scholarly journals Interaction of Adiponectin Genotypes and Insulin Resistance on the Occurrence of Taiwanese Metabolic Syndrome

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Chun-Chieh Chen ◽  
Yu-Hsiang Wei ◽  
Chia-Chen Huang ◽  
Shin-Hui Hung ◽  
Zeng-Wei Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Receptors ◽  
Personal Characteristics ◽  
Chain Reaction ◽  
Tnf Α ◽  
Community Residents ◽  
Polymerase Chain ◽  
Affect Insulin Sensitivity ◽  
Necrosis Factor

Backgrounds. Adiponectin (apM1) may affect insulin sensitivity, and tumor necrosis factor (TNF-α) can inhibit the binding of insulin and insulin receptors. However, whether apM1 and TNF-α genes influence the development of metabolic syndrome (MetS) preceded by insulin resistance is unclear. The current study examines the interactions between the apM1 +45 genotypes, TNF-α -308 genotypes, and insulin resistance on the occurrence of MetS. Methods. A total of 329 community residents were recruited, and their personal characteristics were collected. Waist circumference and biochemical markers were examined for determining MetS. Genotypes were identified by the polymerase chain reaction. Results. After adjusting for the confounding effects, compared to apM1 +45 GG and GT genotypes carriers with HOMR-IR less than 2.0, those carriers with HOMA-IR greater than 2.0 had an increased MetS risk ( OR = 4.35 , 95% CI 2.14-8.85). Further, apM1 +45 TT carriers with HOMA-IR greater than 2.0 experienced a higher MetS risk ( OR = 5.91 , 95% CI 2.78-12.54). A significant interaction of the apM1 +45 genotype and insulin resistance on the MetS development was observed ( P = 0.04 ). Conclusion. Our data suggested that apM1 +45 genotypes might modify the effect of insulin resistance on the development of Taiwanese MetS.

scholarly journals Role of Adipokines in Development of Metabolic Syndrome

2018 ◽  
Vol 54 (04) ◽  
pp. 194-202
Author(s):  
Vani Gupta
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Polymerase Chain Reaction ◽  
Mrna Expression ◽  
Central Obesity ◽  
Premenopausal Women ◽  
Chain Reaction ◽  
Mutant Genotype ◽  
Tnf Α ◽  
Polymerase Chain

ABSTRACTVisceral adipose tissue releases a variety of adipokines which together determine a comprehensive cardiometabolic risk profile. Estrogen deficiency leads to central fat deposition in postmenopausal women. However, premenopausal women are also running high risk of central obesity owing to unhealthy lifestyles, making them prone to development of metabolic syndrome which leads to infertility, polycystic ovary syndrome (PCOS), insulin resistance, and type 2 diabetes (T2D).Premenopausal women with (n=30) and without (n=30) central obesity were studied. Metabolic risk factors and circulatory adipokines were measured. Insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Adipokines' gene polymorphisms were studied by polymerase chain reaction and mRNA expression of leptin, adiponectin, resistin, and interleukin-6 (IL-6). Tumour necrosis factor-α (TNF-α), acylation stimulating protein (ASP) receptor gene (C5L2) were done by real time-polymerase chain reaction in visceral (VAT) and subcutaneous (SAT) adipose tissues was also obtained.Significant high circulating leptin, IL-6, TNF-α, resistin and their VAT mRNA expression and significant low circulating adiponectin and VAT mRNA expression were found in women with metabolic syndrome, irrespective of their menopausal status. Carriers of mutant genotype of TNF-α 308 AA, IL-6 174 CC, resistin 420 GG, leptin 2549 AA, adiponectin 276 TT and C5L2 698 CT had significant association with metabolic syndrome. Conclusively changes in fat distribution modulate the secretion profile of adipokines, therefore elevated circulating leptin, IL-6, TNF-α, ASP, resistin, and low adiponectin may serve as surrogate markers for metabolic syndrome and related morbidities in women with central obesity.

scholarly journals Detection of Tumor Necrosis Factor-α mRNA Induction in Ischemic Brain Tolerance by Means of Real-Time Polymerase Chain Reaction

2000 ◽  
Vol 20 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Xinkang Wang ◽  
Xiang Li ◽  
Joseph A. Erhardt ◽  
Frank C. Barone ◽  
Giora Z. Feuerstein
Keyword(s):  
Polymerase Chain Reaction ◽  
Real Time ◽  
Ischemic Preconditioning ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Chain Reaction ◽  
Tnf Α ◽  
Polymerase Chain ◽  
Factor Α ◽  
Necrosis Factor

A short duration of ischemia (i.e., ischemic preconditioning) results in significant brain protection to subsequent severe ischemic insult. Because previous studies suggest that tumor necrosis factor-α (TNF-α) plays a role in both promoting ischemic damage and neuroprotection, the present work aimed to evaluate the expression of TNF-α mRNA in an established model of ischemic preconditioning using a transient 10-minute occlusion of the middle cerebral artery. Because the level of TNF-α mRNA expression in the brain was too low to be consistently detected by Northern technique, a real-time polymerase chain reaction method was applied to quantitate the absolute copy number of TNF-α transcript in rat brain after the preconditioning procedure. TNF-α mRNA was induced in the ipsilateral cortex as early as 1 hour (27 ± 1 copies of mRNA per microgram of tissue compared to 11 ± 3 copies in sham-operated samples) after preconditioning, reached a peak level at 6 hours (49 ± 10 copies of transcript, n = 4, P < 0.01), and persisted up to 2 days. These data not only demonstrate the utility of real-time polymerase chain reaction for sensitive and accurate measurement of mRNA expression in normal and injured tissues but also suggest a potential role of TNF-α in the phenomenon of ischemic preconditioning.

scholarly journals Tumour necrosis factor-α polymorphism as one of the complex inherited factors in pemphigus

2003 ◽  
Vol 12 (5) ◽  
pp. 303-307 ◽  
Author(s):  
Jolanta Dorota Torzecka ◽  
Joanna Narbutt ◽  
Anna Sysa-jedrzejowska ◽  
Maciej Borowiec ◽  
Anetta Ptasinska ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Tumour Necrosis Factor ◽  
Gene Polymorphisms ◽  
Tumour Necrosis ◽  
Pemphigus Vulgaris ◽  
Pemphigus Foliaceus ◽  
Chain Reaction ◽  
Tnf Α ◽  
Polymerase Chain ◽  
Necrosis Factor

The aim of our study was to analyse a significance of tumour necrosis factor (TNF)-α promoter gene polymorphisms in relation to the HLA-DR locus in genetic predisposition to pemphigus. TNF-α gene polymorphisms in position -238 and -308 were identified using a modified polymerase chain reaction-restriction fragment length polymorphism method in 53 patients with pemphigus (38 with pemphigus vulgaris, 15 with pemphigus foliaceus) and 87 healthy controls. The HLA-DRB1 locus was typed using the polymerase chain reaction SSO method in all the patients and 152 population controls.Carriers of the TNF-α polymorphic -308 A allele were found to be more frequent in the pemphigus foliaceus group in comparison with the control group (odds ratio (OR)=8.12;P=0.0005). A significant association between HLA-DRB1*04 (OR=3.86;Pcor=0.0001) and DRB1*14 (OR=8.4;Pcor=0.0001) and pemphigus vulgaris was found. In this group of patients a decreased frequency of HLA-DRB1*07 (OR=0.08;Pcor=0.006) was also identified.We have shown for the first time a positive association of TNF-α polymorphism in position -308 with pemphigus foliaceus.

Responses of hepatic TNF-α mRNA to repeated hemorrhage in the conscious rat

1998 ◽  
Vol 275 (1) ◽  
pp. E27-E31 ◽  
Author(s):  
Masatomo Yamashita ◽  
Mamoru Yamashita
Keyword(s):  
Blood Pressure ◽  
Tumor Necrosis ◽  
Time Course ◽  
Mrna Level ◽  
Chain Reaction ◽  
Conscious Rat ◽  
Tnf Α ◽  
Polymerase Chain ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

Trauma victims may suffer from repeated hemorrhage, but responses of cytokines to it have not been described. To study this question, we first detected the time course of changes in serum tumor necrosis factor (TNF) activity and hepatic TNF-α mRNA by cytotoxicity against L929 cells and by reverse transcription (RT) and polymerase chain reaction (PCR), respectively, after different sizes of hemorrhage (10–20 ml/kg) with chronically cannulated rats. Then we examined the changes in TNF-α mRNA when two sequential 10 ml/kg hemorrhages were performed. TNF activity showed no significant increases after either size of hemorrhage. At mRNA level, both 15 ml/kg and 20 ml/kg hemorrhages induced significant increases after hemorrhage, whereas a 10 ml/kg hemorrhage did not. When the 10 ml/kg hemorrhage was repeated 24 h later, however, TNF-α mRNA showed a significant increase. There were no significant differences in blood pressure and heart rate after single and repeated 10 ml/kg hemorrhage. This potentiation persisted for ≥48 h. These results show that responses of hepatic TNF-α mRNA are augmented when moderate hemorrhage is repeated.

scholarly journals Emerging roles of C1Q tumor necrosis factor-related proteins in metabolic diseases

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Manjunath Ramanjaneya ◽  
Jayakumar Jerobin ◽  
Ilham Bettahi ◽  
Kodappully Sivaraman Siveen ◽  
Abdul-Badi Abou-Samra
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Metabolic Disorders ◽  
Pharmacological Intervention ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Related Proteins ◽  
Necrosis Factor

AbstractObesity and insulin resistance are key elements of the metabolic syndrome, which includes type 2 diabetes (T2D), dyslipidemia, systemic inflammation, hypertension, elevated risk for cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS). C1Q Tumor necrosis factor-related proteins (CTRPs) have recently emerged as important regulators of metabolism as a core component in the interrelationship between insulin resistance, adiposity and inflammation. To date 15 CTRP members have been identified and most of the CTRPs are dysregulated in obesity, T2D, coronary artery disease and NAFLD. Pharmacological intervention and lifestyle modification alter expression of CTRPs in circulation and in metabolically active tissues. CTRPs enhance metabolism mainly through activation of AMPK/AKT dependent pathways and possess insulin sensitizing properties. Thus dysregulated expression of CTRPs in metabolic disorders could contribute to the pathogenesis of the disease. For these reasons CTRPs appear to be promising targets for early detection, prevention and treatment of metabolic disorders. This review article aims at exploring the role of CTRPs in metabolic syndrome.

scholarly journals Relation of Endothelial Dysfunction and Adipokines Levels to Insulin Resistance in Metabolic Syndrome Patients

2009 ◽  
Vol 63 (4-5) ◽  
pp. 222-227
Author(s):  
Pēteris Tretjakovs ◽  
Antra Jurka ◽  
Inga Bormane ◽  
Indra Miķelsone ◽  
Dace Reihmane ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Doppler Imaging ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Cytokines And Chemokines ◽  
Tnf Α ◽  
Artery Disease ◽  
D 20

Relation of Endothelial Dysfunction and Adipokines Levels to Insulin Resistance in Metabolic Syndrome Patients Obese metabolic syndrome (MS) patients were categorised into three groups: 44 with type 2 diabetes mellitus (T2DM)(D); 20 with T2DM and coronary artery disease (CAD) (DC), and 26 with MS alone (M). Eighteen healthy subjects were selected as controls (C). Insulin resistance (IR) was assessed by HOMA-IR. Adiponectin, tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and interleukin-8 (IL-8) concentrations were measured by xMAP technology. Endothelin-1 (ET-1) was determined by ELISA. We used laser Doppler imaging for evaluating cutaneous endothelium-dependent vasodilatation in the hand. D and DC groups had significantly elevated IR compared with M or C group (P < 0.01). TNF-α, IL-6, IL-8, MCP-1 and ET-1 levels in DC were significantly elevated compared with other groups (P < 0.001). IL-6, IL-8, MCP-1 and ET-1 in D group were higher than those in C group (P < 0.05). TNF-α, IL-6, IL-8, MCP-1 and ET-1 concentrations were correlated with HOMA-IR indexes and adiponectin levels. All patients had lower adiponectin concentrations than controls (P < 0.001), but there were no differences between the patient groups. Only D and DC groups demonstrated a significant and similar decrease in LDI-Ach marker compared to C group (P < 0.001). LDI-Ach values were significantly correlated with HOMA-IR indexes and adiponectin levels (P < 0.001). Our findings show that obese MS patients have significantly increased HOMA-IR, TNF-α, IL-6, MCP-1 and IL-8 levels, decreased adiponectin concentration, and endothelial dysfunction, but the presence of T2DM and CAD in these patients is associated with more pronounced endothelial dysfunction and increased production of inflammatory cytokines and chemokines.

scholarly journals Macrophage migration inhibitory factor may play a protective role in osteoarthritis

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Ming Liu ◽  
Zikun Xie ◽  
Guang Sun ◽  
Liujun Chen ◽  
Dake Qi ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Protective Role ◽  
Macrophage Migration ◽  
Chain Reaction ◽  
Protein Levels ◽  
Tnf Α ◽  
Polymerase Chain

Abstract Background Osteoarthritis (OA) is the most prevalent form of arthritis and the major cause of disability and overall diminution of quality of life in the elderly population. Currently there is no cure for OA, partly due to the large gaps in our understanding of its underlying molecular and cellular mechanisms. Macrophage migration inhibitory factor (MIF) is a procytokine that mediates pleiotropic inflammatory effects in inflammatory diseases such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS). However, data on the role of MIF in OA is limited with conflicting results. We undertook this study to investigate the role of MIF in OA by examining MIF genotype, mRNA expression, and protein levels in the Newfoundland Osteoarthritis Study. Methods One hundred nineteen end-stage knee/hip OA patients, 16 RA patients, and 113 healthy controls were included in the study. Two polymorphisms in the MIF gene, rs755622, and -794 CATT5-8, were genotyped using polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) and PCR followed by automated capillary electrophoresis, respectively. MIF mRNA levels in articular cartilage and subchondral bone were measured by quantitative polymerase chain reaction. Plasma concentrations of MIF, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) were measured by enzyme-linked immunosorbent assay. Results rs755622 and -794 CATT5-8 genotypes were not associated with MIF mRNA or protein levels or OA (all p ≥ 0.19). MIF mRNA level in cartilage was lower in OA patients than in controls (p = 0.028) and RA patients (p = 0.004), while the levels in bone were comparable between OA patients and controls (p = 0.165). MIF protein level in plasma was lower in OA patients than in controls (p = 3.01 × 10−10), while the levels of TNF-α, IL-6 and IL-1β in plasma were all significantly higher in OA patients than in controls (all p ≤ 0.0007). Multivariable logistic regression showed lower MIF and higher IL-1β protein levels in plasma were independently associated with OA (OR per SD increase = 0.10 and 8.08; 95% CI = 0.04–0.19 and 4.42–16.82, respectively), but TNF-α and IL-6 became non-significant. Conclusions Reduced MIF mRNA and protein expression in OA patients suggested MIF might have a protective role in OA and could serve as a biomarker to differentiate OA from other joint disorders.

scholarly journals DETEKSI GEN IL-6 DAN TNF-α DENGAN METODE PCR PADA PENDERITA HEPATITIS B DI LABORATORIUM KLINIK MAXIMA KOTA KENDARI

2021 ◽  
Vol 7 (1) ◽  
pp. 21-28
Author(s):  
Sanatang Abbas ◽  
Sri Anggarini Rasyid ◽  
Tiara Mayang Pratiwi Lio
Keyword(s):  
Tumor Necrosis Factor ◽  
Hepatitis B ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Virus Hepatitis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Polymerase Chain ◽  
Necrosis Factor

Penyakit Hepatitis B adalah inflamasi yang terjadi pada organ hati yang dapat disebabkan oleh virus hepatitis B. Pada saat terjadi inflamasi sitokin yang ada dalam tubuh akan merespon atau mengenali jenis patogen berupa virus yang masuk ke dalam tubuh. Tumor Necrosis Factor (TNF-α) adalah salah satu sitokin pro-inflamasi yang berperan dalam proses inflamasi hati, dan Interleukin-6 (IL-6) adalah sitokin yang disekresikan dari jaringan tubuh pada fase infeksi akut atau kronik. Tujuan dari penelitian ini adalah untuk mendeteksi gen TNF-α dan IL-6 pada penderita hepatitis B dengan metode polymerase chain reaction (PCR). Jenis penelitian yang digunakan dalam penelitian ini adalah semi kuantitatif, dengan desain penelitian eksperimental. Populasi pada penelitian adalah seluruh penderita suspek yang melakukan pemeriksaan rapid Hepatitis B (HbsAg) di Laboratorium Klinik Maxima Kota Kendari sebanyak 7 orang. Teknik penarikan sampel menggunakan total sampling dengan kriteria inklusi sampel yaitu pasien yang tidak memiliki riwayat penyakit lain selain hepatitis B. Berdasarkan hasil penelitian diketahui bahwa dari ketujuh sampel penderita hepatitis B yang diperiksa menggunakan metode PCR 3 sampel dengan hasil positif (45%) terhadap gen TNF-α dan 7 (100%) hasil negative terhadap gen Interleukin 6 (IL-6). Sehingga dapat di simpulkan bahwa jenis sitokin yang berperan saat terjadi inflamasi ketika seseorang terinfeksi Virus Hepatitis B adalah Tumor Necrosis Factor Alpha (TNF-α).

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