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A frequent dyslipidemic characteristic of type 2 diabetes and pre-diabetic conditions is elevated triglyceride levels. One of five acknowledged criteria for identifying persons at high risk for cardiovascular disease and type 2 diabetes, perhaps dubbed the "metabolic syndrome," is a fasting triglyceride level of 150 mg/dl (1.70 mmol/l). Fasting triglyceride levels may help predict type 2 diabetes in the future, according to some research. However, when triglyceride levels were linked with other clinical parameters such as BMI, blood pressure, and other traditional risk factors for cardiovascular disease, or with “high-normal” fasting plasma glucose levels, this was mostly demonstrated. The fed-fasted state, insulin sensitivity, and lifestyle factors such as diet and physical activity all influence the level of circulating triglycerides. These factors make triglyceride levels a highly sensitive lifestyle biomarker at a given time point, but they also suggest that a single triglyceride measurement may not accurately reflect longterm triglyceridemia, especially if lifestyle changes were made during follow-up. It's unclear if assessing triglyceride levels at many time points can enhance the relationship between triglyceride levels and diabetes [1].

Independent of TG levels or other risk factors, the link between low HDL cholesterol and an elevated risk of heart disease is well documented. In fact, in coronary patients, the “low HDL cholesterol” or “hypoalpha” condition is the most common lipoprotein abnormality. Patients with low HDL cholesterol and high TG levels have more widespread coronary atheromas than those with a single increase of LDL cholesterol, according to intravascular ultrasonography studies. Patients with low HDL cholesterol levels have intima-media thicknesses similar to those with familial hypercholesterolemia, but those with preexisting carotid atherosclerosis had plaque development decreased by high HDL cholesterol levels [2,3].

Triglyceride metabolism and diabetic dyslipidemia

During eating and fasting cycles, both fatty acids and glucose play important roles in providing energy to bodily tissues. Triglycerides enable bulk transport of esterified fatty acids in circulating chylomicrons, very low-density lipoproteins (VLDL), and their remains, in addition to energy storage in adipocytes and other cells. Triglyceride-rich lipoproteins are a group of lipoproteins that are high in triglycerides (TRL) [4,5]. Dietary fatty acids are mainly converted to triglycerides in intestinal mucosal cells and released as chylomicrons, which skip the liver and reach the systemic circulation via the thoracic duct via intestinal lymph. Lipoprotein lipase (LPL), which hydrolyzes chylomicron triglyceride to liberate free fatty acids and generates chylomicron remnants in the process, then delivers dietary fatty acids to peripheral tissues through chylomicrons. Additional lipolysis and absorption of residual lipoproteins provide some fatty acids to the liver. De novo hepatic lipogenesis and absorption of nonesterified fatty acids (NEFA) that circulate in plasma bound to albumin are two more major sources of hepatic fatty acids. Hormone sensitive lipase (HSL) and adipocyte triglyceride lipase are enzymes that release NEFA from adipocytes. Insulin inhibits these intracellular enzymes from accessing adipocyte triglycerides, but they become active when insulin levels are very low.

Excessive NEFA production by adipocytes in the presence of insulin resistance and/or insufficiency appears to be a key contributor to dyslipidemia in diabetes and insulin-resistant states like obesity. Circulating VLDL is gradually degraded by LPL in peripheral tissues, releasing fatty acids for usage by muscle and other tissues, as well as storage as triglycerides in adipocytes. VLDL residual particles, known as intermediate-density lipoproteins, are also produced by LPL activity (IDL) [6]. IDL return to the liver, where hepatic lipase partially internalises and partially processes them at the cell surface to become LDL. Insulin promotes LPL activity, therefore insulin resistance leads to poor VLDL particle metabolism. Excess VLDL generation and/or inadequate lipolysis can cause hypertriglyceridemia. In either scenario, TRL participates in cholesteryl ester transfer protein-mediated heteroexchange of neutral lipids (triglycerides and cholesteryl esters) with LDL and HDL, resulting in triglyceride enrichment of LDL and HDL particles. LDL particles grow smaller, denser, and more atherogenic as a result of hepatic lipase activity. HDL particles lose some of their apolipoproteins as a result of comparable lipolysis, which desorb from the decreasing HDL surface and are catabolized in the kidneydisease.