Retinol Binding Protein 4 (RBP-4) Correlates with Triglycerides (TG) and Subcutaneous Adipose Tissue (SAT) but Not Insulin Resistance (IR) in Prepubertal (PP) Children with Premature Adrenarche (PA) and Controls.

2010 ◽  
pp. P3-704-P3-704
Author(s):  
AB Sopher ◽  
E Lee ◽  
EA Frisse ◽  
J Root ◽  
D Gallagher ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Retinol Binding Protein 4 ◽  
Premature Adrenarche ◽  
Subcutaneous Adipose

Effects of rosiglitazone on gene expression in subcutaneous adipose tissue in highly active antiretroviral therapy-associated lipodystrophy

2004 ◽  
Vol 286 (6) ◽  
pp. E941-E949 ◽  
Author(s):  
Jussi Sutinen ◽  
Katja Kannisto ◽  
Elena Korsheninnikova ◽  
Rachel M. Fisher ◽  
Ewa Ehrenborg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Highly Active Antiretroviral Therapy ◽  
Subcutaneous Adipose Tissue ◽  
Binding Protein ◽  
Lipid Binding ◽  
Liver Fat ◽  
Highly Active ◽  
Subcutaneous Adipose

Highly active antiretroviral therapy (HAART) has improved the prognosis of human immunodeficiency virus (HIV)-infected patients but is associated with severe adverse events, such as lipodystrophy and insulin resistance. Rosiglitazone did not increase subcutaneous fat in patients with HAART-associated lipodystrophy (HAL) in a randomized, double-blind, placebo-controlled trial, although it attenuated insulin resistance and decreased liver fat content. The aim of this study was to examine effects of rosiglitazone on gene expression in subcutaneous adipose tissue in 30 patients with HAL. The mRNA concentrations in subcutaneous adipose tissue were measured using real-time PCR. Twenty-four-week treatment with rosiglitazone (8 mg/day) compared with placebo significantly increased the expression of adiponectin, peroxisome proliferator-activated receptor-γ (PPARγ), and PPARγ coactivator 1 and decreased IL-6 expression. Expression of other genes involved in lipogenesis, fatty acid metabolism, or glucose transport, such as acyl-CoA synthase, adipocyte lipid-binding protein, CD45, fatty acid transport protein-1 and -4, GLUT1, GLUT4, keratinocyte lipid-binding protein, lipoprotein lipase, PPARδ, and sterol regulatory element-binding protein-1c, remained unchanged. Rosiglitazone also significantly increased serum adiponectin concentration. The change in serum adiponectin concentration was inversely correlated with the change in fasting serum insulin concentration and liver fat content. In conclusion, rosiglitazone induced significant changes in gene expression in subcutaneous adipose tissue and ameliorated insulin resistance in patients with HAL. Increased expression of adiponectin might have mediated most of the favorable insulin-sensitizing effects of rosiglitazone in these patients.

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 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.

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

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 Minireview: Obesity and LipOdystrophy—Where Do the Circles Intersect?

Endocrinology ◽  
2008 ◽  
Vol 149 (3) ◽  
pp. 925-934 ◽  
Author(s):  
Farid F. Chehab
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Retinol Binding Protein 4 ◽  
Secreted Factors ◽  
Survival And Reproduction

Adipose tissue is unique in that it can undergo significant hypertrophy and atrophy, resulting in wide ranges of obesities and lipodystrophies. At the base of this elasticity is the lipid-filled adipocyte, which can either overfill by storing large amounts of triglycerides or shrink to a tiny cell by depleting its lipids and as such is remarkable in sustaining insults. As a major energy reservoir, the adipocyte may hold considerable calories necessary for survival and reproduction, two functions that are essential for the survival of the species. This review will summarize some of the recent studies that have advanced our understanding of the central and peripheral mechanisms that are initiated by adipocyte-secreted factors such as leptin, adiponectin, resistin, and retinol-binding protein 4. The intersection of obesity and lipodystrophy results in insulin resistance, which may be unlocked by elucidating the roles of these factors in pathways that control insulin sensitivity and glucose uptake.

Fenofibrate reduces serum retinol-binding protein-4 by suppressing its expression in adipose tissue

2009 ◽  
Vol 296 (4) ◽  
pp. E628-E634 ◽  
Author(s):  
Haiya Wu ◽  
Li Wei ◽  
Yuqian Bao ◽  
Junxi Lu ◽  
Ping Huang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Mrna Levels ◽  
Retinol Binding Protein 4 ◽  
Fenofibrate Treatment ◽  
Obese Rats

Fenofibrate is a peroxisome proliferator-activated receptor-α (PPARα) activator that has been clinically used to treat dyslipidemia and insulin resistance. To better understand the molecular mechanisms underlying fenofibrate action, we investigated whether fenofibrate affects serum levels of retinol-binding protein-4 (RBP4), an adipocytokine that has recently been shown to link obesity and insulin resistance. Fenofibrate treatment significantly decreased serum RBP4 levels of dyslipidemic patients, which correlated with reduced body weight and increased insulin sensitivity. To elucidate the biochemical mechanisms of fenofibrate action, we investigated the effect of fenofibrate on RBP4 expression in obese rats. Fenofibrate greatly decreased RBP4 mRNA levels in adipose tissue but not in the liver, which correlated with decreased serum RBP4 levels and increased insulin sensitivity in obese rats. Consistent with a direct effect on RBP4 expression, fenofibrate treatment significantly reduced the mRNA expression levels of RPB4 in 3T3-L1 adipocytes. Together, our results demonstrate for the first time that fenofibrate inhibits RPB4 expression in dyslipidemic human subjects and suggest that inhibition of RBP4 expression in adipocytes may provide a mechanism by which fenofibrate improves insulin sensitivity in dyslipidemic patients.

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