ABSTRACT
INTRODUCTION: Type 2 diabetes mellitus is characterized by increased cardiovascular morbidity and mortality. Atherogenic dyslipidemia is common in this population, consisting of the triad of increased triglycerides, increased small dense low-density lipoprotein (LDL) particles and decreased high-density lipoprotein cholesterol (HDL-C) levels, leading to increased cardiovascular risk. Areas covered: Aim of the review is the presentation of pharmacokinetic characteristics of the currently available sodium-glucose cotransporters 2 (SGLT-2) inhibitors and the effects of these drugs on lipid metabolism. SGLT-2 inhibitors share a common favorable pharmacokinetic profile, are orally administered with long half-lives (allowing for a once daily dosing) and have been proven to be effective in reducing blood glucose levels. However, the SGLT-1 inhibitory capacity differs between these drugs, an effect that may affect their antidiabetic and cardiovascular effects. SGLT-2 inhibitors alter serum lipids modestly in a similar manner. Specifically, an increase of total cholesterol, LDL cholesterol, and HDL-C levels as well as a decrease of triglycerides concentration is observed. Additionally, the administration of these agents may reduce the atherogenic small dense LDL particle levels, an effect that could provide additional cardiovascular protection in the long term. Expert opinion: The effect of SGLT-2 inhibitors on diabetic dyslipidemia may be one of their cardioprotective mechanisms.
Subject(s)
Diabetes Mellitus, Type 2/drug therapy , Hypoglycemic Agents/pharmacology , Atherosclerosis/drug therapy , Atherosclerosis/etiology , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/etiology , Diabetes Mellitus, Type 2/complications , Dyslipidemias/drug therapy , Dyslipidemias/etiology , Half-Life , Humans , Hypoglycemic Agents/pharmacokinetics , Lipids/blood , Risk Factors , Sodium-Glucose Transporter 2ABSTRACT
AIM: To evaluate the presence of the so called "statin escape" phenomenon among hyperlipidemic subjects attending a lipid clinic. METHODS: This was a retrospective analysis of 1240 hyperlipidemic individuals followed-up for ≥ 3 years. We excluded those individuals meeting one of the following criteria: Use of statin therapy at baseline visit, discontinuation of statin treatment at most recent visit, change in statin treatment during follow-up and poor compliance to treatment. Statin escape phenomenon was defined as an increase in low-density lipoprotein cholesterol (LDL-C) levels at the most recent visit by > 10% compared with the value at 6 mo following initiation of statin treatment. RESULTS: Of 181 eligible subjects, 31% exhibited the statin escape phenomenon. No major differences regarding baseline characteristics were found between statin escapers and non-statin escapers. Both escapers and non-escapers had similar baseline LDL-C levels [174 (152-189) and 177 (152-205) mg/dL, respectively]. In comparison with non-escapers, statin escapers demonstrated lower LDL-C levels at 6 mo after treatment initiation [88 (78-97) mg/dL vs 109 (91-129) mg/dL, P < 0.05], but higher levels at the most recent visit [103 (96-118) mg/dL vs 94 (79-114) mg/dL, P < 0.05]. CONCLUSION: These data confirm the existence of an escape phenomenon among statin-treated individuals. The clinical significance of this phenomenon remains uncertain.
