scholarly journals Sepsis-Induced Adipokine Change with regard to Insulin Resistance

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Andreas Hillenbrand ◽  
Manfred Weiss ◽  
Uwe Knippschild ◽  
Anna Maria Wolf ◽  
Markus Huber-Lang
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Plasminogen Activator Inhibitor ◽  
Retinol Binding Protein ◽  
Plasminogen Activator Inhibitor 1 ◽  
Necrosis Factor Alpha ◽  
Retinol Binding Protein 4 ◽  
Chemotactic Protein ◽  
Pubmed Search ◽  
Anti Inflammatory

Background. Assessment of white adipose tissue has changed in recent years, with WAT now being considered as an active endocrine organ, secreting a large number of bioactive mediators, so-called adipokines. Besides other functions, these adipokines are involved in inflammatory response thereby exhibiting predominantly proinflammatory or anti-inflammatory properties and contribute to insulin resistance.Methods. Comprehensive review of the literature of the role of adipokines relevant to critical care medicine using PubMed search.Results. Adiponectin—the prototype of an anti-inflammatory and insulin-sensitizing adipokine—is diminished in sepsis, while resistin—a protein with proinflammatory properties—is elevated. Plasminogen activator inhibitor-1, interleukin (IL)-1, IL-6, IL-8, and IL-10, and tumor-necrosis-factor-alpha mediate insulin resistance and are elevated in sepsis, while retinol-binding protein-4 concentrations are significantly reduced in sepsis. Chemerin displays potent anti-inflammatory and insulin-resistance properties, while monocyte chemotactic protein-1—increased in sepsis—contributes to macrophage infiltration in adipose tissue and insulin resistance.Conclusions. The expression of adipokines in humans is altered as well in obese as in septic patients with elevated levels of proinflammatory adipokines. Changes in adipokine levels in acute sepsis could contribute to insulin resistance. Consequently, in critically ill patients, these alterations underline a possible contribution of adipokines in the development of hyperglycemia.

Role of adiponectin and PBEF/visfatin as regulators of inflammation: involvement in obesity-associated diseases

2008 ◽  
Vol 114 (4) ◽  
pp. 275-288 ◽  
Author(s):  
Herbert Tilg ◽  
Alexander R. Moschen
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Clinical Medicine ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Acid Oxidation ◽  
Endothelial Cell Function ◽  
Retinol Binding Protein 4 ◽  
Associated Diseases ◽  
Anti Inflammatory

Obesity and obesity-related disorders play an important role in clinical medicine. Adipose tissue, with its soluble mediators called adipocytokines, has emerged as a major endocrine organ. These adipocytokines comprise many mediators such as adiponectin, PBEF (pre-B-cell-enhancing factor)/visfatin, leptin, resistin, retinol-binding protein-4 and others. They play major roles in key aspects of metabolism, such as insulin resistance, fatty acid oxidation, inflammation and immunity. Adiponectin, a prototypic adipocytokine, is of importance in the regulation of insulin resistance, as circulating levels are decreased in obesity and diseases associated with insulin resistance. Besides its major role in regulation of insulin sensitivity, recent evidence suggests potent anti-inflammatory functions for adiponectin. These effects are paralleled by other immune-regulatory properties, such as regulation of endothelial cell function. The in vitro effects of adiponectin have been corroborated by several studies demonstrating potent in vivo anti-inflammatory effects. Many other adipocytokines, such as PBEF/visfatin, leptin, resistin or retinol binding protein-4, are involved in the physiology and pathophysiology of adipocytes, adipose tissue and related diseases. PBEF/visfatin, another recently characterized adipocytokine, has been linked to several inflammatory disease states beyond insulin resistance, such as acute lung injury or inflammatory bowel diseases. It has been recognized for many decades that obesity is accompanied by an increase in cancer and potentially some immune-mediated diseases. Understanding this new exciting world of adipocytokines will be of importance in the development of novel therapies for obesity-associated diseases.

scholarly journals Subcutaneous adipose tissue biology in metabolic syndrome

2018 ◽  
Vol 33 (1) ◽  
Author(s):  
Ishwarlal Jialal ◽  
Sridevi Devaraj
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Interleukin 1 ◽  
Plasminogen Activator Inhibitor ◽  
Retinol Binding Protein ◽  
Plasminogen Activator Inhibitor 1 ◽  
Amyloid A ◽  
Subcutaneous Adipose

AbstractMetabolic syndrome (MetS) is a common global problem that comprises the cardio-metabolic cluster and predisposes to both diabetes and cardiovascular diseases. Although the pathogenic mechanisms have not been elucidated, both increased inflammation and insulin resistance play a pivotal role. It appears that both monocyte/macrophages and adipose tissue (AT) conspire to accentuate both the pro-inflammatory state and increased insulin resistance. Whilst there are scant data on visceral adipose tissue (VAT) and epicardial adipose tissue (EAT) biology, there are data on subcutaneous adipose tissue (SAT) dysregulation. There is a significant increase in macrophages and crown-like structures in the SAT of patients with MetS. With respect to adipokines, there is an increase in plasma leptin, plasminogen activator inhibitor-1, retinol-binding protein-4 (RBP-4), chemerin, serum amyloid-A, C-reactive protein (CRP), interleukin-1, -6, -8, lipopolysaccharide, fetuin A (FetA) and a decrease in adiponectin and omentin-1. All of the abnormalities in plasma were also confirmed for SAT-secreted adipokines except for adiponectin and RBP-4 which derive largely from VAT. As many of these biomediators correlate with both insulin resistance and increased inflammation, we can posit that dysregulation of SAT is detrimental and contributes to both the pathogenesis of MetS and its sequalae. Furthermore, as future directions, much work is needed with respect to VAT/EAT biology, autophagy, sirtuins, the gut microbiome, browning of AT, to further elucidate this common syndrome and identify potential therapeutic targets to forestall its serious complications.

scholarly journals Increased adipose tissue secretion of interleukin-6, but not of leptin, plasminogen activator inhibitor-1 or tumour necrosis factor alpha, in Graves' hyperthyroidism

2002 ◽  
pp. 607-611 ◽  
Author(s):  
H Wahrenberg ◽  
A Wennlund ◽  
J Hoffstedt
Keyword(s):  
Adipose Tissue ◽  
Plasminogen Activator Inhibitor ◽  
Tumour Necrosis Factor Alpha ◽  
Tnf Alpha ◽  
Plasminogen Activator Inhibitor 1 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Activator Inhibitor ◽  
Necrosis Factor ◽  
Pai 1

OBJECTIVE: This study was designed to investigate adipose tissue secretion of interleukin-6 (IL-6), leptin, tumour necrosis factor alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) in Graves' hyperthyroidism. DESIGN: We studied 10 patients before and during (after 8 weeks) anti-thyroid treatment for Graves' hyperthyroidism and 16 healthy, euthyroid control subjects. METHODS: Plasma levels of thyroid hormones and serum/plasma levels of IL-6, leptin, TNF-alpha and PAI-1 were analysed. Subcutaneous fat biopsies were taken for subsequent measurement of IL-6, leptin, TNF-alpha and PAI-1 protein secretion. RESULTS: In patients with Graves' disease, the anti-thyroid treatment resulted in significant reductions of plasma thyroxine and triiodothyronine levels. No differences in serum concentration or adipose tissue secretion of leptin or TNF-alpha were observed either before, as compared with during, anti-thyroid treatment, or in comparison with euthyroid controls. In contrast, plasma PAI-1 activity, but not adipose tissue secretion of PAI-1, was increased both in Graves' disease before as compared with during anti-thyroid treatment (P=0.01) and in thyrotoxic patients compared with euthyroid controls (P=0.0001). Finally, adipose secretion of IL-6 was increased both before (8-fold, P=0.001) and during (6-fold, P<0.0001) treatment as compared with control subjects. Accordingly, serum concentration of IL-6 was also increased by about 50% in thyrotoxic patients as compared with healthy controls (P=0.03). CONCLUSIONS: In Graves' hyperthyroidism regardless of thyroid status, adipose tissue secretion of IL-6, but not of leptin, TNF-alpha or PAI-1, is markedly increased in comparison with euthyroid controls. This suggests that autoimmune thyroidal disorder may regulate adipose tissue release of IL-6.

scholarly journals RBP4: A Culprit for Insulin Resistance in End Stage Renal Disease That Can Be Cleared by Hemodiafiltration

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Fabrizio Grosjean ◽  
Pasquale Esposito ◽  
Rosario Maccarrone ◽  
Carmelo Libetta ◽  
Antonio Dal Canton ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Kidney Transplant ◽  
Glucose Transporter ◽  
Serum Levels ◽  
Tissue Expression ◽  
Serum Glucose ◽  
Retinol Binding Protein ◽  
Retinol Binding Protein 4 ◽  
Glut4 Expression

Introduction. Retinol Binding Protein 4 (RBP4) is mainly excreted by the kidney and plays a pivotal role in insulin resistance (IR). In our study, we evaluated the association between RBP4 and IR in hemodialysis subjects (HD). We also assessed how circulating RBP4 could be influenced by kidney transplant or different dialytic techniques.Methods. RBP4 serum levels were evaluated in HD (n=16) and matched healthy controls (C;n=16). RBP4 and glucose transporter type 4 (GLUT4) mRNA expressions were also determined in adipose tissue. Circulating RBP4 was evaluated after kidney transplant (n=7) and in hemodialysis patients (n=10) enrolled in a cross-over study treated with standard bicarbonate dialysis (BD) or hemodiafiltration (HDF).Results. HOMA index (P<0.05) and serum RBP4 (P<0.005) were higher in HD compared to C. RBP4 levels positively correlated with fasting serum glucose (P<0.05). RBP4 mRNA was lower in HD compared to C (P<0.05) and positively correlated with kidney function (P<0.05) and GLUT4 mRNA (P<0.001). Transplant or HDF reduced circulating RBP4 (P<0.01andP<0.05, resp.). Our results demonstrate that IR is associated with high circulating RBP4 and that suppressed RBP4 adipose tissue expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF are effective in lowering serum RBP4 levels.

scholarly journals Inflammation, obesity, and thrombosis

Blood ◽  
2013 ◽  
Vol 122 (20) ◽  
pp. 3415-3422 ◽  
Author(s):  
Fahumiya Samad ◽  
Wolfram Ruf
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Hepatic Steatosis ◽  
Plasminogen Activator Inhibitor ◽  
Epidemiological Studies ◽  
Clinical Markers ◽  
Plasminogen Activator Inhibitor 1 ◽  
Protease Activated Receptors ◽  
The Metabolic Syndrome

Abstract Clinical and epidemiological studies support a connection between obesity and thrombosis, involving elevated expression of the prothrombotic molecules plasminogen activator inhibitor-1 and tissue factor (TF) and increased platelet activation. Cardiovascular diseases and metabolic syndrome–associated disorders, including obesity, insulin resistance, type 2 diabetes, and hepatic steatosis, involve inflammation elicited by infiltration and activation of immune cells, particularly macrophages, into adipose tissue. Although TF has been clearly linked to a procoagulant state in obesity, emerging genetic and pharmacologic evidence indicate that TF signaling via G protein-coupled protease-activated receptors (PAR2, PAR1) additionally drives multiple aspects of the metabolic syndrome. TF–PAR2 signaling in adipocytes contributes to diet-induced obesity by decreasing metabolism and energy expenditure, whereas TF–PAR2 signaling in hematopoietic and myeloid cells drives adipose tissue inflammation, hepatic steatosis, and insulin resistance. TF-initiated coagulation leading to thrombin–PAR1 signaling also contributes to diet-induced hepatic steatosis and inflammation in certain models. Thus, in obese patients, clinical markers of a prothrombotic state may indicate a risk for the development of complications of the metabolic syndrome. Furthermore, TF-induced signaling could provide new therapeutic targets for drug development at the intersection between obesity, inflammation, and thrombosis.

scholarly journals Associations between Tissue Visfatin/Nicotinamide, Phosphoribosyltransferase (Nampt), Retinol Binding Protein-4, and Vaspin Concentrations and Insulin Resistance in Morbidly Obese Subjects

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Zeynep Goktas ◽  
Shannon Owens ◽  
Mallory Boylan ◽  
David Syn ◽  
Chwan-Li Shen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Morbidly Obese ◽  
Tissue Samples ◽  
Blood Concentrations ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Retinol Binding Protein 4 ◽  
Obese Subjects

Visfatin/Nampt, vaspin, and retinol binding protein-4 (RBP-4) play an important role in insulin resistance. The objectives of this study were to measure visfatin/Nampt, vaspin, and RBP-4 concentrations in blood, liver, muscle, subcutaneous, omental, and mesenteric adipose tissues in morbidly obese subjects and investigate their relationship to insulin resistance. Blood and tissue samples were collected from 38 morbidly obese subjects during Roux-en-Y surgery. Insulin resistance biomarkers were measured using standard kits. Visfatin/Nampt, vaspin, and RBP-4 gene expression levels in tissues were measured using real-time PCR. Their protein concentrations in blood and tissues were measured using ELISA kits. Diabetic subjects had significantly higher homeostasis model of assessment-insulin resistance and age and lower blood HDL-cholesterol concentrations than nondiabetic and prediabetic subjects. Diabetic and prediabetic subjects had significantly higher blood concentrations of visfatin/Nampt and vaspin than nondiabetic subjects. Liver RBP-4 concentrations were positively associated with blood glucose concentrations. Blood insulin resistance biomarker levels were positively associated with visfatin/Nampt concentrations in omental adipose tissue and liver, and vaspin concentrations in mesenteric adipose tissue. In conclusion, the correlations of visfatin/Nampt, vaspin, and RBP-4 with insulin resistance are tissue dependent.

PAI-1 gene 4G/5G polymorphism, cytokine levels and their relations with metabolic parameters in obese children

2008 ◽  
Vol 99 (02) ◽  
pp. 352-356 ◽  
Author(s):  
Muammer Yuce ◽  
Ayse Yazici ◽  
Hasibe Verdi ◽  
F. Belgin Ataç ◽  
Sibel Kinik ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Plasminogen Activator Inhibitor ◽  
Control Group ◽  
Model Assessment ◽  
Obese Children ◽  
Plasminogen Activator Inhibitor 1 ◽  
Necrosis Factor Alpha ◽  
Pai 1

SummaryObesity is associated with the changes of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-alpha (TNFα) and transforming growth factor beta (TGFβ) levels. However, the precise effect of the 4G allele on obesity is still contradictory. Here, we aimed to elucidate the role of the 4G/5G polymorphism of the PAI-1 gene on the PAI-1 level and determine the associations between cytokines, glucose and lipid metabolism parameters in obese children. Thirty-nine obese children (mean age 11.4 ± 3.3 years) and 38 age-matched healthy control group (mean age 10.3 ± 3.5 years) were included in the study. In all cases, serum levels of glucose, lipid and insulin were measured, homeostasis model assessment of insulin resistance (HOMAIR) was calculated, and 4G/5G polymorphism of PAI-1 gene, plasma PAI-1 level and serum TNFα and TGFβ levels were studied. The mean relative body mass index (BMI) and HOMA-IR score, VLDL,TG, insulin, PAI-1,TNFα levels were higher, and HDL and TGFβ levels were lower in the obese group. The frequency of the 4G/4G genotype was considerably higher in obese children than in controls. Also, a positive correlation was found between PAI-1 and TNFα levels, and relative BMI, HOMA-IR score, insulin,TG, HDL levels. TGFβ was inversely correlated only with relative BMI. There was no correlation among three cytokines. In conclusion, childhood obesity contributes to higher PAI-1 andTNFα and lowerTGFβ levels. Especially PAI-1 andTNFα accompany insulin resistance and dyslipidemia.

scholarly journals Visceral Adipose Tissue was Associated with Increased Risk of Insulin Resistance in Lean Polycystic Ovarian Syndrome, Independent with Retinol Binding Protein-4

2020 ◽  
pp. 168-173
Author(s):  
Vita Silvana ◽  
Andon Hestiantoro ◽  
Muharam Natadisastra ◽  
Kanadi Sumapraja ◽  
Budi Wiweko
Keyword(s):  
Insulin Resistance ◽  
Body Mass Index ◽  
Adipose Tissue ◽  
Body Mass ◽  
Visceral Adipose Tissue ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Receiver Operating Curve ◽  
Retinol Binding Protein 4 ◽  
Visceral Adipose

Objective: To determine whether visceral adipose tissue or serum RBP-4 were related with the risk increment of insulin resistance in normal BMI PCOS patients. Methods: This was a cross-sectional study conducted in normal body mass index PCOS patients at Yasmin Clinic, RSCM, Jakarta from July 2014 until March 2015. Diagnosis of PCOS was established using Rotterrdam (2003) criteria. Insulin resistance was confirmed by using ratio of HOMA-IR >1.4. Results: Among 40 subjects, 20 subjects (50%) belong insulin resistance group. Serum RBP-4 level was higher in insulin resistance group (p=0.06). After ROC analysis was conducted, area under curve for of serum RBP-4 was 69.9% (CI 95% -3754.77 - (186.60-7696.14, p=0.061)). Cut-off level of serum RBP-4 was 23814.5 ng/mL yielded sensitivity and specificity to a level of 60% and 60%, respectively. After logistic regression were analyzed, visceral adipose tissue demonstrated substantial association with the risk increment of insulin resistance in normal BMI PCOS patients. Conclusions: Visceral adipose tissue demonstrated substantial association with the risk increment of insulin resistance in normal BMI PCOS patients, independent with serum RBP-4 levels. Key words: body mass index, diagnosis, insulin resistance, PCOS, retinol binding protein-4   Abstrak Tujuan: Untuk menentukan apakah jaringan adiposa viseral atau serum RBP-4 berhubungan dengan peningkatan risiko resistensi insulin pada Sindrom Ovarium Polikistik dengan indeks masa tubuh normal. Metode: Studi potong lintang dilakukan pada subjek SOPK dengan IMT normal di Klinik Yasmin, RSCM, Jakarta sejak Juli 2014 sampai dengan Maret 2015. Penegakan diagnosis SOPK dilakukan dengan kriteria Rotterdam (2003). Resistensi insulin dikonfirmasi dengan pemeriksaan rasio HOMA-IR > 1.4 Hasil: Diantara 40 subjek, sebanyak 20 subjek (50%) mengalami resistensi insulin. Kadar serum RBP-4 lebih tinggi pada kelompok resistensi insulin (p=0.06). Setelah dilakukan analisis Receiver Operating Curve (ROC), serum RBP-4 memiliki Area Under the Curve  (AUC) sebesar 69.9% (IK 95% -3754.77 - (186.60-7696.14, p=0,061)). Titik potong kadar serum RBP-4 adalah 23814.5 ng/mL dengan sensitivitas dan spesifisitas masing-masing 60% dan 60%. Setelah dilakukan analisis regresi logistik, jaringan adiposa viseral menunjukan asosiasi yang kuat dengan terjadinya resistensi insulin pada pasien SOPK dengan IMT normal. Kesimpulan: Jaringan adiposa viseral menunjukan asosiasi yang kuat dengan terjadinya resistensi insulin pada SOPK dengan IMT normal, independen terhadap kadar serum RBP-4. Kata kunci: diagnosis, indeks masa tubuh, resistensi insulin, retinol binding protein-4, SOPK

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