Treatment of Dyslipidemias to Prevent Cardiovascular Disease in Patients with Type 2 Diabetes

Abstract

Purpose of Review Current preventive and treatment guidelines for type 2 diabetes have failed to decrease the incidence of comorbidities, such as dyslipidemia and ultimately heart disease. The goal of this review is to describe the physiological and metabolic lipid alterations that develop in patients with type 2 diabetes mellitus. Questions addressed include the differences in lipid and lipoprotein metabolism that characterize the dyslipidemia of insulin resistance and type 2 diabetes mellitus. We also examine the relevance of the new AHA/ADA treatment guidelines to dyslipidemic individuals. Recent Findings In this review, we provide an update on the pathophysiology of diabetic dyslipidemia, including the role of several apolipoproteins such as apoC-III. We also point to new studies and new agents for the treatment of individuals with type 2 diabetes mellitus who need lipid therapies. Summary Type 2 diabetes mellitus causes cardiovascular disease via several pathways, including dyslipidemia characterized by increased plasma levels of apoB-lipoproteins and triglycerides, and low plasma concentrations of HDL cholesterol. Treatments to normalize the dyslipidemia and reduce the risk for cardiovascular events include the following: lifestyle and medication, particularly statins, and if necessary, ezetimibe, to significantly lower LDL cholesterol. Other treatments, more focused on triglycerides and HDL cholesterol, are less well supported by randomized clinical trials and should be used on an individual basis. Newer agents, particularly the PCSK9 inhibitors, show a great promise for even greater lowering of LDL cholesterol, but we await the results of ongoing clinical trials.

Effects of short‐term add‐on ezetimibe to statin treatment on expression of adipokines and inflammatory markers in diabetic and dyslipidemic patients

“…Add-on ezetimibe and other nonstatin therapies have been prescribed to reduce the residual cardiovascular risk in diabetic patients. 14,15 The effect of the add-on ezetimibe to simvastatin treatment on the LDL cholesterol levels in HC (21% reduction) and DM (24% reduction) observed in this study was similar to the effect of the combined therapy using different types and regular dosages of statins in diabetic and nondiabetic hypercholesterolemics as well as subjects with coronary heart disease. [16][17][18][19][20] Interestingly, add-on ezetimibe also reduced the levels of triglycerides and VLDL cholesterol in DM patients, suggesting that ezetimibe contributes to better metabolic control in diabetics.…”

“…Statins are the first line of treatment for diabetic dyslipidemia that substantially reduces LDL cholesterol as well as the risk of CVD. Add‐on ezetimibe and other nonstatin therapies have been prescribed to reduce the residual cardiovascular risk in diabetic patients …”

Antidiabetic Activity of Pistia strateotes L.Aqueous Extract in Alloxan-induced Diabetic Rats

“…The data on the effect of P. stratiotes aqueous extract on lipid profile is presented in Table 3.Studies have shown that dyslipidemia is a crucial feature of diabetes. [20][21][22] The key components of diabetic dyslipidemia include alterations on the plasma lipid profiles (LDLcholesterol, TG and lowered HDL-cholesterol), which were evidently observed in the present study ( Table 3). The TC, TG and LDLcholesterols of the untreated diabetic group were significantly (p<0.05) elevated while the HDL-cholesterol was significantly (p<0.05) lowered compared to the normal untreated group (Table 3).…”

Hyperglycemia induces inflammatory mediators in the human chorionic villous

“…These receptors recognize conserved pathogens-associated molecular patterns (PAMPs), inducing innate immune responses which are essential for host defenses [14]. They can also be activated by endogenous molecules (damage-associated molecular patterns, DAMPs) released under conditions of cellular stress or tissue injury [15] as free fatty acids and glycation end products [16]. TLRs and nucleotide binding and oligomerization domain (NOD)-like receptors (NLRs) trigger the formation of an inflammasome in the cytoplasm, a multiprotein complex, when active, recruits inactive procaspase-1 molecules to form activated caspase-1 [17].…”