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(%) Normal (18.5–<25 kg/m 2 ) 18 (28.1) Overweight (25–<30 kg/m 2 ) 29 (45.3) Obese (≥30 kg/m 2 ) 15 (23.4) Missing data 2 (3.1) Total cholesterol (mmol/L) 6.26 (±1.49) Low-density lipoprotein cholesterol (mmol/L) 3
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of low-density lipoprotein cholesterol (LDL-C) is strongly associated with CVD. Hundreds of studies with millions of participants have suggested that LDL-C is a strong predictor of atherosclerosis that eventually leads to atherosclerotic
Department of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu, China
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analysis method (North Biotechnology Research Co, Ltd, Beijing, China). Serum total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) concentrations were measured by enzymatic
Department of Pediatrics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China
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differences in age, sex or height between the obese and control groups. Obese children and adolescents had higher levels of obesity descriptors, such as BMI, BMI z -score and WC. Serum low-density lipoprotein cholesterol (LDL-C) levels were higher in obese
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Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar S. João, Alameda Professor Hernâni Monteiro, Porto, Portugal
Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
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Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar S. João, Alameda Professor Hernâni Monteiro, Porto, Portugal
Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
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Tromso study . Journal of Internal Medicine 2006 260 53 – 61 . ( doi:10.1111/j.1365-2796.2006.01652.x ) 26 Mikhail GS Alshammari SM Alenezi MY Mansour M Khalil NA. Increased atherogenic low-density lipoprotein cholesterol in
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-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and glycated hemoglobin (HbA1c) levels were measured by high-performance liquid chromatography. Circulating fetuin-B(JM-1455H1), adiponectin (ADI) and ET-1 concentrations were
School of Life Science and Engineering, Southwest Jiaotong University, Chengdu, Sichuan, China
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-stimulating hormone; Glu, glucose; GSH, glutathione; HDL-C, high-density lipoprotein cholesterol; HOMA-IR, index homeostatic model assessment of insulin resistance; Ins, insulin; LDL-C, low-density lipoprotein cholesterol; LH, luteinizing hormone; MDA, malondialdehyde
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Shanghai Pituitary Tumor Center, Shanghai, China
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Shanghai Pituitary Tumor Center, Shanghai, China
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; HDL-c, high-density lipoprotein cholesterol; LDL-c, low-density lipoprotein cholesterol; n , number; SBP, systolic blood pressure; TG, triglyceride. An association was detected between SBP values and lipid profile including CHO ( r = 0
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Objective
This study aimed to reveal associations between metabolic hormones in cerebral spinal fluid (CSF) and cigarette smoking-induced weight gain and to explore the underlying mechanism.
Methods
A total of 156 adult men were included, comprising active smokers and nonsmokers. In addition to demographic information and body mass index (BMI), plasma levels of ApoA1 and ApoB, high-density lipoprotein, low-density lipoprotein, cholesterol, triglyceride, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase in the participants were measured. Moreover, the metabolic hormones adiponectin, fibroblast growth factor 21 (FGF21), ghrelin, leptin, and orexin A, as well as the trace elements iron and zinc in CSF, were assessed.
Results
Compared to nonsmokers, active smokers showed higher BMI, and elevated CSF levels of FGF21, Zn, and Fe, but decreased levels of metabolic hormones adiponectin, ghrelin, leptin, and orexin A. Negative correlations existed between CSF FGF21 and ghrelin, between CSF Zn and ghrelin, as well as between CSF Fe and orexin A in active smokers. Furthermore, elevated CSF FGF21 and Zn predicted ghrelin level decrease in the smokers.
Conclusion
These data relate smoking-induced weight gain to its neurotoxic effect on the neurons that synthesize metabolic hormones such as adiponectin, ghrelin, leptin, or orexin A in the brain, by disrupting mitochondrial function and causing oxidative stress in the neurons.
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Background:
Evidence has demonstrated that visceral fat area (VFA) and subcutaneous fat area (SFA) had different influences on cardiovascular disease (CVD) risk in patients with type 2 diabetes mellitus (T2DM). We aimed to investigate the relationship between the visceral fat area (VFA) to subcutaneous fat area (SFA) ratio (V/S) and carotid atherosclerosis (CAS) in patients with T2DM.
Methods:
From January 2018 to May 2023, 1,838 patients with T2DM admitted to the National Metabolic Management Centre in our hospital were assigned to two groups based on comorbid CAS. Dual bioelectrical impedance analysis was used to measure the VAF and SFA, and the V/S was calculated. Patient characteristics and serum biochemical indices were compared between groups. Factors influencing comorbid CAS were determined, and correlations between V/S and other clinical indices were analyzed.
Results:
The group with comorbid CAS included 858 individuals and 980 without comorbid CAS. Those with comorbid CAS were older and had a longer disease duration, more significant systolic blood pressure, and greater V/S. The proportions of patients with comorbid hypertension increased significantly with the V/S ratio. The V/S ratio positively correlated with triglyceride (TG), low-density lipoprotein cholesterol levels, and waist circumference. According to binary logistic regression analysis, V/S was an independent risk factor for CAS.
Conclusion:
Elevated V/S is an independent risk factor for CAS in patients with T2DM.