Contribution of Maladaptive Adipose Tissue Expansion to Development of Cardiovascular Disease

2016 ◽  
pp. 253-262 ◽  
Author(s):  
Guanghong Jia ◽  
Yan Jia ◽  
James R. Sowers
Keyword(s):  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Tissue Expansion

Adipokines and the cardiovascular system: mechanisms mediating health and disease

2012 ◽  
Vol 90 (8) ◽  
pp. 1029-1059 ◽  
Author(s):  
Josette M. Northcott ◽  
Azadeh Yeganeh ◽  
Carla G. Taylor ◽  
Peter Zahradka ◽  
Jeffrey T. Wigle
Keyword(s):  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Cardiovascular System ◽  
Cardiac Fibroblasts ◽  
Tissue Expansion ◽  
Cell Types ◽  
Vessel Growth ◽  
Major Cell Type ◽  
Health And Disease ◽  
Cardiovascular Cells

This review focuses on the role of adipokines in the maintenance of a healthy cardiovascular system, and the mechanisms by which these factors mediate the development of cardiovascular disease in obesity. Adipocytes are the major cell type comprising the adipose tissue. These cells secrete numerous factors, termed adipokines, into the blood, including adiponectin, leptin, resistin, chemerin, omentin, vaspin, and visfatin. Adipose tissue is a highly vascularised endocrine organ, and different adipose depots have distinct adipokine secretion profiles, which are altered with obesity. The ability of many adipokines to stimulate angiogenesis is crucial for adipose tissue expansion; however, excessive blood vessel growth is deleterious. As well, some adipokines induce inflammation, which promotes cardiovascular disease progression. We discuss how these 7 aforementioned adipokines act upon the various cardiovascular cell types (endothelial progenitor cells, endothelial cells, vascular smooth muscle cells, pericytes, cardiomyocytes, and cardiac fibroblasts), the direct effects of these actions, and their overall impact on the cardiovascular system. These were chosen, as these adipokines are secreted predominantly from adipocytes and have known effects on cardiovascular cells.

scholarly journals Roles of the Chemokine System in Development of Obesity, Insulin Resistance, and Cardiovascular Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Longbiao Yao ◽  
Oana Herlea-Pana ◽  
Janet Heuser-Baker ◽  
Yitong Chen ◽  
Jana Barlic-Dicen
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Nutrient Intake ◽  
Nutrient Deficiency ◽  
Tissue Expansion ◽  
Low Grade ◽  
Chemokine Production ◽  
Increase Risk

The escalating epidemic of obesity has increased the incidence of obesity-induced complications to historically high levels. Adipose tissue is a dynamic energy depot, which stores energy and mobilizes it during nutrient deficiency. Excess nutrient intake resulting in adipose tissue expansion triggers lipid release and aberrant adipokine, cytokine and chemokine production, and signaling that ultimately lead to adipose tissue inflammation, a hallmark of obesity. This low-grade chronic inflammation is thought to link obesity to insulin resistance and the associated comorbidities of metabolic syndrome such as dyslipidemia and hypertension, which increase risk of type 2 diabetes and cardiovascular disease. In this review, we focus on and discuss members of the chemokine system for which there is clear evidence of participation in the development of obesity and obesity-induced pathologies.

Heat shock proteins in obesity: links to cardiovascular disease

2015 ◽  
Vol 21 (2) ◽  
Author(s):  
Christiane Habich ◽  
Henrike Sell
Keyword(s):  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Heat Shock ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
Tissue Expansion ◽  
Heme Oxygenase 1 ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Shock Proteins

AbstractAdipose tissue expansion is associated with adipocyte dysfunction and increased inflammatory processes. In the obese state, adipose tissue is characterized by an impaired intracellular stress defense system and dysbalanced heat shock response. Several members of the heat shock protein (HSP) family have been identified as novel adipokines released upon cellular stress, which might be a molecular link from adipose tissue inflammation to the cardiovascular system. Therefore, this review aims at summarizing and discussing our recent knowledge on HSPs in relation to obesity and their potential links to cardiovascular disease. Of particular importance/interest are two members of the HSP family, HSP60 and heme oxygenase 1 (HO-1), which have been well described as adipokines, and studied in the context of obesity and cardiovascular disease. HSP60 is regarded as a novel molecular link between adipose tissue inflammation and obesity-associated insulin resistance. The role of HO-1 induction in the obese state is well-documented, but a causal relationship between increased HO-1 levels and obesity-associated metabolic diseases is still controversial. Both HSP60 and HO-1 are also forthcoming targets for the treatment of cardiovascular disease, and the current knowledge will also be discussed in this review.

scholarly journals LMO3 reprograms visceral adipocyte metabolism during obesity

2021 ◽  
Author(s):  
Gabriel Wagner ◽  
Anna Fenzl ◽  
Josefine Lindroos-Christensen ◽  
Elisa Einwallner ◽  
Julia Husa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Visceral Adipose Tissue ◽  
Tissue Expansion ◽  
Oxidative Capacity ◽  
Glut4 Translocation ◽  
Mitochondrial Oxidative Capacity ◽  
Visceral Adipose

Abstract Obesity and body fat distribution are important risk factors for the development of type 2 diabetes and metabolic syndrome. Evidence has accumulated that this risk is related to intrinsic differences in behavior of adipocytes in different fat depots. We recently identified LIM domain only 3 (LMO3) in human mature visceral adipocytes; however, its function in these cells is currently unknown. The aim of this study was to determine the potential involvement of LMO3-dependent pathways in the modulation of key functions of mature adipocytes during obesity. Based on a recently engineered hybrid rAAV serotype Rec2 shown to efficiently transduce both brown adipose tissue (BAT) and white adipose tissue (WAT), we delivered YFP or Lmo3 to epididymal WAT (eWAT) of C57Bl6/J mice on a high-fat diet (HFD). The effects of eWAT transduction on metabolic parameters were evaluated 10 weeks later. To further define the role of LMO3 in insulin-stimulated glucose uptake, insulin signaling, adipocyte bioenergetics, as well as endocrine function, experiments were conducted in 3T3-L1 adipocytes and newly differentiated human primary mature adipocytes, engineered for transient gain or loss of LMO3 expression, respectively. AAV transduction of eWAT results in strong and stable Lmo3 expression specifically in the adipocyte fraction over a course of 10 weeks with HFD feeding. LMO3 expression in eWAT significantly improved insulin sensitivity and healthy visceral adipose tissue expansion in diet-induced obesity, paralleled by increased serum adiponectin. In vitro, LMO3 expression in 3T3-L1 adipocytes increased PPARγ transcriptional activity, insulin-stimulated GLUT4 translocation and glucose uptake, as well as mitochondrial oxidative capacity in addition to fatty acid oxidation. Mechanistically, LMO3 induced the PPARγ coregulator Ncoa1, which was required for LMO3 to enhance glucose uptake and mitochondrial oxidative gene expression. In human mature adipocytes, LMO3 overexpression promoted, while silencing of LMO3 suppressed mitochondrial oxidative capacity. LMO3 expression in visceral adipose tissue regulates multiple genes that preserve adipose tissue functionality during obesity, such as glucose metabolism, insulin sensitivity, mitochondrial function, and adiponectin secretion. Together with increased PPARγ activity and Ncoa1 expression, these gene expression changes promote insulin-induced GLUT4 translocation, glucose uptake in addition to increased mitochondrial oxidative capacity, limiting HFD-induced adipose dysfunction. These data add LMO3 as a novel regulator improving visceral adipose tissue function during obesity. Key messages LMO3 increases beneficial visceral adipose tissue expansion and insulin sensitivity in vivo. LMO3 increases glucose uptake and oxidative mitochondrial activity in adipocytes. LMO3 increases nuclear coactivator 1 (Ncoa1). LMO3-enhanced glucose uptake and mitochondrial gene expression requires Ncoa1.

scholarly journals PHYSIOLOGICAL ROLES AND ASSOCIATED DISORDERS OF ADIPONECTIN

2016 ◽  
Vol 10 (1) ◽  
pp. 32
Author(s):  
Preeti Sharma ◽  
Shailaza Shrestha ◽  
Pradeep Kumar ◽  
Saxena Sp ◽  
Rachna Sharma
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Human Plasma ◽  
Mode Of Action ◽  
Skeletal Muscles ◽  
High Concentration ◽  
Peripheral Tissues ◽  
Cardioprotective Effects

ABSTRACTAmong the adipokines, adiponectin is the first one to be described just over a decade ago. It is produced exclusively by adipose tissue and circulatesin high concentration in human plasma accounting for 0.01% of proteins in plasma, almost thousand times higher than that of leptin. The normalcirculating level of adiponectin ranges from 2 to 30 µg/ml. It is now observed that besides adipose tissue, adiponectin can also be produced byseveral other tissues such as hepatocytes, cardiomyocytes, and placenta. Adiponectin executes its action via autocrine as well as and paracrine effects.Researchers working in this area have revealed that adiponectin has insulin-sensitizing, anti-inflammatory and cardioprotective effects. Our reviewfocuses on adiponectin, its mode of action on different peripheral tissues such as skeletal muscles, heart, liver, brain and its the correlative accountin various diseases.Keywords: Adiponectin, Obesity, Type 2 diabetes, Inflammation, Malignancies, Cardiovascular disease.

Fibroblast growth factor receptor 1 is a key regulator of early adipogenic events in human preadipocytes

2009 ◽  
Vol 296 (1) ◽  
pp. E121-E131 ◽  
Author(s):  
C. H. Widberg ◽  
F. S. Newell ◽  
A. W. Bachmann ◽  
S. N. Ramnoruth ◽  
M. C. Spelta ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Tissue Expansion ◽  
Cell Number ◽  
Fibroblast Growth ◽  
Tissue Mass ◽  
Proliferation And Differentiation ◽  
Adipose Tissue Mass ◽  
Human Preadipocytes

Cell number is an important determinant of adipose tissue mass, and the coordinated proliferation and differentiation of preadipocytes into mature lipid-laden adipocytes underpins the increased adipose tissue mass associated with obesity. Despite this, the molecular cues governing such adipose tissue expansion are poorly understood. We previously reported that fibroblast growth factor-1 (FGF-1) promotes both proliferation and differentiation of human preadipocytes and that the major adipogenic effect of FGF-1 occurs during proliferation, priming the cells for adipose conversion. In the current study, we examined whether this effect was linked to the mitogenic action of FGF-1 by investigating the mitogenic and adipogenic potential of other growth factors, platelet-derived growth factor (PDGF; AA and BB) and vascular endothelial growth factor. Although PDGF-AA and PDGF-BB showed comparable mitogenic potential to FGF-1, only FGF-1 treatment resulted in priming and subsequent differentiation. Pharmacological inhibition of FGF receptor (FGFR) tyrosine kinase activity, using the FGFR-specific inhibitors PD-173074 and SU-5402, revealed an obligate requirement for FGFR activity in these processes. A combination of biochemical and genetic approaches revealed an important role for FGFR1. Knock down of FGFR1 expression by small-interfering RNA reduced FGF-1-stimulated signaling events, proliferation, and priming. Together these data highlight the unique nature of the role of FGF-1 during the earliest stages of adipogenesis and establish a role for FGFR1 in human adipogenesis, identifying FGFR1 as a potential therapeutic target to reduce obesity.

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