T-lymphocyte Infiltration in Visceral Adipose Tissue

Kintscher, Ulrich; Hartge, Martin; Heß, Katharina; Foryst‐Ludwig, Anna; Clemenz, Markus; Wabitsch, Martin; Fischer‐Posovszky, Pamela; Barth, Thomas F.E.; Dragun, Duska; Skurk, Thomas; Hauner, Hans; Blüher, Matthias; Unger, Thomas; Wolf, Anna-Maria; Knippschild, Uwe; Hombach, Vinzenz; Marx, Nikolaus

doi:10.1161/atvbaha.108.165100

Cited by 597 publications

(335 citation statements)

References 23 publications

Supporting

Mentioning

315

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, RANTES and CCR5 expression were significantly higher in the visceral adipose depot that correlated positively with T-cell CD3 and macrophage CD11b VAT expression (71,72) . T-cell accumulation may be a primary event in adipose tissue inflammation (74) . Immunohistochemical staining and mRNA analysis demonstrated CD3 + T-cells were present in the adipose tissue after just 5 weeks of high-fat feeding.…”

Section: Adipose Tissue T-cells Infiltration and Dietary Fatmentioning

confidence: 99%

Fats, inflammation and insulin resistance: insights to the role of macrophage and T-cell accumulation in adipose tissue

et al. 2011

View full text Add to dashboard Cite

High-fat diet-induced obesity is associated with a chronic state of low-grade inflammation, which pre-disposes to insulin resistance (IR), which can subsequently lead to type 2 diabetes mellitus. Macrophages represent a heterogeneous population of cells that are instrumental in initiating the innate immune response. Recent studies have shown that macrophages are key mediators of obesity-induced IR, with a progressive infiltration of macrophages into obese adipose tissue. These adipose tissue macrophages are referred to as classically activated (M1) macrophages. They release cytokines such as IL-1β, IL-6 and TNFα creating a pro-inflammatory environment that blocks adipocyte insulin action, contributing to the development of IR and type 2 diabetes mellitus. In lean individuals macrophages are in an alternatively activated (M2) state. M2 macrophages are involved in wound healing and immunoregulation. Wound-healing macrophages play a major role in tissue repair and homoeostasis, while immunoregulatory macrophages produce IL-10, an anti-inflammatory cytokine, which may protect against inflammation. The functional role of T-cell accumulation has recently been characterised in adipose tissue. Cytotoxic T-cells are effector T-cells and have been implicated in macrophage differentiation, activation and migration. Infiltration of cytotoxic T-cells into obese adipose tissue is thought to precede macrophage accumulation. T-cell-derived cytokines such as interferon γ promote the recruitment and activation of M1 macrophages augmenting adipose tissue inflammation and IR. Manipulating adipose tissue macrophages/T-cell activity and accumulation in vivo through dietary fat modification may attenuate adipose tissue inflammation, representing a therapeutic target for ameliorating obesity-induced IR.

show abstract

Section: Adipose Tissue T-cells Infiltration and Dietary Fatmentioning

confidence: 99%

Fats, inflammation and insulin resistance: insights to the role of macrophage and T-cell accumulation in adipose tissue

et al. 2011

View full text Add to dashboard Cite

show abstract

“…A prominent characteristic of diabetes-promoting lifestyle change is weight gain. Since the first reports of local inflammation in obese adipose tissue in 2003 [51,52] it has become clear that fat tissue with hypertrophic adipocytes often gives rise to the influx and activation of immune cells, mostly macrophages but also of T cells [53]. This is more pronounced in visceral, hepatic and epicardial than in subcutaneous fat [54].…”

Section: Excess Nutrients/obesitymentioning

confidence: 99%

The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation

Kolb¹,

2009

View full text Add to dashboard Cite

The recent major increase in the global incidence of type 2 diabetes suggests that most cases of this disease are caused by changes in environment and lifestyle. All major risk factors for type 2 diabetes (overnutrition, low dietary fibre, sedentary lifestyle, sleep deprivation and depression) have been found to induce local or systemic low-grade inflammation that is usually transient or milder in individuals not at risk for type 2 diabetes. By contrast, inflammatory responses to lifestyle factors are more pronounced and prolonged in individuals at risk of type 2 diabetes and appear to occur also in the pancreatic islets. Chronic low-grade inflammation will eventually lead to overt diabetes if counter-regulatory circuits to inflammation and metabolic stress are compromised because of a genetic and/or epigenetic predisposition. Hence, it is not the lifestyle change per se but a deficient counter-regulatory response in predisposed individuals which is crucial to disease pathogenesis. Novel approaches of intervention may target these deficient defence mechanisms.

show abstract

“…This syndrome has attracted much attention, because it seems to be caused by an excess of nutrients (Kimokoti and Brown 2011). Most of these studies focused on the physiology and underlying molecular mechanisms in liver (Kreeft et al 2005;Akagiri et al 2008), skeletal muscle (Anderson et al 2008) and adipose tissue (Akagiri et al 2008;Kintscher et al 2008), as these organs are targets of insulin-modulated metabolism. However, increasing evidence links the intake of a HF diet (HFD) to gut local inflammatory events, being gut the first organ to be exposed to dietary components.…”

Section: Introductionmentioning

confidence: 99%

The nutrigenomic investigation of C57BL/6N mice fed a short-term high-fat diet highlights early changes in clock genes expression

et al. 2013

View full text Add to dashboard Cite

Mice fed long-term high-fat diets (HFD) are an established model for human metabolic disorders, such as obesity and diabetes. However, also the effects of shortterm HFD feeding should be investigated to understand which are the first events that trigger the onset of a predisease condition, the so-called metabolic syndrome, that increases the risk of developing clinical diseases. In this study, C57BL/6N mice were fed a control diet (CTR) or a HFD for 1 (T1) or 2 weeks (T2). Metabolic and histological effects were examined. Cecum transcriptomes of HFD and CTR mice were compared at T2 by microarray analysis. Differentially expressed genes were validated by real-time PCR in the cecum and in the liver. After 2 weeks of diet administration, HFD mice showed an altered expression pattern in only seven genes, four of which are involved in the circadian clock regulatory pathway. Real-time PCR confirmed microarray results of the cecum and revealed the same trend of clock gene expression changes in the liver. These findings suggest that clock genes may play an important role in early controlling gut output systems in response to HFD in mice and that their expression change may also represent an early signaling of the development of an intestinal pro-inflammatory status.

show abstract

T-lymphocyte Infiltration in Visceral Adipose Tissue

Cited by 597 publications

References 23 publications

Fats, inflammation and insulin resistance: insights to the role of macrophage and T-cell accumulation in adipose tissue

Fats, inflammation and insulin resistance: insights to the role of macrophage and T-cell accumulation in adipose tissue

The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation

The nutrigenomic investigation of C57BL/6N mice fed a short-term high-fat diet highlights early changes in clock genes expression

Contact Info

Product

Resources

About