IL-1β mediates leptin induction during inflammation

1998 ◽  
Vol 274 (1) ◽  
pp. R204-R208 ◽  
Author(s):  
Raffaella Faggioni ◽  
Giamila Fantuzzi ◽  
John Fuller ◽  
Charles A. Dinarello ◽  
Kenneth R. Feingold ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Host Response ◽  
Tumor Necrosis ◽  
Local Inflammation ◽  
Protein Levels ◽  
Infection And Inflammation ◽  
Leptin Expression ◽  
Necrosis Factor

Interleukins (IL) are key mediators of the host response to infection and inflammation. Leptin is secreted by adipose tissue and plays an important role in the control of food intake. Administration of lipopolysaccharide (LPS), tumor necrosis factor (TNF), or IL-1 acutely increases leptin mRNA and protein levels. To investigate the role of IL-1β and IL-6 in leptin expression during inflammation, we used IL-1β-deficient (−/−) and IL-6 −/− mice. Mice were injected intraperitoneally with LPS or subcutaneously with turpentine, as models of systemic or local inflammation, respectively. In IL-1β +/+ mice, both LPS and turpentine increased leptin mRNA and circulating leptin. In contrast, neither LPS nor turpentine increased leptin levels in IL-1β −/− mice. In IL-6 +/+ or IL-6 −/− mice, turpentine increased leptin protein to comparable levels. We conclude that IL-1β is essential for leptin induction by both LPS and turpentine in mice, but IL-6 is not.

scholarly journals TNFRSF14 deficiency protects against ovariectomy-induced adipose tissue inflammation

2014 ◽  
Vol 220 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Eun-Kyung Choi ◽  
Woon-Ki Kim ◽  
Ok-Joo Sul ◽  
Yun-Kyung Park ◽  
Eun-Sook Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Adipose Tissue ◽  
Tumor Necrosis ◽  
Ovarian Function ◽  
Tumor Necrosis Factor Receptor ◽  
Oxygen Species ◽  
Adipose Tissue Inflammation ◽  
Metabolic Perturbation ◽  
Necrosis Factor

To elucidate the role of tumor necrosis factor receptor superfamily member 14 (TNFRSF14) in metabolic disturbance due to loss of ovarian function, ovariectomy (OVX) was performed in TNFRSF 14-knockout mice. OVX increased fat mass and infiltration of highly inflammatory CD11c cells in the adipose tissue (AT), which was analyzed by flow cytometry, and resulted in disturbance of glucose metabolism, whereas TNFRSF14 deficiency attenuated these effects. TNFRSF14 deficiency decreased recruitment of CD11c-expressing cells in AT and reduced the polarization of bone marrow-derived macrophages to M1. Upon engagement of LIGHT, a TNFRSF14 ligand, TNFRSF14 enhanced the expression of CD11c via generation of reactive oxygen species, suggesting a role of TNFRSF14 as a redox modulator. TNFRSF14 participated in OVX-induced AT inflammation via upregulation of CD11c, resulting in metabolic perturbation. TNFRSF14 could be used as a therapeutic target for the treatment of postmenopausal syndrome by reducing AT inflammation.

scholarly journals Systemic Inflammation, Adipose Tissue Tumor Necrosis Factor, and Leptin Expression

2003 ◽  
Vol 11 (4) ◽  
pp. 525-531 ◽  
Author(s):  
Monica Bulló ◽  
Pilar García-Lorda ◽  
Isabel Megias ◽  
Jordi Salas-Salvadó
Keyword(s):  
Adipose Tissue ◽  
Tumor Necrosis Factor ◽  
Systemic Inflammation ◽  
Tumor Necrosis ◽  
Tissue Tumor ◽  
Leptin Expression ◽  
Necrosis Factor

LPS-induced anorexia in leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) mice

1997 ◽  
Vol 273 (1) ◽  
pp. R181-R186 ◽  
Author(s):  
R. Faggioni ◽  
J. Fuller ◽  
A. Moser ◽  
K. R. Feingold ◽  
C. Grunfeld
Keyword(s):  
Food Intake ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Leptin Receptor ◽  
Per Se ◽  
Necrosis Factor

Administration of endotoxin (lipopolysaccharide, LPS) induces profound anorexia. Injection of leptin decreases food intake in mice. Recently, we reported that LPS and cytokines increase leptin levels in hamsters. To further investigate the role of leptin in the LPS-induced anorexia, we administered LPS to leptin receptor-deficient (db/db) and leptin-deficient (ob/ob) mice. We found that LPS caused anorexia in both db/db and ob/ob mice. As might be predicted if leptin had a role in anorexia, the db/db mice were somewhat resistant to LPS-induced anorexia. However the ob/ob mice were more sensitive to LPS-induced anorexia. No differences between db/db and ob/ob mice and their respective littermate were observed in circulating tumor necrosis factor levels after LPS. These data suggest that leptin per se is not essential for LPS-induced anorexia.

scholarly journals Endogenous brain IL-1 mediates LPS-induced anorexia and hypothalamic cytokine expression

2000 ◽  
Vol 279 (1) ◽  
pp. R93-R98 ◽  
Author(s):  
Sophie Layé ◽  
Gilles Gheusi ◽  
Sandrine Cremona ◽  
Chantal Combe ◽  
Keith Kelley ◽  
...  
Keyword(s):  
Food Intake ◽  
Plasma Levels ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Intraperitoneal Administration ◽  
Cytokine Mrna ◽  
Enhanced Expression ◽  
Factor Α ◽  
Necrosis Factor

The present study was designed to determine the role of endogenous brain interleukin (IL)-1 in the anorexic response to lipopolysaccharide (LPS). Intraperitoneal administration of LPS (5–10 μg/mouse) induced a dramatic, but transient, decrease in food intake, associated with an enhanced expression of proinflammatory cytokine mRNA (IL-1β, IL-6, and tumor necrosis factor-α) in the hypothalamus. This dose of LPS also increased plasma levels of IL-1β. Intracerebroventricular pretreatment with IL-1 receptor antagonist (4 μg/mouse) attenuated LPS-induced depression of food intake and totally blocked the LPS-induced enhanced expression of proinflammatory cytokine mRNA measured in the hypothalamus 1 h after treatment. In contrast, LPS-induced increases in plasma levels of IL-1β were not altered. These findings indicate that endogenous brain IL-1 plays a pivotal role in the development of the hypothalamic cytokine response to a systemic inflammatory stimulus.

TNF-α tolerance blocks LPS-induced hypophagia but LPS tolerance fails to prevent TNF-α-induced hypophagia

1998 ◽  
Vol 274 (3) ◽  
pp. R741-R745 ◽  
Author(s):  
M. H. Porter ◽  
M. Arnold ◽  
W. Langhans
Keyword(s):  
Food Intake ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Male Rats ◽  
Cross Tolerance ◽  
Dark Cycle ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

To investigate the role of tumor necrosis factor-α (TNF-α) in bacterial lipopolysaccharide (LPS)-induced hypophagia, we tested whether a cross tolerance between LPS and TNF-α exists with respect to their anorectic effects. Only the first of three subsequent intraperitoneal injections of LPS (100 μg/kg body wt) given every second day at dark onset (12:12-h light-dark cycle) led to a significant reduction of food intake in male rats. Likewise, intraperitoneal injections of human recombinant TNF-α (150 μg ≥ 3 × 106U/kg body wt) also resulted in tolerance to its hypophagic effect. LPS tolerance did not alter the hypophagic response to subsequently injected TNF-α ( n = 14). However, TNF-α pretreatment completely blocked the hypophagic response to LPS ( n = 14). The results demonstrate that tolerance to the hypophagic effect of exogenous TNF-α is sufficient to eliminate LPS-induced hypophagia. This is consistent with the hypothesis that endogenous TNF-α plays a major role in LPS-induced hypophagia. The ineffectiveness of LPS tolerance to attenuate TNF-α-induced hypophagia is compatible with findings demonstrating that reduced TNF-α production is an important feature of LPS tolerance.

scholarly journals Estrogen as a Contributing Factor to the Development of Lipedema

2021 ◽  
Author(s):  
Sara Al-Ghadban ◽  
Mary L. Teeler ◽  
Bruce A. Bunnell
Keyword(s):  
Estrogen Receptor ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Food Intake ◽  
Estrogen Receptor Alpha ◽  
Hormonal Change ◽  
Increase Insulin Sensitivity ◽  
Diet And Exercise ◽  
Leptin Expression

Lipedema is an underdiagnosed painful adipose tissue disorder that occurs almost exclusively in women, with onset manifesting at puberty or at times of hormonal change. Unlike many fat disorders, diet and exercise have little to no impact on the prevention or progression of this disease. Estrogens control the distribution of body fat and food intake, regulate leptin expression, increase insulin sensitivity, and reduce inflammation through signaling pathways mediated by its receptors, estrogen receptor alpha (ERα) and ERβ. This review will focus on understanding the role of estrogen in the pathogenesis of the disease and envisage potential hormonal therapy for lipedema patients.

Paradoxical role of tumor necrosis factor on metabolic dysfunction and adipose tissue expansion in mice

Nutrition ◽  
2018 ◽  
Vol 50 ◽  
pp. 1-7 ◽  
Author(s):  
Laís Bhering Martins ◽  
Marina Chaves de Oliveira ◽  
Zélia Menezes-Garcia ◽  
Débora Fernandes Rodrigues ◽  
Jaqueline Pereira Lana ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tissue Expansion ◽  
Metabolic Dysfunction ◽  
Necrosis Factor
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