Serum Level of Endogenous Secretory Receptor for Advanced Glycation End Products and Other Factors in Type 2 Diabetic Patients With Mild Cognitive Impairment

Abstract

OBJECTIVEDetermine the serum levels of endogenous secretory receptor for advanced glycation end products (esRAGEs) in patients with type 2 diabetes and mild cognitive impairment (MCI) and in control patients with type 2 diabetes but no MCI, and examine the relationship of esRAGE and MCI with other clinical factors.RESEARCH DESIGN AND METHODSA total of 101 patients with type 2 diabetes who were hospitalized in the Department of Endocrinology at Fujian Provincial Hospital between January 2010 and January 2011 were enrolled. There were 58 patients with MCI and 43 patients without MCI (control). Serum levels of esRAGE were measured using an enzyme-linked immunosorbent assay (ELISA). Other clinical parameters were also measured.RESULTSType 2 diabetic patients with MCI had a longer duration of diabetes; elevated HbA1c, total cholesterol (CHOL), LDL cholesterol (LDL-C), triglyceride (TG), intima-media thickness, C-reactive protein (CRP), and brachial-ankle pulse wave velocity (ba-PWV); and lower ankle brachial index (ABI) and esRAGE relative to the control group. Among patients with MCI, the Montreal Cognitive Assessment (MoCA) score was positively correlated with serum esRAGE but negatively correlated with CHOL. Spearman rank correlation analysis indicated that esRAGE was positively correlated with MoCA score and ABI but negatively correlated with ba-PWV, CHOL, TG, and CRP in all subjects.CONCLUSIONSOur results suggest that esRAGE may be a potential protective factor for dyslipidemia, atherosclerosis, and MCI in patients with type 2 diabetes.

Effect of Circular ANRIL on the Inflammatory Response of Vascular Endothelial Cells in a Rat Model of Coronary Atherosclerosis

“…Skrzep-Poloczek et al demonstrated that AS patients had an increased level of total CHOL and LDL and decreased level of HDL [20]. Chen et al showed that AS patients had elevated levels of total CHOL, LDL and TGs [21]. In rats with AS, the ECs were irregular; for example, the number if ECs vanished, and nuclei were irregular with nuclear pore expansion, while heterochromatin gathered at the periphery of the nuclear membrane and physalides increased in the cytoplasm.…”

Associations of Advanced Glycation End-Products With Cognitive Functions in Individuals With and Without Type 2 Diabetes: The Maastricht Study

“…Studies that found associations with plasma AGEs mostly investigated this in individuals with cognitive impairment or dementia (16,47). In addition, in one recent study, SAF was associated with cognitive impairment (score Ͻ Ϫ1.5 SD in any domain from age-, sex-, and education-adjusted norms) (12).…”

“…Yaffe et al (15) have shown that the AGE pentosidine, measured in its free form in urine, was associated with a greater 9-year cognitive decline in older people independent of diabetes status. Furthermore, Chen et al (16) showed that higher levels of serum AGEs were cross-sectionally associated with mild cognitive impairment in diabetes patients. No study to date has investigated the relationship between SAF and cognitive performance on multiple cognitive domains.…”

Glyco-oxidation and cardiovascular complications in type 2 diabetes: a clinical update

“…Another interesting finding that was not emphasized enough was that sRAGEs and esRAGEs seem to have no significant association with classical CVD risk factors such as smoking, lipids, blood pressure, or duration of diabetes, and no more than 6 and 10 % of the variance in sRAGE and esRAGE levels, respectively, was explained by BMI, ethnicity, HbA1c, or eGFR, which goes to show their independent role in predicting CHD events. In a cross-sectional study [70] examining a situation of frank cardiovascular damage, lower serum esRAGE levels and higher serum AGE levels were found associated with dyslipidemia and atherosclerosis in patients with type 2 diabetes. The authors attributed the decrease in serum esRAGE to three possible mechanisms: (1) chronic hyperglycemia directly inhibiting the synthesis and secretion of esRAGEs, (2) the accumulated AGEs binding to esRAGEs and leading to their greater clearance, and (3) inflammation interfering with esRAGE synthesis.…”