Effects of pro-inflammatory cytokines and chemokines on leptin production in human adipose tissue in vitro

Bruun, Jens Meldgaard; Pedersen, Steen B.; Kristensen, Kurt; Richelsen, Bjørn

doi:10.1016/s0303-7207(02)00007-2

Cited by 126 publications

(97 citation statements)

References 44 publications

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“…A decrease in leptin secretion has also been reported in humans with other chronic inflammatory illnesses, such as tuberculosis or inflammatory bowel disease (van Crevel et al 2002, Karmiris et al 2006. Furthermore, long-term incubation with cytokines inhibits leptin mRNA and leptin release from adipocytes (Bruun et al 2002). The cause of leptin decrease in arthritic rats can be a combination of two factors: the decrease in adipose mass and chronic inflammation.…”

Section: Discussionmentioning

confidence: 92%

Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis

Martín¹,

Castillero²,

Granado³

et al. 2008

Journal of Endocrinology

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Adjuvant-induced arthritis is a model of rheumatoid arthritis that induces cachexia. In other cachectic situations, there is an increase in lipolysis resulting in a loss of adipose tissue mass. The aim of this work was to analyse the effect of chronic arthritis, induced by adjuvant injection, on white adipose tissue (WAT). For this purpose, rats were killed 10 days after adjuvant injection, when the first external symptoms appeared, on days 15 and 22 when the external signs of the illness reach their severest level. As arthritis decreases food intake, a pair-fed group was also included. Serum concentrations of insulin, leptin, adiponectin, glycerol and nitrites, as well as gene expression of leptin, adiponectin, hormonesensitive lipase (HSL), fatty acid synthase (FAS), tumour necrosis factor a and zinc-a 2 -glycoprotein (ZAG) were determined. Arthritis decreased food intake between days 5 and 16, but not during the last 5 days of the experiment. There was a marked decrease in relative adipose tissue weight and in serum leptin and adiponectin as well as in their gene expression in WAT in arthritic rats. Arthritis decreased the gene expression of FAS in the WAT. However, none of these effects was found in pair-fed rats. Arthritis did not increase lipolysis, since arthritic rats have lower serum concentrations of glycerol, HSL mRNA in WAT, as well as liver ZAG mRNA than the pair-fed or control rats. These data suggest that in chronic arthritis the decrease in white adipose mass is secondary to a reduced adipose lipogenesis, and this effect is not mainly due to the decrease in food intake.

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Section: Discussionmentioning

confidence: 92%

Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis

Martín¹,

Castillero²,

Granado³

et al. 2008

Journal of Endocrinology

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“…These cytokines are also involved in the regulation of metabolism and food intake. For example, TNF-α and IL1-β decrease the production and expression of leptin, an anorexigenic hormone formed in the adipose tissue [32]. Polymorphisms of the genes encoding TNF-α receptor have been associated with leptin-resistance and obesity [33,34].…”

Section: Discussionmentioning

confidence: 99%

Weight gain in relation to plasma levels of complement factor 3: results from a population-based cohort study

et al. 2005

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Aims/hypothesis: Mice that are deficient for complement factor 3 (C3) have shown resistance to weight gain, despite increased food intake. Cross-sectional studies of humans have reported correlations between C3 and obesity. This longitudinal study explored whether C3 predicts a large weight gain in middle-aged men. Methods: Plasma concentrations of C3 and complement factor 4 (C4) were measured in 2,706 non-diabetic healthy men aged between 38 and 50 years, who were re-examined after a mean period of 6.1 years. Results: After adjustments for initial weight, age, height and follow-up time, the odds of incurring large weight gain (75th percentile, ≥3.8 kg) were 1.00 (reference), 0.96 (95% CI:0.7-1.2), 1.1 (CI:0.9-1.5) and 1.4 (CI: 1.1-1.8), respectively, among men with C3 levels in the first, second, third and fourth quartiles (p for trend= 0.01) respectively. This relationship remained significant after further adjustments for lifestyle factors (physical inactivity, alcohol, smoking), metabolic factors (glucose or homeostasis model assessment values, cholesterol, triglycerides), inflammatory markers (fibrinogen, haptoglobin, ceruloplasmin, orosomucoid, α1-antitrypsin) and for C4. C4 was associated with weight gain after adjustments for initial weight, height, follow-up time and lifestyle factors, but not after adjustments for C3. Conclusions/interpretation: C3 is a risk factor for incurring large weight gain in middleaged men.

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“…Obesity, insulin resistance and diabetes mellitus share a chronic, low-grade inflammatory component [4,5,6,7], as reflected by increased expression of proinflammatory cytokines such as TNF-α [8], IL-6 [9], and monocyte chemoattractant protein-1 (MCP-1) [6,7,10,11]. Adipose tissue functions as an endocrine organ that secretes a number of biologically active proteins, including TNF-α [8], IL-6 [6,12], IL-8 [13], C-reactive protein, inducible nitric oxide synthase [6], TGF-β1, plasminogen-activator inhibitor-1 (PAI-1) [14], adiponectin [15], resistin [16], leptin [13,17], macrophage inflammatory protein-1α (MIP-1α) [7,13] and MCP-1 [6,7,10,11,17]. Obesity alters adipose tissue endocrine function and leads to the increased secretion of proinflammatory cytokines (so-called "adipokines"), hormones and fatty acids [6,7,10].…”

Section: Introductionmentioning

confidence: 99%

Association between the A?2518G polymorphism in the monocyte chemoattractant protein-1 gene and insulin resistance and Type 2 diabetes mellitus

et al. 2004

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Aims/hypothesis. The molecular mechanisms of obesity-related insulin resistance are incompletely understood. Macrophages accumulate in adipose tissue of obese individuals. In obesity, monocyte chemoattractant protein-1 (MCP-1), a key chemokine in the process of macrophage accumulation, is overexpressed in adipose tissue. MCP-1 is an insulin-responsive gene that continues to respond to exogenous insulin in insulin-resistant adipocytes and mice. MCP-1 decreases insulin-stimulated glucose uptake into adipocytes. The A-2518G polymorphism in the distal regulatory region of MCP-1 may regulate gene expression. The aim of this study was to investigate the impact of this gene polymorphism on insulin resistance. Methods. We genotyped the Ludwigshafen Risk and Cardiovascular Health (LURIC) cohort (n=3307). Insulin resistance, estimated by homeostasis model assessment, and Type 2 diabetes were diagnosed in 803 and 635 patients respectively. Results. Univariate analysis revealed that plasma MCP-1 levels were significantly and positively correlated with WHR (p=0.011), insulin resistance (p=0.0097) and diabetes (p<0.0001). Presence of the MCP-1 G-2518 allele was associated with decreased plasma MCP-1 (p=0.017), a decreased prevalence of insulin resistance (odds ratio [OR]=0.82, 95% CI: 0.70-0.97, p=0.021) and a decreased prevalence of diabetes (OR=0.80, 95% CI: 0.67-0.96, p=0.014). In multivariate analysis, the G allele retained statistical significance as a negative predictor of insulin resistance (OR=0.78, p=0.0060) and diabetes (OR=0.80, p=0.018). Conclusions/interpretation. In a large cohort of Caucasians, the MCP-1 G-2518 gene variant was significantly and negatively correlated with plasma MCP-1 levels and the prevalence of insulin resistance and Type 2 diabetes. These results add to recent evidence supporting a role for MCP-1 in pathologies associated with hyperinsulinaemia.

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Effects of pro-inflammatory cytokines and chemokines on leptin production in human adipose tissue in vitro

Cited by 126 publications

References 44 publications

Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis

Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis

Weight gain in relation to plasma levels of complement factor 3: results from a population-based cohort study

Association between the A?2518G polymorphism in the monocyte chemoattractant protein-1 gene and insulin resistance and Type 2 diabetes mellitus

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