Dyslipidemia is a common feature of diabetes characterized by hypertriglyceridemia (HTG) with decreased levels of high-density lipoprotein (HDL)-cholesterol. This condition includes hypertriglyceridemia, low HDL-C, and mildly elevated low-density lipoprotein (LDL)-C which appears to be more atherogenic. Dyslipidemia and hyperglycemia play fundamental roles in clinical medicine thereby, mediating the risk of cardiovascular disease in diabetes mellitus. The origin of low HDL-C and the predominance of small dense LDL is closely linked to hypertriglyceridemia which is directly related to insulin resistance, adipocytokines, and beta-cell dysfunction. The majority of type 2 diabetic patients exhibit dyslipidemia. This condition is divided into two types: primary (inherited) and secondary (acquired) which are further caused by
- Familial combined hyperlipidemia
- Familial hyperapobetalipoproteinemia
- Familial hypertriglyceridemia
- Polygenic hypercholesterolemia
- Diabetes mellitus
- Alcohol overuse
- Chronic kidney disease
- Primary biliary cirrhosis
Familial combined hyperlipidemia is an inherited disorder that causes isolated triglyceride or low-density lipoprotein (LDL) cholesterol elevations. Familial hypobetalipoproteinemia is characterized by low levels of plasma cholesterol. It impairs the body’s ability to absorb and transport fats called hepatic steatosis. In familial hypertriglyceridemia, there is excessive production of very-low-density lipoproteins (VLDL) from the liver. Dyslipidemia treatment includes the modification of diet and lifestyle, intake of plant sterols, walnut-rich diet, decrease intake of saturated and trans-fatty acids, and increased physical activity. A rich fiber diet can decrease total cholesterol by up to 18%. Non-HDL cholesterol levels, including very-low-density lipoprotein (VLDL) and LDL cholesterol, should be targeted in cholesterol-lowering therapy. Statins have become the first-line drug therapy for diabetic dyslipidemia which inhibits 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the key enzyme in cholesterol biosynthesis, leading to up-regulation of LDL receptors and increased LDL clearance. Bile acid sequestrants are effective cholesterol-lowering agents with non-insulin-dependent diabetes mellitus (NIDDM). They block intestinal bile acid reabsorption and prove to reduce cardiovascular mortality. Ezetimibe inhibits intestinal absorption of cholesterol, lowering LDL cholesterol by 15 to 20%, causing small increases in HDL and a mild decrease in triglycerides. Fibrates reduce the triglyceride level by 30%-50% by stimulating lipoprotein lipase activity. They are activators of peroxisomal proliferator-activating receptor alpha and have an equal effect on microvascular and macrovascular disorders. Nicotinic acid, a water-soluble vitamin B3 increases HDL-cholesterol levels and lowers triglyceride levels. Alirocumab and Evolocumab, PCSK 9 inhibitors reduce LDL cholesterol levels in patients with prior atherosclerotic cardiovascular disease.
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