Adipose tissue, adipokines, and inflammation

Fantuzzi, Giamila

doi:10.1016/j.jaci.2005.02.023

Cited by 2,201 publications

(1,916 citation statements)

References 90 publications

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“…Leptin secretion by T cells seems to have, at most, a marginal role in experimentally induced hepatitis, in which no differences have been found in the ability of T cells from ob/ob and wild-type mice to induce inflammation. 6 Other authors observed protection of ob/ob mice from autoimmunity in experimentally induced hepatitis. 88 The activation of T cells and macrophages is one of the initial events during viral or autoimmune hepatitis.…”

Section: Leptin Connective Tissue Diseases and Organ-specific Autoimmentioning

confidence: 97%

“…Leptin deficiency is also associated with increased susceptibility to the toxicity of proinflammatory stimuli, such as endotoxin and TNF-a. 6 Furthermore, starvation and malnutrition, two conditions characterized by low leptin levels, are also associated with alterations in immune responses and thymic atrophy, which can be reversed by leptin administration. 57 Similarly, low circulating CD4 1 cells, impaired T-cell proliferation and impaired release of T-cell cytokines exhibited by patients with congenital leptin deficiency are ameliorated by the administration of recombinant human leptin.…”

Section: Leptin and Autoimmunity M Vadacca Et Al 205mentioning

confidence: 99%

“…Furthermore, leptin mRNA is upregulated in mesenteric adipose tissue of these patients. 6 The role of leptin has also been investigated in spontaneous models of autoimmunity, such as nonobese diabetic (NOD) mice. The NOD mouse strains have increased basal serum leptin before disease onset.…”

Section: Leptin Connective Tissue Diseases and Organ-specific Autoimmentioning

confidence: 99%

“…5 The current view of WAT states that it is an active contributor to body homeostasis by sending out and responding to signals that modulate appetite, energy expenditure, insulin sensitivity, the endocrine and reproductive systems, bone metabolism, inflammation and immunity. 6 Several findings have converged to indicate that adipocytes share certain properties with immune cells, such as complement activation 7 and proinflammatory cytokine production. 8 Fat cell precursors also share features with macrophages.…”

Section: Introductionmentioning

confidence: 99%

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Leptin in immuno-rheumatological diseases

et al. 2011

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Leptin is one of the most important hormones secreted by adipocytes, with a variety of physiological roles related to the control of metabolism and energy homeostasis. Since its discovery in 1994, leptin has attracted increasing interest in the scientific community for its pleiotropic actions. One of these functions is the relationship between nutritional status and immune competence. It structurally resembles proinflammatory cytokines, such as IL-6 and IL-12. The cytokine-like structural characteristic of leptin is implicative of its function in regulating immune responses. The role of leptin in regulating immune responses has been assessed in vitro as well as in clinical studies. It has been shown that disease conditions of reduced leptin production are associated with increased infection susceptibility. Conversely, immune-mediated disorders, such as autoimmune diseases, are associated with the increased secretion of leptin and the production of proinflammatory pathogenic cytokines. In this paper, we review the most recent advances of the role of leptin in immune-rheumatological diseases, and we discuss whether strategies aimed at modifying leptin levels could represent innovative and therapeutic tools for autoimmune disorders. Keywords: adipokines; autoimmune diseases; leptin; rheumatic diseases INTRODUCTIONThe existence of a factor secreted by white adipose tissue (WAT), which acts to control feeding, weight and WAT mass, was first proposed by Kennedy 1 and is supported by monogenic mutations resulting in obesity. [2][3][4] WAT is composed of adipocytes filled mainly with triacylglycerol and embedded in loose connective tissue containing adipocyte precursors, fibroblasts, immune and other cells. Obesity, the condition that originally motivated the research on WAT, is characterized by low-grade systemic inflammation. It is thought that excess WAT can contribute to the maintenance of obesity through inflammation-inducing lipotoxicity by secreting factors that stimulate the synthesis of inflammatory agents in other organs and by secreting inflammatory agents itself. 5 The current view of WAT states that it is an active contributor to body homeostasis by sending out and responding to signals that modulate appetite, energy expenditure, insulin sensitivity, the endocrine and reproductive systems, bone metabolism, inflammation and immunity. 6 Several findings have converged to indicate that adipocytes share certain properties with immune cells, such as complement activation 7 and proinflammatory cytokine production. 8 Fat cell precursors also share features with macrophages. Numerous genes that code for transcription factors, cytokines, inflammatory signaling molecules, and fatty acid transporters are essential for adipocyte biology and are also expressed and functional in macrophages. 9 Adipose tissue secrets a variety of factors: the term 'adipokine' is generally given to any protein that can be synthesized and secreted by adipocytes. Among these factors, only leptin and adiponectin (and possibly resistin, adipsi...

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Section: Leptin Connective Tissue Diseases and Organ-specific Autoimmentioning

confidence: 97%

Section: Leptin and Autoimmunity M Vadacca Et Al 205mentioning

confidence: 99%

Section: Leptin Connective Tissue Diseases and Organ-specific Autoimmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Leptin in immuno-rheumatological diseases

et al. 2011

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“…The increase in body weight causes limitation of diaphragmatic mobility and reduced back movement, with impaired pulmonary gas exchange and breathing pattern control 710 Moreover, excess adipose tissue is associated with increased inflammatory mediators and cytokines, which could alter the pulmonary airways of these subjects and contribute to the development of bronchial hyperreactivity 11…”

Section: Introductionmentioning

confidence: 99%

Effects of obesity on lung volume and capacity in children and adolescents: a systematic review

Winck

Heinzmann‐Filho

Soares

et al. 2016

Revista Paulista de Pediatria (English Edition)

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Objective:To assess the effects of obesity on lung volume and capacity in children and adolescents.Data source:This is a systematic review, carried out in Pubmed, Lilacs, Scielo and PEDro databases, using the following Keywords: Plethysmography; Whole Body OR Lung Volume Measurements OR Total Lung Capacity OR Functional Residual Capacity OR Residual Volume AND Obesity. Observational studies or clinical trials that assessed the effects of obesity on lung volume and capacity in children and adolescents (0-18 years) without any other associated disease; in English; Portuguese and Spanish languages were selected. Methodological quality was assessed by the Agency for Healthcare Research and Quality.Data synthesis:Of the 1,030 articles, only four were included in the review. The studies amounted to 548 participants, predominantly males, with sample size ranging from 45 to 327 individuals. 100% of the studies evaluated nutritional status through BMI (z-score) and 50.0% reported the data on abdominal circumference. All demonstrated that obesity causes negative effects on lung volume and capacity, causing a reduction mainly in functional residual capacity in 75.0% of the studies; in the expiratory reserve volume in 50.0% and in the residual volume in 25.0%. The methodological quality ranged from moderate to high, with 75.0% of the studies classified as having high methodological quality.Conclusions:Obesity causes deleterious effects on lung volume and capacity in children and adolescents, mainly by reducing functional residual capacity, expiratory reserve volume and residual volume.

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