Dyslipidaemia in Type 1 Diabetes: Molecular Mechanisms and Therapeutic Opportunities
Stephen T O'Brien1, Orla M Neylon1, Timothy O'Brien2
1Department of Paediatrics, University Hospital Limerick, V94 F858 Limerick, Ireland.
Insights
Cardiovascular disease (CVD) is the leading cause of death in Type 1 Diabetes (T1D). Research explores unique atherosclerosis mechanisms in T1D to improve CVD risk assessment and management.
Area of Science:
- Endocrinology
- Cardiology
- Metabolic Diseases
Background:
- Cardiovascular disease (CVD) is the primary cause of mortality in individuals with Type 1 Diabetes (T1D).
- Hyperglycemia significantly contributes to atherosclerosis in T1D through atherogenic modifications of low-density lipoprotein (LDL).
- Existing CVD risk assessment tools are limited for T1D patients, especially younger populations.
Purpose of the Study:
- To review the distinct pathophysiology of atherosclerosis in T1D.
- To highlight the impact of hyperglycemia and LDL modifications on CVD risk.
- To discuss current challenges in managing dyslipidemia and CVD risk in T1D.
Main Methods:
- Literature review focusing on the molecular basis of atherosclerosis in T1D.
- Analysis of hyperglycemia-induced damage and LDL alterations.
- Examination of clinical management strategies and evidence gaps.
Main Results:
- Atherosclerosis in T1D is characterized by unique pathways influenced by hyperglycemia.
- Atherogenic LDL modifications exacerbate CVD risk in T1D patients.
- Current management guidelines often extrapolate from Type 2 Diabetes (T2D) data, lacking T1D-specific evidence.
Conclusions:
- Understanding T1D-specific atherosclerosis mechanisms is crucial for developing novel CVD risk prediction tools.
- Improved lipid-lowering therapies and risk management strategies are needed for T1D populations.
- Addressing evidence gaps and treatment barriers is essential for better patient outcomes.
Abstract:
Cardiovascular disease (CVD) is the leading cause of death in Type 1 Diabetes (T1D). The molecular basis for atherosclerosis in T1D is heavily influenced by hyperglycaemia and its atherogenic effects on LDL. Ongoing research into the distinct pathophysiology of atherosclerosis in T1D offers exciting opportunities for novel approaches to calculate CVD risk in patients with T1D and to manage this risk appropriately. Currently, despite the increased risk of CVD in the T1D population, there are few tools available for estimating the risk of CVD in younger patients. This poses significant challenges for clinicians in selecting which patients might benefit from lipid-lowering therapies over the long term. The current best practice guidance for the management of dyslipidaemia in T1D is generally based on evidence from patients with T2D and the opinion of experts in the field. In this review article, we explore the unique pathophysiology of atherosclerosis in T1D, with a specific focus on hyperglycaemia-induced damage and atherogenic LDL modifications. We also discuss the current clinical situation of managing these patients across paediatric and adult populations, focusing on the difficulties posed by a lack of strong evidence and various barriers to treatment.
Related Concept Videos
01:15Diabetes: Management and Pharmacotherapy
Insulin remains the cornerstone of treatment for most patients with type 1 and many...
01:22Diabetes Mellitus: Overview and Type I Subtype
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
01:24Glucagon-like Receptor Agonists
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
01:22Diabetes Mellitus: Type 2 and Gestational
01:20Lipid-Lowering Drugs: Statins and Miscellaneous Agents
01:20Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...