High density lipoprotein downregulates angiotensin II type 1 receptor and inhibits angiotensin II-induced cardiac hypertrophy

Purpose: Adiponectin (ApN) is considered to be responsible for reduction of inflammation and is known to be included in lipid metabolism. This study was designed to assess the role of adiponectin in patients with type 1 and type 2 diabetes and to determine parameters important in the prediction of adiponectin. Methods: Adiponectin, high sensitive C-reactive protein, fibrinogen, homocysteine, C-peptide, and lipid panel in addition to clinical and laboratory parameters important for the definition of diabetes, obesity and the metabolic syndrome were measured in 118 patients. Results: The best model (R2=0.989) for predicting adiponectin in type 1 diabetes included fibrinogen, white blood cell count, uric acid and triglycerides. In type 2 diabetes the best model (R2=0.751) included C-peptide, white blood cell count, systolic blood pressure, fasting blood glucose, glycated hemoglobin and high-density lipoprotein cholesterol. ANOVA showed among-group differences in adiponectin (P=0.028), body mass index (P < 0.001), fasting blood glucose (P < 0.001) and high-density lipoprotein cholesterol (P =0.012) according to the type of diabetes. Between-group differences were also observed in adiponectin (P =0.033) and high-density lipoprotein cholesterol (P =0.009) according to sex. Adiponectin correlated (P < 0.05) with body mass index, C-peptide, pulse pressure and high-density lipoprotein cholesterol. Conclusion: Adiponectin levels were higher in type 1 diabetes. The association between C-peptide and adiponectin is probably one of the reasons for their different respective levels in different types of diabetes. Interrelations between adiponectin and inflammation, dyslipidemia, C-peptide levels and sex appear to be important for complex adiponectin modulation and action.

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Associations between epicardial adipose tissue, subclinical atherosclerosis and high-density lipoprotein composition in type 1 diabetes

Cardiovascular Diabetology ◽

10.1186/s12933-018-0794-9 ◽

2018 ◽

Vol 17 (1) ◽

Cited By ~ 10

Author(s):

Cristina Colom ◽

David Viladés ◽

Montserrat Pérez-Cuellar ◽

Rubén Leta ◽

Andrea Rivas-Urbina ◽

...

Keyword(s):

Type 1 Diabetes ◽

Adipose Tissue ◽

High Density Lipoprotein ◽

Epicardial Adipose Tissue ◽

Subclinical Atherosclerosis ◽

Density Lipoprotein ◽

High Density ◽

Lipoprotein Composition

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Abstract 407: High Density Lipoprotein Mediated Protection of Macrophages Against Apoptosis Requires Scavenger Receptor Class B Type 1 Activity and Sphingosine-1-Phosphate

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.37.suppl_1.407 ◽

2017 ◽

Vol 37 (suppl_1) ◽

Author(s):

Kevin Chathely ◽

Leticia González ◽

Bernardo Trigatti

Keyword(s):

High Density Lipoprotein ◽

Fluorescent Microscopy ◽

Scavenger Receptor ◽

Density Lipoprotein ◽

High Density ◽

Terminal Deoxynucleotidyl Transferase ◽

Scavenger Receptor Class ◽

Class B ◽

Sphingosine 1 Phosphate

Background/Objectives: Prevention of macrophage apoptosis in advanced atherosclerotic lesions can help stop atherosclerosis progression to vulnerable plaques. High density lipoprotein (HDL) can protect macrophages from apoptosis that has been induced by a variety of agents. We hypothesize that this is the consequence of the sphingolipid, sphingosine-1-phosphate (S1P), specifically carried by HDL, and transferred to S1P receptor 1 (S1PR1) on the cells via the HDL receptor, scavenger receptor class B type 1 (SR-B1). Methods: Apoptosis was induced in murine peritoneal macrophages from wild type and different knockout mice with the ER stress inducing agent tunicamycin. Apoptosis was then observed and detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling through fluorescent microscopy. All experiments were conducted with an n of 3 or 4. Results: Treatment of cells with HDL protected them against tunicamycin induced apoptosis. In contrast, pre-treatment of HDL with S1P lyase, which irreversibly cleaves S1P, eliminated the ability of HDL to protect macrophages. Furthermore, HDL-dependent protection of macrophages against apoptosis required both the HDL receptor SRB1 and the S1PR1. Inhibitor of SRB1’s lipid transport activity also prevented HDL dependant protection against apoptosis. Conclusions: These results suggest that the HDL mediated protection of macrophages against apoptosis may involve SRB1 mediated delivery of S1P from HDL to the S1PR1. Understanding the mechanisms by which HDL elicits atheroprotective signalling in macrophages will provide insight into new targets for therapeutic intervention.

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