Interactions between adipose tissue and the immune system in health and malnutrition

Wensveen, Felix M.; Valentić, Sonja; Šestan, Marko; Wensveen, Tamara Turk; Polić, Bojan

doi:10.1016/j.smim.2015.10.006

Cited by 77 publications

(54 citation statements)

References 198 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hypertrophic adipocytes therefore induce expression of stress ligands on their cell membrane, thus activating the local immune system and driving a sterile inflammatory response in adipose tissue[116]. As obesity progresses, adipose tissue inflammation is aggravated, ultimately leading to the release of pro-inflammatory cytokines[116-118]. The increased amount of free fatty acids (FFAs) in circulation, caused by IR, stimulates FFA uptake by the liver, thus contributing to lipid accumulation and inflammation in the liver and development of NAFLD[119].…”

Section: Diabetes Mellitus and Nafldmentioning

confidence: 99%

Nonalcoholic fatty liver disease - A multisystem disease?

Mikolašević

Milić

Wensveen

et al. 2016

WJG

Self Cite

150

155

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) is one of the most common comorbidities associated with overweight and metabolic syndrome (MetS). Importantly, NAFLD is one of its most dangerous complications because it can lead to severe liver pathologies, including fibrosis, cirrhosis and hepatic cellular carcinoma. Given the increasing worldwide prevalence of obesity, NAFLD has become the most common cause of chronic liver disease and therefore is a major global health problem. Currently, NAFLD is predominantly regarded as a hepatic manifestation of MetS. However, accumulating evidence indicates that the effects of NAFLD extend beyond the liver and are negatively associated with a range of chronic diseases, most notably cardiovascular disease (CVD), diabetes mellitus type 2 (T2DM) and chronic kidney disease (CKD). It is becoming increasingly clear that these diseases are the result of the same underlying pathophysiological processes associated with MetS, such as insulin resistance, chronic systemic inflammation and dyslipidemia. As a result, they have been shown to be independent reciprocal risk factors. In addition, recent data have shown that NAFLD actively contributes to aggravation of the pathophysiology of CVD, T2DM, and CKD, as well as several other pathologies. Thus, NAFLD is a direct cause of many chronic diseases associated with MetS, and better detection and treatment of fatty liver disease is therefore urgently needed. As non-invasive screening methods for liver disease become increasingly available, detection and treatment of NAFLD in patients with MetS should therefore be considered by both (sub-) specialists and primary care physicians.

show abstract

Section: Diabetes Mellitus and Nafldmentioning

confidence: 99%

Nonalcoholic fatty liver disease - A multisystem disease?

Mikolašević

Milić

Wensveen

et al. 2016

WJG

Self Cite

150

155

View full text Add to dashboard Cite

show abstract

“…It has become increasingly clear that obesity promotes a chronic inflammatory state, mediated in large part by macrophages, and that this chronic inflammation underlies many of the diseases associated with obesity (24)(25)(26)(27). In lean adipose tissue, adipose tissue macrophages (ATMs) are largely M2 or reparative in nature (28).…”

mentioning

confidence: 99%

The Ron Receptor Tyrosine Kinase Regulates Macrophage Heterogeneity and Plays a Protective Role in Diet-Induced Obesity, Atherosclerosis, and Hepatosteatosis

Allen

Dey

et al. 2016

The Journal of Immunology

View full text Add to dashboard Cite

Obesity is a chronic inflammatory disease mediated in large part by the activation of inflammatory macrophages. This chronic inflammation underlies a whole host of diseases including atherosclerosis, hepatic steatosis, insulin resistance, type 2 diabetes, and cancer, among others. Macrophages are generally classified as either inflammatory or alternatively activated. Some tissue-resident macrophages are derived from yolk sac erythromyeloid progenitors and fetal liver progenitors that seed tissues during embryogenesis and have the ability to repopulate through local proliferation. These macrophages tend to be anti-inflammatory in nature and are generally involved in tissue remodeling, repair, and homeostasis. Alternatively, during chronic inflammation induced by obesity, bone marrow monocyte-derived macrophages are recruited to inflamed tissues, where they produce proinflammatory cytokines and exacerbate inflammation. The extent to which these two populations of macrophages are plastic in their phenotype remains controversial. We have demonstrated previously that the Ron receptor tyrosine kinase is expressed on tissue-resident macrophages, where it limits inflammatory macrophage activation and promotes a repair phenotype. In this study, we demonstrate that Ron is expressed in a subpopulation of macrophages during chronic inflammation induced by obesity that exhibit a repair phenotype as determined by the expression of arginase 1. In addition, we demonstrate that the Ron receptor plays a protective role in the progression of diet-induced obesity, hepatosteatosis, and atherosclerosis. These results suggest that altering macrophage heterogeneity in vivo could have the potential to alleviate obesity-associated diseases.

show abstract

“…In addition, the immune system plays a key role in the development of diet‐induced metabolic disease, such as DM2 and non‐alcoholic fatty liver disease . Obesity is commonly associated with insulin resistance which can progress towards DM2 .…”

Section: Immune–endocrine Interactions In Absence Of Infectionmentioning

confidence: 99%

‘Beauty and the beast’ in infection: How immune–endocrine interactions regulate systemic metabolism in the context of infection

et al. 2019

Self Cite

View full text Add to dashboard Cite

The immune and endocrine systems ensure two vital functions in the body. The immune system protects us from lethal pathogens, whereas the endocrine system ensures proper metabolic function of peripheral organs by regulating systemic homeostasis. These two systems were long thought to operate independently. The immune system uses cytokines and immune receptors, whereas the endocrine system uses hormones to regulate metabolism. However, recent findings show that the immune and endocrine systems closely interact, especially regarding regulation of glucose metabolism. In response to pathogen encounter, cytokines modify responsiveness of peripheral organs to endocrine signals, resulting in altered levels of blood hormones such as insulin, which promotes the ability of the body to fight infection. Here we provide an overview of recent literature describing various mechanisms, which the immune system utilizes to modify endocrine regulation of systemic metabolism. Moreover, we will describe how these immuneendocrine interactions derail in the context of obesity. From a clinical perspective we will elaborate how infection and obesity aggravate the development of metabolic diseases such as diabetes mellitus type 2 in humans. In summary, this review provides a comprehensive overview of immune-induced changes in systemic metabolism following infection, with a focus on regulation of glucose metabolism.Keywords: diabetes r glucose r infection r insulin resistance r metabolic disease P. A., Lordan, J. L. et al., Ceramide is increased in the lower airway epithelium of people with advanced cystic fibrosis lung disease. Am. J.

show abstract

Interactions between adipose tissue and the immune system in health and malnutrition

Cited by 77 publications

References 198 publications

Nonalcoholic fatty liver disease - A multisystem disease?

Nonalcoholic fatty liver disease - A multisystem disease?

The Ron Receptor Tyrosine Kinase Regulates Macrophage Heterogeneity and Plays a Protective Role in Diet-Induced Obesity, Atherosclerosis, and Hepatosteatosis

‘Beauty and the beast’ in infection: How immune–endocrine interactions regulate systemic metabolism in the context of infection

Contact Info

Product

Resources

About