Association of serum chemerin and inflammatory factors with type 2 diabetes macroangiopathy and waist-to-stature ratio

Yang, Gangyi; Zhou, Xue; Xu, Jie; Yang, Bo; Gong, Qihai; Zhang, Xuan; Sun, Xiaohua; Zhang, Qun; Xia, Jun; Li, Jianhui

doi:10.17305/bjbms.2019.4002

Cited by 10 publications

(9 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiRNAs promotes mRNA degradation or inhibits translation process to affect the progression of NSCLC by complementary pairing with the 3’UTR of the target mRNA. For example, miR-608 impedes proliferation and metastasis of NSCLC cells via targeting the BRD4 [ 31 ]. MiR-7-5p functions as a tumor suppressor o block the progression of NSCLC via targeting PAK2 [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

Zhang

et al. 2021

Cancer Cell Int

View full text Add to dashboard Cite

Background Long non-coding RNAs (lncRNAs) have been reported to exert crucial functions in regulating the progression of human cancers. However, the function and mechanism of long intergenic non-protein coding RNA 01089 (LINC01089) in non-small cell lung cancer (NSCLC) have not been revealed. Methods The expression level of LINC01089, microRNA (miRNA, miR)-152-3p and phosphatase and tensin homolog deleted onc hromosome ten (PTEN) mRNA was detected by quantitative real-time PCR (qRT-PCR). After gain-of-function and loss-of-function models were established with NSCLC cell lines, the proliferation, migration and invasion of NSCLC cells were detected by cell counting kit-8 (CCK-8) assay, scratch healing assay, Transwell assay, respectively. Dual luciferase reporter assay was employed to validate the binding relationship between miR-152-3p and LINC01089 or the 3’UTR of PTEN. Western blot was used to detect PTEN expression in NSCLC cells after LINC01089 and miR-152-3p were selectively modulated. Results LINC01089 was down-regulated in NSCLC tissues and cells. Functional experiments showed that knockdown of LINC01089 could promote the proliferation, migration and invasion of NSCLC cells, while over-expression of LINC01089 had the opposite effects. miR-152-3p was identified as a functional target for LIN01089, and miR-152-3p could reverse the function of LINC01089. Additionally, LINC01089 could up-regulate the expression level of PTEN via repressing miR-152-3p. Conclusions Down-regulation of LINC01089 promoted the progression of NSCLC through regulating miR-152-3p/PTEN axis.

show abstract

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

Zhang

et al. 2021

Cancer Cell Int

View full text Add to dashboard Cite

show abstract

“…Our results are corroborated by earlier and recent findings [ 62 , 67 ]. In the current study, higher levels of chemerin were observed in the T2DM patients and were closely associated increasing WHR and BMI, which is in agreement with the work of Yang et al, who reported a positive correlation between chemerin levels and BMI and other anthropometric indices [ 68 ]. Our results are also in agreement with a previous study conducted on a section of Saudi women by Habib et al, who reported higher levels of chemerin in T2DM patients, and a good correlation with insulin resistance and adiposity [ 69 ].…”

Section: Discussionsupporting

confidence: 93%

Differential Association of Selected Adipocytokines, Adiponectin, Leptin, Resistin, Visfatin and Chemerin, with the Pathogenesis and Progression of Type 2 Diabetes Mellitus (T2DM) in the Asir Region of Saudi Arabia: A Case Control Study

Mir

Alghamdi

et al. 2022

JPM

View full text Add to dashboard Cite

Background: Sedentary lifestyles, urbanization and improvements in socio-economic status have had serious effects on the burden of diabetes across the world. Diabetes is one of the 10 leading causes of death globally, and individuals with diabetes have a 2–3-fold increased risk of all-cause mortality. Adipose tissue is increasingly understood as a highly active endocrine gland that secretes many biologically active substances, including adipocytokines. However, the exact and discrete pathophysiological links between obesity and T2DM are not yet fully elucidated. Methods: In the current study, we present the association of five diverse adipocytokines, adiponectin, leptin, resistin, visfatin and chemerin, with T2DM in 87 patients (46 males and 41 females) with type 2 diabetes mellitus and 85 healthy controls (44 males and 41 females) from the Asir region of Saudi Arabia. The patients were divided into four groups: normal BMI, overweight, obese and severely obese. The baseline biochemical characteristics, including HbA1c and anthropometric lipid indices, such as BMI and waist–hip ratio, were determined by standard procedures, whereas the selected adipokine levels were assayed by ELISA. Results: The results showed significantly decreased levels of adiponectin in the T2DM patients compared to the control group, and the decrease was more pronounced in obese and severely obese T2DM patients. Serum leptin levels were significantly higher in the females compared to the males in the controls as well as all the four groups of T2DM patients. In the male T2DM patients, a progressive increase was observed in the leptin levels as the BMI increased, although these only reached significantly altered levels in the obese and severely obese patients. The serum leptin levels were significantly higher in the severely obese female patients compared to the controls, patients with normal BMI, and overweight patients. The leptin/adiponectin ratio was significantly higher in the obese and severely obese patients compared to the controls, patients with normal BMI, and overweight patients in both genders. The serum resistin levels did not show any significant differences between the males and females in thr controls or in the T2DM groups, irrespective of the BMI status of the T2DM patients. The visfatin levels did not reveal any significant gender-based differences, but significantly higher levels of visfatin were observed in the T2DM patients, irrespective of their level of obesity, although the higher values were observed in the obese and highly obese patients. Similarly, the serum chemerin levels in the controls, as well as in T2DM patients, did not show any significant gender-based differences. However, in the T2DM patients, the chemerin levels showed a progressive increase, with the increase in BMI reaching highly significant levels in the obese and severely obese patients, respectively. Conclusion: In summary, it is concluded that significantly altered concentrations of four adipokines, adiponectin, leptin, visfatin and chemerin, were found in the T2DM patient group compared to the controls, with more pronounced alterations observed in the obese and highly obese patients. Thus, it can be surmised that these four adipokines play a profound role in the onset, progression and associated complications of T2DM. In view of the relatively small sample size in our study, future prospective studies are needed on a large sample size to explore the in-depth relationship between adipokines and T2DM.

show abstract

“…A number of studies have shown an association between increased circulating chemerin levels with obesity and T2DM in humans, correlating with markers of insulin resistance and inflammation [ 101 , 102 , 103 , 104 ], while exercise, diet intervention, and bariatric surgery decrease its levels [ 105 , 106 , 107 , 108 ]. Moreover, both chemerin and CMKLR1 are upregulated in adipose tissue from obese patients, where the pro-inflammatory cytokine TNFα increases chemerin mRNA expression in visceral adipocytes [ 109 ], which suggests that the low-grade inflammation observed in obesity could contribute to chemerin expression in the adipose tissue [ 110 ].…”

Section: Role Of Some Adipokines In Inflammatory Processes Associamentioning

confidence: 99%

Adipokines and Inflammation: Focus on Cardiovascular Diseases

Feijóo‐Bandín

Aragón-Herrera

Moraña-Fernández

et al. 2020

IJMS

View full text Add to dashboard Cite

It is well established that adipose tissue, apart from its energy storage function, acts as an endocrine organ that produces and secretes a number of bioactive substances, including hormones commonly known as adipokines. Obesity is a major risk factor for the development of cardiovascular diseases, mainly due to a low grade of inflammation and the excessive fat accumulation produced in this state. The adipose tissue dysfunction in obesity leads to an aberrant release of adipokines, some of them with direct cardiovascular and inflammatory regulatory functions. Inflammation is a common link between obesity and cardiovascular diseases, so this review will summarise the role of the main adipokines implicated in the regulation of the inflammatory processes occurring under the scenario of cardiovascular diseases.

show abstract

Association of serum chemerin and inflammatory factors with type 2 diabetes macroangiopathy and waist-to-stature ratio

Cited by 10 publications

References 25 publications

RETRACTED ARTICLE: LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

RETRACTED ARTICLE: LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

Differential Association of Selected Adipocytokines, Adiponectin, Leptin, Resistin, Visfatin and Chemerin, with the Pathogenesis and Progression of Type 2 Diabetes Mellitus (T2DM) in the Asir Region of Saudi Arabia: A Case Control Study

Adipokines and Inflammation: Focus on Cardiovascular Diseases

Contact Info

Product

Resources

About