Samir Awadallah1, Mohammed Madkour2, Reem Al Hamidi3, Esraa Abo Alwafa3, Maram Hattab3, Buhour Zakkour3, Amna Al-Matroushi4, Eslah Ahmed4, Mariam Al-Kitbi4. 1. Department of Medical Lab Sciences, College of Health Sciences, University of Sharjah, United Arab Emirates; Metabolic Syndrome and Related Disorders (MSRD) Research Group, Research Institute of Health and Medical Sciences, University of Sharjah, United Arab Emirates. Electronic address: sawadallah@sharjah.ac.ae. 2. Department of Medical Lab Sciences, College of Health Sciences, University of Sharjah, United Arab Emirates; Metabolic Syndrome and Related Disorders (MSRD) Research Group, Research Institute of Health and Medical Sciences, University of Sharjah, United Arab Emirates. 3. Department of Medical Lab Sciences, College of Health Sciences, University of Sharjah, United Arab Emirates. 4. Medical Services of the Ministry of Interior, Sharjah, United Arab Emirates.
Abstract
BACKGROUND: Previous studies have demonstrated that hemoglobin-haptoglobin (Hb-Hp) complex plays a role in developing vascular complications in type 2 diabetes mellitus (T2DM). The complexes bind with Apolipoprotein A1 (ApoA1) of high-density lipoprotein (HDL), affecting the function of Lecithin:Cholesterol Acyltransferase (LCAT), and impairing the reverse cholesterol transport mechanism (RCT). This study investigated the influence of Hp phenotypes on serum levels of ApoA1 and LCAT in patients with T2DM. METHODS: The study comprised 131 T2DM patients and 111 matching healthy controls. Fasting blood glucose, HbA1C, and lipid profile were determined by chemistry autoanalyzer, LCAT and ApoA1 by ELISA, and Hp phenotypes by gel electrophoresis. RESULTS: Irrespective of Hp phenotypes, fasting blood glucose, HbA1C, and lipid profile were significantly higher in patients than in controls, while HDL-cholesterol, ApoA1, and LCAT were lower. ApoA1 correlated positively with LCAT (r=0.223, p=0.024) and HDL-cholesterol (r=0.255, 0.003) in patients only. When Hp polymorphism was taken into account, the levels of LCAT and ApoA1 were significantly lower in patients with Hp2-2 than that in patients of Hp1-1 and/or Hp2-1. Correlations between ApoA1 and each of HDL-cholesterol and LCAT (r=0.239, p=0.046, and r=0.252, p=0.040, respectively) were also observed, but only in patients with Hp2-2 phenotype. CONCLUSIONS: The reduced levels of LCAT and ApoA1 observed in this study support the suggestion that T2DM patients with Hp2-2 phenotype could have altered RCT mechanism and increased risk of developing cardiovascular disease.
BACKGROUND: Previous studies have demonstrated that hemoglobin-haptoglobin (Hb-Hp) complex plays a role in developing vascular complications in type 2 diabetes mellitus (T2DM). The complexes bind with Apolipoprotein A1 (ApoA1) of high-density lipoprotein (HDL), affecting the function of Lecithin:Cholesterol Acyltransferase (LCAT), and impairing the reverse cholesterol transport mechanism (RCT). This study investigated the influence of Hp phenotypes on serum levels of ApoA1 and LCAT in patients with T2DM. METHODS: The study comprised 131 T2DM patients and 111 matching healthy controls. Fasting blood glucose, HbA1C, and lipid profile were determined by chemistry autoanalyzer, LCAT and ApoA1 by ELISA, and Hp phenotypes by gel electrophoresis. RESULTS: Irrespective of Hp phenotypes, fasting blood glucose, HbA1C, and lipid profile were significantly higher in patients than in controls, while HDL-cholesterol, ApoA1, and LCAT were lower. ApoA1 correlated positively with LCAT (r=0.223, p=0.024) and HDL-cholesterol (r=0.255, 0.003) in patients only. When Hp polymorphism was taken into account, the levels of LCAT and ApoA1 were significantly lower in patients with Hp2-2 than that in patients of Hp1-1 and/or Hp2-1. Correlations between ApoA1 and each of HDL-cholesterol and LCAT (r=0.239, p=0.046, and r=0.252, p=0.040, respectively) were also observed, but only in patients with Hp2-2 phenotype. CONCLUSIONS: The reduced levels of LCAT and ApoA1 observed in this study support the suggestion that T2DM patients with Hp2-2 phenotype could have altered RCT mechanism and increased risk of developing cardiovascular disease.