scholarly journals Circulating glucagon is associated with inflammatory mediators in metabolically compromised subjects

2011 ◽  
Vol 165 (4) ◽  
pp. 639-645 ◽  
Author(s):  
Francisco J Ortega ◽  
José M Moreno-Navarrete ◽  
Mónica Sabater ◽  
Wifredo Ricart ◽  
Gema Frühbeck ◽  
...  
Keyword(s):  
Weight Loss ◽  
Glucose Tolerance ◽  
Acute Phase ◽  
Low Grade ◽  
Complement Factor ◽  
Acute Phase Reactants ◽  
Cross Sectional ◽  
Altered Glucose ◽  
Obese Subjects ◽  
Low Grade Inflammation

BackgroundAcute phase mediators promote metabolic changes by modifying circulating hormones. However, there is virtually no data about the link between glucagon and inflammatory parameters in obesity-related chronic low-grade inflammation.Study designWe performed both cross-sectional and longitudinal (diet-induced weight loss) studies.MethodsCirculating glucagon concentrations (ELISA), parameters of glucose and lipid metabolism, interleukin 6 (IL6), and complement factor B (CFB) were analyzed in 316 subjects (250 men and 66 women). The effects of weight loss were investigated in an independent cohort of 20 subjects.ResultsCirculating glucagon significantly correlated with glucose (r=0.407,P<0.0001), HbAlc (r=0.426,P<0.0001), fasting triglycerides (r=0.356,P=0.001), and parameters of innate immune response system such as IL6 (r=0.342,P=0.050) and CFB (r=0.404,P=0.002) in obese subjects with altered glucose tolerance, but not in individuals with normal glucose tolerance (NGT). In obese and NGT subjects, glucagon was associated with fasting triglycerides (r=0.475,P=0.003) and CFB (r=0.624,P=0.001). In obese subjects, glucagon (P=0.019) and CFB (P=0.002) independently contributed to 26% of fasting triglyceride variance (P<0.0001) after controlling for the effects of age and fasting serum glucose concentration in multiple lineal regression models. Moreover, concomitant with fat mass, fasting triglycerides, and CFB, weight loss led to significantly decreased circulating glucagon (−23.1%,P=0.004).ConclusionsAccording to the current results, acute phase reactants such as IL6 and CFB are associated with fasting glucagon in metabolically compromised subjects. This suggests that glucagon may be behind the association between inflammatory and metabolic parameters in obesity-associated chronic low-grade inflammation.

Lysozyme is a component of the innate immune system linked to obesity associated-chronic low-grade inflammation and altered glucose tolerance

2020 ◽  
Author(s):  
José María Moreno-Navarrete ◽  
Jèssica Latorre ◽  
Aina Lluch ◽  
Francisco J. Ortega ◽  
Ferran Comas ◽  
...  
Keyword(s):  
Immune System ◽  
Glucose Tolerance ◽  
Innate Immune System ◽  
Innate Immune ◽  
Low Grade ◽  
Altered Glucose ◽  
Low Grade Inflammation

scholarly journals Obesity and Low-Grade Inflammation Increase Plasma Follistatin-Like 3 in Humans

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Claus Brandt ◽  
Maria Pedersen ◽  
Anders Rinnov ◽  
Anne S. Andreasen ◽  
Kirsten Møller ◽  
...  
Keyword(s):  
Fat Mass ◽  
Cross Sectional Study ◽  
Low Grade ◽  
Cross Sectional ◽  
Obese Subjects ◽  
Plasma Leptin ◽  
Low Grade Inflammation ◽  
Diabetes And Obesity

Background. Rodent models suggest that follistatin-like 3 (fstl3) is associated with diabetes and obesity. In humans, plasma fstl3 is reduced with gestational diabetes.In vitro, TNF-αinduces fstl3 secretion, which suggests a link to inflammation.Objective. To elucidate the association between plasma fstl3 and obesity, insulin resistance, and low-grade inflammation in humans.Study Design. Plasma fstl3 levels were determined in a cross-sectional study including three groups: patients with type 2 diabetes, impaired glucose tolerance, and healthy controls. In addition, lipopolysaccharide (LPS), TNF-α, or interleukin-6 (IL-6) as well as a hyperinsulinemic euglycemic clamp were used to examine if plasma fstl3 was acutely regulated in humans.Results. Plasma fstl3 was increased in obese subjects independent of glycemic state. Moreover, plasma fstl3 was positively correlated with fat mass, plasma leptin, fasting insulin, and HOMA B and negatively with HOMA S. Furthermore plasma fstl3 correlated positively with plasma TNF-αand IL-6 levels. Infusion of LPS and TNF-α, but not IL-6 and insulin, increased plasma fstl3 in humans.Conclusion. Plasma fstl3 is increased in obese subjects and associated with fat mass and low-grade inflammation. Furthermore, TNF-αincreased plasma fstl3, suggesting that TNF-αis one of the inflammatory drivers of increased systemic levels of fstl3.

scholarly journals Decreased TLR3 in Hyperplastic Adipose Tissue, Blood and Inflamed Adipocytes is Related to Metabolic Inflammation

2018 ◽  
Vol 51 (3) ◽  
pp. 1051-1068 ◽  
Author(s):  
Jèssica Latorre ◽  
José M. Moreno-Navarrete ◽  
Mónica Sabater ◽  
Maria Buxo ◽  
José I. Rodriguez-Hermosa ◽  
...  
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Inflammation ◽  
Fat Depots ◽  
Acute Surgery ◽  
Obese Subjects ◽  
Anti Inflammatory ◽  
The Impact

Background/Aims: Obesity is characterized by the immune activation that eventually dampens insulin sensitivity and changes metabolism. This study explores the impact of different inflammatory/ anti-inflammatory paradigms on the expression of toll-like receptors (TLR) found in adipocyte cultures, adipose tissue, and blood. Methods: We evaluated by real time PCR the impact of acute surgery stress in vivo (adipose tissue) and macrophages (MCM) in vitro (adipocytes). Weight loss was chosen as an anti-inflammatory model, so TLR were analyzed in fat samples collected before and after bariatric surgery-induced weight loss. Associations with inflammatory and metabolic parameters were analyzed in non-obese and obese subjects, in parallel with gene expression measures taken in blood and isolated adipocytes/ stromal-vascular cells (SVC). Treatments with an agonist of TLR3 were conducted in human adipocyte cultures under normal conditions and upon conditions that simulated the chronic low-grade inflammatory state of obesity. Results: Surgery stress raised TLR1 and TLR8 in subcutaneous (SAT), and TLR2 in SAT and visceral (VAT) adipose tissue, while decreasing VAT TLR3 and TLR4. MCM led to increased TLR2 and diminished TLR3, TLR4, and TLR5 expressions in human adipocytes. The anti-inflammatory impact of weight loss was concomitant with decreased TLR1, TLR3, and TLR8 in SAT. Cross-sectional associations confirmed increased V/ SAT TLR1 and TLR8, and decreased TLR3 in obese patients, as compared with non-obese subjects. As expected, TLR were predominant in SVC and adipocyte precursor cells, even though expression of all of them but TLR8 (very low levels) was also found in ex vivo isolated and in vitro differentiated adipocytes. Among SVC, CD14+ macrophages showed increased TLR1, TLR2, and TLR7, but decreased TLR3 mRNA. The opposite patterns shown for TLR2 and TLR3 in V/ SAT, SVC, and inflamed adipocytes were observed in blood as well, being TLR3 more likely linked to lymphocyte instead of neutrophil counts. On the other hand, decreased TLR3 in adipocytes challenged with MCM dampened lipogenesis and the inflammatory response to Poly(I:C). Conclusion: Functional variations in the expression of TLR found in blood and hypertrophied fat depots, namely decreased TLR3 in lymphocytes and inflamed adipocytes, are linked to metabolic inflammation.

scholarly journals Serum and urinary concentrations of calprotectin as markers of insulin resistance and type 2 diabetes

2012 ◽  
Vol 167 (4) ◽  
pp. 569-578 ◽  
Author(s):  
Francisco J Ortega ◽  
Mónica Sabater ◽  
José M Moreno-Navarrete ◽  
Neus Pueyo ◽  
Patricia Botas ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Weight Loss ◽  
Lipid Metabolism ◽  
Inflammatory Markers ◽  
Low Grade ◽  
Model Assessment ◽  
Glucose And Lipid Metabolism ◽  
Obese Subjects

ObjectiveIncreased circulating calprotectin has been reported in obese subjects but not in association with measures of insulin resistance and type 2 diabetes (T2D). The main aim of this study was to determine whether calprotectins in plasma and urine are associated with insulin resistance.DesignWe performed both cross-sectional and longitudinal (diet-induced weight loss) studies.MethodsCirculating calprotectin concentrations (ELISA), other inflammatory markers, homeostasis model assessment of insulin resistance (HOMA-IR), and parameters of glucose and lipid metabolism were evaluated in 298 subjects (185 with normal (NGT) and 62 with impaired (IGT) glucose tolerance and 51 T2D subjects). Calprotectin was also evaluated in urine samples from 71 participants (50 NGT and 21 subjects with IGT). Insulin sensitivity (SI, Minimal Model) was determined in a subset of 156 subjects, and the effects of weight loss were investigated in an independent cohort of obese subjects (n=19).ResultsCirculating calprotectin was significantly increased in IGT–T2D (independently of BMI) and positively associated with HOMA-IR, obesity measures, inflammatory markers, and parameters of glucose and lipid metabolism. Similar findings were reported for calprotectin concentrations in urine. In the subset of subjects, the association of calprotectin withSIwas independent of BMI and age. In fact,SItogether with C-reactive protein contributed to 27.4% of calprotectin variance after controlling for age and blood neutrophils count. Otherwise, weight loss led to decreased circulating calprotectin in parallel to fasting glucose and HOMA-IR.ConclusionThese findings suggest that circulating and urinary concentrations of calprotectin are linked to chronic low-grade inflammation and insulin resistance beyond obesity.

scholarly journals Association of GWAS-Based Candidate Genes with HDL-Cholesterol Levels before and after Bariatric Surgery in the Swedish Obese Subjects Study

2011 ◽  
Vol 96 (6) ◽  
pp. E953-E957 ◽  
Author(s):  
Mark A. Sarzynski ◽  
Peter Jacobson ◽  
Tuomo Rankinen ◽  
Björn Carlsson ◽  
Lars Sjöström ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Weight Loss ◽  
Candidate Genes ◽  
Association Studies ◽  
Statistical Significance ◽  
Genome Wide Association Studies ◽  
Nucleotide Polymorphisms ◽  
Cross Sectional ◽  
Time Points ◽  
Obese Subjects

Context and Objective: The magnitude of weight loss-induced high-density lipoprotein cholesterol (HDL-C) changes may depend on genetic factors. We examined the associations of eight candidate genes, identified by genome-wide association studies, with HDL-C at baseline and 10 yr after bariatric surgery in the Swedish Obese Subjects study. Methods: Single-nucleotide polymorphisms (SNP) (n = 60) in the following gene loci were genotyped: ABCA1, APOA5, CETP, GALNT2, LIPC, LIPG, LPL, and MMAB/MVK. Cross-sectional associations were tested before (n = 1771) and 2 yr (n = 1583) and 10 yr (n = 1196) after surgery. Changes in HDL-C were tested between baseline and yr 2 (n = 1518) and yr 2 and 10 (n = 1149). A multiple testing corrected threshold of P = 0.00125 was used for statistical significance. Results: In adjusted multivariate models, CETP SNP rs3764261 explained from 3.2–4.2% (P &lt; 10−14) of the variation in HDL-C at all three time points, whereas CETP SNP rs9939224 contributed an additional 0.6 and 0.9% at baseline and yr 2, respectively. LIPC SNP rs1077834 showed consistent associations across all time points (R2 = 0.4–1.1%; 3.8 × 10−6 &lt; P &lt; 3 × 10−3), whereas LPL SNP rs6993414 contributed approximately 0.5% (5 × 10−4 &lt; P &lt; 0.0012) at yr 2 and 10. In aggregate, four SNP in three genes explained 4.2, 6.8, and 5.6% of the HDL-C variance at baseline, yr 2, and yr 10, respectively. None of the SNP was significantly associated with weight loss-related changes in HDL-C. Conclusions: SNP in the CETP, LIPC, and LPL loci contribute significantly to plasma HDL-C levels in obese individuals, and the associations persist even after considerable weight loss due to bariatric surgery. However, they are not associated with surgery-induced changes in HDL-C levels.

Immunology of Eating Disorders

2018 ◽  
pp. 241-250
Author(s):  
Adaliene Versiani Matos Ferreira ◽  
Laís Bhering Martins ◽  
Nayara Mussi Monteze ◽  
Geneviève Marcelin ◽  
Karine Clément
Keyword(s):  
Eating Disorders ◽  
Body Weight ◽  
Anorexia Nervosa ◽  
Immune Cells ◽  
Eating Behaviors ◽  
Viral Infections ◽  
Low Grade ◽  
Obese People ◽  
Obese Subjects ◽  
Low Grade Inflammation

Eating disorders (EDs) are characterized by dysregulation in eating behavior leading to extreme increase or decrease in food intake that, in turn, changes body weight, adiposity, and physical health. Anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) are the three major eating disorders. Peculiar immune abnormalities occur in these conditions. Previous studies have reported a higher number of CD4+ T lymphocytes in patients with AN, which are related to a relative resistance to viral infections, even in the presence of leukopenia. It has also been proposed that a cluster of cytokines is altered in these patients. A chronic low-grade inflammation has been observed in obese people with BED and in patients with AN, but with a different profile in each condition. In this context, antagonist drugs of specific cytokines, such as anti-TNF, showed improvement of AN-related symptoms, but increased weight gain in obese subjects. The identification of specific molecules and/or immune cells that impair neuronal circuits implicated in eating behaviors may contribute to the development of pharmacological strategies for eating disorders.

scholarly journals Hypomagnesemia and its relation with chronic low-grade inflammation in obesity

2017 ◽  
Vol 63 (2) ◽  
pp. 156-163 ◽  
Author(s):  
Ana Raquel Soares de Oliveira ◽  
Kyria Jayanne Clímaco Cruz ◽  
Juliana Soares Severo ◽  
Jennifer Beatriz Silva Morais ◽  
Taynáh Emannuelle Coelho de Freitas ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Metabolic Disorder ◽  
Magnesium Deficiency ◽  
Scientific Evidence ◽  
Low Grade ◽  
Mineral Deficiency ◽  
Keywords Obesity ◽  
Obese Subjects ◽  
Metabolic Reactions ◽  
Low Grade Inflammation

Summary Introduction: The accumulation of visceral fat in obesity is associated with excessive production of proinflammatory adipokines, which contributes to low-grade chronic inflammation state. Moreover, the literature has shown that mineral deficiency, in particular of magnesium, has important role in the pathogenesis of this metabolic disorder with relevant clinical repercussions. Objective: To bring updated information about the participation of hypomagnesemia in the manifestation of low-grade chronic inflammation in obese individuals. Method: Articles published in PubMed, SciELO, LILACS and ScienceDirect, using the following keywords: "obesity," "magnesium" and "low grade inflammation." Results: Scientific evidence suggests that magnesium deficiency favors the manifestation of low-grade chronic inflammation in obese subjects. Conclusion: From literature data, it is evident the participation of magnesium through biochemical and metabolic reactions in protecting against this metabolic disorder present in obesity.

Sign in / Sign up

Export Citation Format

Share Document