays a central role in its pathogenesis, intensive glycemic control provides only partial protection, suggesting the involvement of additional metabolic pathways. The primary objective of this systematic review was to evaluate the role of lipid metabolism disturbances and advanced lipidomic alterations in the development and progression of DPN in patients with obesity and T2D. Secondary objectives included identifying specific lipid species associated with DPN and exploring their potential pathophysiological and clinical implications. Methods: This systematic review included 8 studies that met the inclusion criteria and was conducted according to PRISMA guidelines and registered in PROSPERO/2026/CRD420261288920. Study quality was assessed using the Newcastle–Ottawa Scale. Results: Large population-based cohorts reported a consistent association between hypertriglyceridemia and DPN prevalence, with triglyceride levels >204 mg/dL associated with an approximately 40% increased risk. Lipidomic analysis revealed alterations in acylcarnitine, sphingolipids, and phospholipids. However, the evidence remains limited and heterogeneous, and neuropathy-specific outcomes were insufficiently evaluated in interventional studies. Conclusions: Lipid metabolism disturbances, particularly hypertriglyceridemia and specific lipidomic alterations, may contribute to DPN beyond the effects of hyperglycemia. Although not yet clinically actionable, lipidomic alterations may represent promising future biomarkers and therapeutic targets in DPN. However, the current evidence is limited by heterogeneity and predominantly observational designs. Further well-designed longitudinal and interventional studies are needed to clarify causal relationships and clinical relevance.
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Mocanu et al. (2026) conducted a systematic review in Diabetic peripheral neuropathy in obesity and type 2 diabetes. Hypertriglyceridemia and lipidomic alterations was evaluated on Diabetic peripheral neuropathy prevalence (40% increased risk). Hypertriglyceridemia (>204 mg/dL) was associated with an approximately 40% increased risk of diabetic peripheral neuropathy in patients with obesity and type 2 diabetes.
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