Review reveals how insulin resistance affects lipid metabolism in type 2 diabetes, implicating dyslipidemia complications.
Diabetes Mellitus (DM) is one of the most prevalent chronic conditions worldwide, with an estimated incidence of 592 million globally by 2035. DM can lead to various serious complications, including diabetic nephropathy, peripheral arterial disease, central and peripheral neuropathy, coronary artery disease, diabetic retinopathy, stroke, and cardiomyopathy. One of the most important macrovascular complications of DM is diabetic dyslipidemia. It is more prevalent in type 2 diabetes (T2D) than in type 1 diabetes (T1D), as T2D is associated with insulin resistance. In normal states, lipid metabolism is mainly regulated by insulin; thus, IR linked to T2D leads to multiple lipid metabolism aberrations. Under normal conditions, insulin promotes hepatic lipid storage and synthesis while suppressing fatty acid oxidation. It also induces de novo lipogenesis through stimulating the expression of lipogenic genes. In healthy conditions, insulin suppresses very-low-density lipoprotein (VLDL) production, preventing excessive lipid export into circulation. However, insulin resistance is associated with increased VLDL secretion, contributing to hypertriglyceridemia. Although a correlation between hyperinsulinemia and hypertriglyceridemia was observed, the exact mechanisms of how insulin affects lipid metabolism, especially in diabetes dyslipidemia, are still not fully understood. The aim of this review is to discuss dyslipidemia in diabetes, its pathophysiology and treatment, as well as the role of insulin in lipid metabolism.
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Alsubhi et al. (2025) studied this question.
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