Serum fetuin-A levels in obese and non-obese subjects with and without type 2 diabetes mellitus

Zhou, Zhongwei; Ju, Huixiang; Sun, Mingzhong; Chen, Hongmei; Fu, Qing-ping; Jiang, Dongmei

doi:10.1016/j.cca.2017.11.023

Cited by 17 publications

(19 citation statements)

References 30 publications

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“…This assessment demonstrated that obesity increased risk of dyslipidemia by 64% in metabolically healthy adults, however, obesity increased risk of diabetes by 240% in metabolically healthy adults (Fingeret et al, 2018). T2DM patients with obesity had higher fetuin-A levels as compared to non-obese patients and obese glucose tolerance (NGT) subjects (p < 0.001) (Zhou et al, 2018). The miR-144 was one of the highly upregulated miRNAs that showed a linear increase in expression with increasing glycaemic status.…”

Section: Discussionmentioning

confidence: 98%

Lipid metabolism disorder induced by up-regulation of miR-125b and miR-144 following β-diketone antibiotic exposure to F0-zebrafish (Danio rerio)

Wang

Zheng

et al. 2018

Ecotoxicology and Environmental Safety

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β-Diketone antibiotics (DKAs) are widely used in human and veterinary medicine to prevent and treat a large variety of infectious diseases. Long-term DKA exposure to zebrafish can result in lipid metabolism disorders and liver function abnormalities. Based on our previous miRNA-seq analyses, miR-144 and miR-125b were identified as target genes regulating lipid metabolism. DKA-exposure at 12.5 and 25 mg/L significantly increased the expressions of miR-144 and miR-125b. The expression levels for the two miRNAs exhibited an inverse relationship with their lipid-metabolism-related target genes (ppardb, bcl2a, pparaa and pparda). Over-expression and inhibition of miR-144 and miR-125b were observed by micro-injection of agomir-144, agomir-125b, antagomir-144 and antagomir-125b. The over-expression of miR-144 and miR-125b enhanced lipid accumulation and further induced lipid-metabolism-disorder syndrome in F1-zebrafish. The expression of ppardb and bcl2a in whole-mount in situ hybridization was in general agreement with results from qRT-PCR and was concentration-dependent. Oil red O and H&E staining, as well as related physiological and biochemical indexes, showed that chronic DKA exposure resulted in lipid-metabolism-disorder in F0-adults, and in F1-larvae fat accumulation, increased lipid content, abnormal liver function and obesity. The abnormal levels of triglyceride (TG) and total cholesterol (TCH) in DKA-exposed zebrafish increased the risk of hyperlipidemia, atherosclerosis and coronary heart disease. These observations improve our understanding of mechanisms leading to liver disease from exposure to environmental pollution, thereby having relevant practical significance in health prevention, early intervention, and gene therapy for drug-induced diseases.

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Section: Discussionmentioning

confidence: 98%

Lipid metabolism disorder induced by up-regulation of miR-125b and miR-144 following β-diketone antibiotic exposure to F0-zebrafish (Danio rerio)

Wang

Zheng

et al. 2018

Ecotoxicology and Environmental Safety

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“…The incidence of diabetes mellitus (DM), a common chronic disease in clinical practice that affected over 100 million people in China, is increasing each year (1). It has been reported that DM is a persistent metabolic disorder, which can be induced by hypoglycemia and impaired glucose tolerance due to insulin deficiency and resistance (2,3). Type 1 DM is caused by the reduction of insulin due to the destruction of islet cells and accounts for a minority of patients with DM (4,5).…”

Section: Introductionmentioning

confidence: 99%

Reduced expression of microRNA‑199a‑3p is associated with vascular endothelial cell injury induced by type 2 diabetes mellitus

Wang

Tang

2018

Exp Ther Med

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The aim of the present study was to investigate the function and mechanism of action of microRNA (miRNA or miR)-199a-3p in vascular endothelial cell injury induced by type 2 diabetes mellitus (T2DM). A total of 36 patients with T2DM (26 males and 10 females; mean age, 52.5±7.0 years) and 20 healthy subjects (10 males and 10 females; mean age, 55.6±4.5 years) were included in the present study. Peripheral blood samples were obtained from all participants and total RNA was extracted Reverse transcription-quantitative polymerase chain reaction was performed to determine the expression of miR-199a-3p. Following the transfection of human umbilical vein endothelial cells (HUVECs) with a negative control (NC) miRNA or miR-199a-3p mimics, cell proliferation was assessed using a Cell Counting kit-8 assay. Cell migration was investigated using Transwell assays and flow cytometry was performed to detect the apoptosis of HUVECs. HUVECs were infected with Ad-GFP-LC3B and laser-scanning confocal microscopy was performed to observe autophagosomes in HUVECs. Western blotting was used to measure the expression of proteins associated with autophagy and the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/nuclear factor (NF)-κB signaling pathway. MiR-199a-3p was downregulated in peripheral blood from patients with T2DM compared with healthy subjects. Transfection with miR-199a-3p mimics promoted the proliferation and migration of HUVECs. However, miR-199a-3p overexpression inhibited the apoptosis of HUVECs. MiR-199a-3p facilitated HUVEC autophagy by affecting autophagy-associated signaling pathways. Furthermore, miR-199a-3p regulated the biological functions of HUVECs via the PI3K/AKT/NF-κB signaling pathway. The results of the present study suggest that miR-199a-3p expression was reduced in patients with T2DM compared with healthy subjects and may be associated with vascular endothelial cell injury. In addition, miR-199a-3p promoted the proliferation, migration and autophagy of HUVECs, potentially by regulating the PI3K/AKT/NF-κB signaling pathway. Therefore, miR-199a-3p may function as protector of vascular endothelia.

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“…This hepatokin has many different functions due to its complex structure and its binding to different toll-like receptors (TLR) in different tissues [5]. Studies have reported that TLR4 is associated with obesity-related in ammation and insulin resistance, and fetuin-A acts as the endogenous ligand of TLR4 [6,7,8]. It also reduces the insulin response in muscle and adipose tissue by inhibiting the autophosphorylation of the insulin receptor [4,9,10].…”

Section: Introductionmentioning

confidence: 99%

“…Fetuin-A is known as one of the mediators of in ammation. In adult studies, fetuin-A is associated with many diseases such as infections, renal diseases, cardiovascular diseases, cirrhosis, cancer, insulin resistance and metabolic syndrome [6,11,12,13]. There are a limited number of children studies [14,15,16,17,18].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Fetuin-A level and related factors in obese adolescents

Küçükali¹,

Çeti̇nkaya²,

Kurnaz³

et al. 2021

Preprint

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Inflammation is thought to be responsible for insülin resistance and fatty liver in obese cases. The contribution of fetuin-A the inflammation process is not clear. We aimed to evaluate fetuin-A levels in obese adolescents and to evaluate its relationship with anthropometric data, insulin levels and high-sensitive CRP. We found that there was no difference in fetuin-A levels between obese and healthy cases in the whole group. However, hs-CRP levels of obese patients were found to be significantly higher than healthy subjects. There was no difference in terms of fetuin-A and hs-CRP levels between the insulin-resistance and non-resistance group. There was no correlation between lipid parameters and fetuin-A levels. There was no difference in terms of fetuin-A and hs-CRP in cases with and without fatty liver. This may suggest that although systemic inflammation starts in obese patients, fetuin-A is not involved in this process or that the negative effect of fetuin-A on inflammation with other factors is still balanced in the adolescent age group. As a conclusion, further studies are needed to evaluate at what stage and how fetuin-A participates in systemic inflammation physiopathologically.

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Serum fetuin-A levels in obese and non-obese subjects with and without type 2 diabetes mellitus

Cited by 17 publications

References 30 publications

Lipid metabolism disorder induced by up-regulation of miR-125b and miR-144 following β-diketone antibiotic exposure to F0-zebrafish (Danio rerio)

Lipid metabolism disorder induced by up-regulation of miR-125b and miR-144 following β-diketone antibiotic exposure to F0-zebrafish (Danio rerio)

Reduced expression of microRNA‑199a‑3p is associated with vascular endothelial cell injury induced by type 2 diabetes mellitus

Evaluation of Fetuin-A level and related factors in obese adolescents

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