Interleukin-6 and obesity

El-Kadre, Luciana; Tinoco, Augusto

doi:10.1097/mco.0b013e32836410e6

Cited by 17 publications

(12 citation statements)

References 30 publications

(31 reference statements)

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“…The pro-inflammatory function of IL6 has been challenged by the observations that mice with null deletion of this cytokine develop obesity, systemic insulin resistance, hepatosteatosis and hepatic inflammation [63,64], and that this cytokine can acutely exert an anti-inflammatory action in skeletal muscle during exercise. As surmised by several studies and reviewed recently [65], IL6 can exert differential site-and cell-specific inflammatory effect.…”

Section: Recruitment Of Macrophages and Other Inflammatory Cells To Amentioning

confidence: 97%

“…In addition to macrophages, IL6 could be released from B cells, as part of the adaptive immune response [198], to induce differentiation of hepatic stellate cells to myofibroblasts and mediate hepatic fibrosis in response to CCl4 in mice, independently of T-cell or antibody stimulation [199]. However, the pro-inflammatory effect of IL6 has been challenged by the observations that it can also play an anti-inflammatory role [65]. For instance, some studies show that IL6 exerts a protective mechanism against liver fibrosis by promoting hepatocyte regeneration and proliferation [200], and preventing oxidative stress and mitochondrial dysfunction [201].…”

Section: Il-6mentioning

confidence: 99%

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CEACAM1 loss links inflammation to insulin resistance in obesity and non-alcoholic steatohepatitis (NASH)

Najjar

Russo

2013

Semin Immunopathol

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Mounting epidemiological evidence points to an association between metabolic syndrome and non-alcoholic steatohepatitis (NASH), an increasingly recognized new epidemic. NASH pathologies include hepatocellular ballooning, lobular inflammation, hepatocellular injury, apoptosis and hepatic fibrosis. We will review the relationship between insulin resistance and inflammation in visceral obesity and NASH in an attempt to shed more light on the pathogenesis of these major metabolic diseases. Moreover, we will identify loss of the Carcinoembryonic antigen-related cell adhesion molecule 1 as a unifying mechanism linking the immunological and metabolic abnormalities in NASH.

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Section: Recruitment Of Macrophages and Other Inflammatory Cells To Amentioning

confidence: 97%

Section: Il-6mentioning

confidence: 99%

CEACAM1 loss links inflammation to insulin resistance in obesity and non-alcoholic steatohepatitis (NASH)

Najjar

Russo

2013

Semin Immunopathol

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“…Consequently, choline and PC homeostasis not only impact on liver metabolism, but also affect extrahepatic, clinically important parameters in CF: the lungs are compromised by chronic inflammation, even in the absence of bacterial or viral infection [33]. The release of IL-6 induces the formation of acute phase proteins by the liver, and is involved in the cross-talk between organs during inflammatory processes including lungs and liver [34,35,36]. The C20:4 and C22:6 moieties of plasma PC are important precursors of prostaglandins, leucotrienes and resolvins, being involved in inflammation and organ integrity [37].…”

Section: Discussionmentioning

confidence: 99%

Plasma Phosphatidylcholine Alterations in Cystic Fibrosis Patients: Impaired Metabolism and Correlation with Lung Function and Inflammation

Grothe

Riethmüller²,

Tschürtz³

et al. 2015

Cell Physiol Biochem

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Background: Liver impairment, ranging from steatosis to cirrhosis, is frequent in cystic fibrosis (CF) patients and is becoming increasingly significant due to their improved life expectancy. One aspect of hepatic alterations is caused by increased fecal loss of the essential nutrient choline, following enterohepatic bile phosphatidylcholine (PC) cycle impairment. Hepatic PC synthesis, both de novo and via phosphatidylethanolamine-N-methyl-transferase (PEMT), is essential for very low-density lipoprotein (VLDL) secretion. VLDL-PC in particular contributes to the organism's supply with polyunsaturated fatty acids (LC-PUFA), namely arachidonic (C20:4) and docosahexaenoic acid (C22:6). Consequently, choline deprivation and altered hepatic PC metabolism may affect plasma PC homeostasis and extrahepatic organ function. Objectives: To investigate relationships between altered plasma choline and PC homeostasis and markers of lung function and inflammation in CF. To assess alterations in hepatic choline and PC metabolism of CF patients. Design: Quantification of plasma/serum choline and PC species in adult CF patients compared to controls. Correlation of PC with forced expiratory vital capacity (FEV₁) and interleukin 6 (IL-6) concentrations. Analysis of choline and PC metabolism in CF compared to controls, using deuterated choline ([D₉-methyl]-choline) labeling in vivo. Results: Mean choline and PC concentrations in CF patients were lower than in controls. Choline and PC concentrations as well as fractions of C22:6-PC and C20:4-PC correlated directly with FEV₁, but inversely with IL-6. Plasma concentrations of deuterated PC were decreased for both pathways, whereas only in PC synthesized via PEMT precursor enrichment was decreased. Conclusion: In CF patients, hepatic and plasma homeostasis of choline and PC correlate with lung function and inflammation. Impaired hepatic PC metabolism, exemplarily shown in three CF patients, provides an explanation for such correlations. Larger studies are required to understand the link between hepatic PC metabolism and overall clinical performance of CF patients, and the perspective of choline substitution of these patients.

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“…Specifically, higher IL-6 was related to poorer insulin sensitivity with a P value of 0.05 in bivariate analyses and a trend towards statistical significance in a multi-variable model. In persons without systemic inflammatory disease, IL-6 has shown a complex relationship with insulin sensitivity (25). Acutely, increases in IL-6 associated with exercise have been shown to improve insulin sensitivity, but chronic elevations appear to worsen insulin sensitivity (25).…”

Section: Discussionmentioning

confidence: 99%

“…In persons without systemic inflammatory disease, IL-6 has shown a complex relationship with insulin sensitivity (25). Acutely, increases in IL-6 associated with exercise have been shown to improve insulin sensitivity, but chronic elevations appear to worsen insulin sensitivity (25). Here, in persons with elevated systemic concentrations of IL-6, this cytokine was related to poorer insulin sensitivity in contrast to other disease-related variables.…”

Section: Discussionmentioning

confidence: 99%

Adipose Depots, Not Disease-related Factors, Account for Skeletal Muscle Insulin Sensitivity in Established and Treated Rheumatoid Arthritis

AbouAssi

Tune

Gilmore³

et al. 2014

J Rheumatol

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Objectives In prior reports, individuals with rheumatoid arthritis (RA) exhibited increased insulin resistance. However, these studies were limited by either suboptimal assessment methods for insulin sensitivity or a failure to account for important determinants, adiposity and physical activity. Our objectives were to carefully assess, compare and determine predictors of skeletal muscle insulin sensitivity (SI) in RA, accounting for adiposity and physical activity. Methods Thirty-nine individuals with established (seropositive or erosions) and treated RA and 39 age, gender, race, BMI, and physical activity-matched controls underwent a frequently-sampled intravenous glucose tolerance test to determine SI. Inflammation, body composition, and physical activity were assessed with systemic cytokine measurements, CT scans, and accelerometry, respectively. Exclusions were diabetes, cardiovascular disease, medication changes within three months, and prednisone use over 5 mg/d. This investigation was powered to detect a clinically significant, moderate effect size for SI difference. Results Despite elevated systemic inflammation (interleukin (IL)-6, IL-18, tumor necrosis factor-alpha; P<0.05 for all), persons with RA were not less insulin sensitive (SI geometric mean (SD): RA 4.0 (2.4) versus Control 4.9 (2.1)*10−5 min−1/[pmol/l]; P=0.39). Except for visceral adiposity being slightly greater in controls (P=0.03), there were no differences in body composition or physical activity. Lower SI was independently associated with increased abdominal and thigh adiposity, but not with cytokines, disease activity, duration, disability, or disease modifying medication use. Conclusions In established and treated RA, traditional risk factors, specifically excess adiposity, play more of a role in predicting skeletal muscle insulin sensitivity than systemic inflammation or other disease-related factors.

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Interleukin-6 and obesity

Cited by 17 publications

References 30 publications

CEACAM1 loss links inflammation to insulin resistance in obesity and non-alcoholic steatohepatitis (NASH)

CEACAM1 loss links inflammation to insulin resistance in obesity and non-alcoholic steatohepatitis (NASH)

Plasma Phosphatidylcholine Alterations in Cystic Fibrosis Patients: Impaired Metabolism and Correlation with Lung Function and Inflammation

Adipose Depots, Not Disease-related Factors, Account for Skeletal Muscle Insulin Sensitivity in Established and Treated Rheumatoid Arthritis

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