scholarly journals Whole grain-rich diet reduces body weight and systemic low-grade inflammation without inducing major changes of the gut microbiome: a randomised cross-over trial

Gut ◽  
2017 ◽  
Vol 68 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Henrik Munch Roager ◽  
Josef K Vogt ◽  
Mette Kristensen ◽  
Lea Benedicte S Hansen ◽  
Sabine Ibrügger ◽  
...  
Keyword(s):  
Body Weight ◽  
Insulin Sensitivity ◽  
Gut Microbiome ◽  
Inflammatory Markers ◽  
Dietary Intervention ◽  
Short Chain Fatty Acids ◽  
Low Grade ◽  
Whole Grain ◽  
Intestinal Transit Time ◽  
Low Grade Inflammation

ObjectiveTo investigate whether a whole grain diet alters the gut microbiome and insulin sensitivity, as well as biomarkers of metabolic health and gut functionality.Design60 Danish adults at risk of developing metabolic syndrome were included in a randomised cross-over trial with two 8-week dietary intervention periods comprising whole grain diet and refined grain diet, separated by a washout period of ≥6 weeks. The response to the interventions on the gut microbiome composition and insulin sensitivity as well on measures of glucose and lipid metabolism, gut functionality, inflammatory markers, anthropometry and urine metabolomics were assessed.Results50 participants completed both periods with a whole grain intake of 179±50 g/day and 13±10 g/day in the whole grain and refined grain period, respectively. Compliance was confirmed by a difference in plasma alkylresorcinols (p<0.0001). Compared with refined grain, whole grain did not significantly alter glucose homeostasis and did not induce major changes in the faecal microbiome. Also, breath hydrogen levels, plasma short-chain fatty acids, intestinal integrity and intestinal transit time were not affected. The whole grain diet did, however, compared with the refined grain diet, decrease body weight (p<0.0001), serum inflammatory markers, interleukin (IL)-6 (p=0.009) and C-reactive protein (p=0.003). The reduction in body weight was consistent with a reduction in energy intake, and IL-6 reduction was associated with the amount of whole grain consumed, in particular with intake of rye.ConclusionCompared with refined grain diet, whole grain diet did not alter insulin sensitivity and gut microbiome but reduced body weight and systemic low-grade inflammation.Trial registration numberNCT01731366; Results.

scholarly journals Estradiol regulates insulin signaling and inflammation in adipose tissue

2014 ◽  
Vol 17 (2) ◽  
Author(s):  
Minqian Shen ◽  
Shiva P.D. Senthil Kumar ◽  
Haifei Shi
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Active Form ◽  
Biologically Active ◽  
Low Grade ◽  
Energy Status ◽  
Body Weights ◽  
Low Grade Inflammation

AbstractObesity-associated low-grade inflammation at white adipose tissue (WAT) leads to metabolic defects. Sex steroid hormone estrogen may be protective against high-fat diet (HFD)-induced obesity and insulin resistance. This has been tested by many previous studies utilizing rodent models of ovariectomy (OVX) and/or treatment of estradiol (E2), the major biologically active form of estrogen. Body weight and adiposity are increased by OVX and reduced following E2 treatment, however. Thus, the protective roles of E2 may be secondary effects to the changes in body weight and adiposity. We hypothesize that E2 directly prevents inflammation and maintains insulin sensitivity in WAT independent of energy status using mice with similar body weights and adiposity.Four groups of female C57BL/6 mice were used, including sham-operated mice treated with vehicle for E2 and fed with either a low-fat diet (LFD; Sham-Veh-LFD) or a HFD (Sham-Veh-HFD), and HFD-fed OVX mice treated with either vehicle (OVX-Veh-HFD) or E2 (OVX-E2-HFD). Body weight and abdominal parametrial WAT mass, insulin signaling, and expression levels of genes related to low-grade inflammation in WAT were compared between these groups pair-fed with equal amounts of calories for a period of 4 days.Body weights and WAT mass were similar in all four groups. OVX-Veh-HFD mice had impaired insulin signaling associated with rapid activation of inflammation, whereas OVX-E2-HFD group maintained insulin sensitivity without showing inflammation in WAT.E2 directly contributed to the maintenance of insulin sensitivity during the early phase of development of metabolic dysfunction, possibly via preventing low-grade inflammation in WAT.

Diet and exercise reduce low-grade inflammation and macrophage infiltration in adipose tissue but not in skeletal muscle in severely obese subjects

2006 ◽  
Vol 290 (5) ◽  
pp. E961-E967 ◽  
Author(s):  
Jens M. Bruun ◽  
Jørn W. Helge ◽  
Bjørn Richelsen ◽  
Bente Stallknecht
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Inflammatory Markers ◽  
Macrophage Infiltration ◽  
Hypocaloric Diet ◽  
Low Grade ◽  
Severely Obese ◽  
Obese Subjects ◽  
Low Grade Inflammation

Obesity is associated with low-grade inflammation, insulin resistance, type 2 diabetes, and cardiovascular disease. This study investigated the effect of a 15-wk lifestyle intervention (hypocaloric diet and daily exercise) on inflammatory markers in plasma, adipose tissue (AT), and skeletal muscle (SM) in 27 severely obese subjects (mean body mass index: 45.8 kg/m2). Plasma samples, subcutaneous abdominal AT biopsies, and vastus lateralis SM biopsies were obtained before and after the intervention and analyzed by ELISA and RT-PCR. The intervention reduced body weight ( P < 0.001) and increased insulin sensitivity (homeostasis model assessment; P < 0.05). Plasma adiponectin ( P < 0.001) increased, and C-reactive protein ( P < 0.05), IL-6 ( P < 0.01), IL-8 ( P < 0.05), and monocyte chemoattractant protein-1 ( P < 0.01) decreased. AT inflammation was reduced, determined from an increased mRNA expression of adiponectin ( P < 0.001) and a decreased expression of macrophage-specific markers (CD14, CD68), IL-6, IL-8, and tumor necrosis factor-α ( P < 0.01). After adjusting for macrophage infiltration in AT, only IL-6 mRNA was decreased ( P < 0.05). Only very low levels of inflammatory markers were found in SM. The intervention had no effect on adiponectin receptor 1 and 2 mRNA in AT or SM. Thus hypocaloric diet and increased physical activity improved insulin sensitivity and reduced low-grade inflammation. Markers of inflammation were particularly reduced in AT, whereas SM does not contribute to this attenuation of whole body inflammation.

scholarly journals Dietary Fiber's Effect on High Sensitivity C-reactive Protein Serum in Sedentary Workers

2021 ◽  
Vol 5 (1) ◽  
pp. 40
Author(s):  
Livia Kurniati Saputra ◽  
Dian Novita Chandra ◽  
Ninik Mudjihartini
Keyword(s):  
Body Weight ◽  
High Sensitivity ◽  
The Body ◽  
Low Grade ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Dietary Fiber Intake ◽  
Anti Inflammatory ◽  
Low Grade Inflammation ◽  
Inflammatory Effect

Low grade inflammation has been recognized of being involved in the pathogenesis of chronic disease pandemic. Individual lifestyle plays a major role in the development of low grade inflammation. Sedentary workers are at risk of low grade inflammation due to the nature of their work. Dietary habit also contributes to inflammatory status in the body. Dietary fiber intake indirectly affects the immune system. It has been hypothesized that fiber has anti-inflammatory effects, both body weight-related and body weight-unrelated This review will focus more on body weight-unrelated anti-inflammatory effect of fiber, especially through fiber’s fermentation metabolites, the short chain fatty acid (SCFA). Its anti-inflammatory effect can be seen by monitoring a biomarker of inflammation in the body, the high sensitivity C-reactive protein (hsCRP). This review’s objective is to cover the mechanisms and role of dietary fiber intake on serum hsCRP level as a marker of low grade inflammation on sedentary workers. 

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 The Prebiotic Inulin Beneficially Alters the Gut Microbiome and Associated Metabolites in an APOE4 Mouse Model (P08-133-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lucille Yanckello ◽  
Jared Hoffman ◽  
Ishita Parikh ◽  
Jessie Hoffman ◽  
Stefan Green ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
Dietary Intervention ◽  
Disease Risk ◽  
Short Chain Fatty Acids ◽  
Apoe4 Allele ◽  
Funding Sources ◽  
Tryptophan Metabolites ◽  
Host Metabolism ◽  
Microbiota Diversity

Abstract Objectives The APOE4 allele is a genetic risk factor for certain diseases, due in part to alterations in lipid and glucose metabolism. The gut microbiota is also known to impact metabolic and can be beneficially modulated by prebiotics. Prebiotics are fermented into metabolites by the gut microbiota. These metabolites act as gut-brain axis components. However, the interaction of the APOE4 allele, gut microbiota, and prebiotics are unknown. The goal of the study was to use prebiotic diet to restore the gut microbiome of mice with human APOE4 (E4FAD) genes. We hypothesized that the microbial compositions of E4 mice fed inulin, compared to control fed, will correlate to metabolites being produced by the microbiome that confer benefit to host metabolism. Methods At 3 months of age the E4FAD mice were fed for 4 months with either control or inulin diet. We used 16S rRNA sequencing to determine gut microbiota diversity and species variations; non-targeted UPLC-MS/MS and GC-MS analysis was used to determine metabolic profiles of blood. Results The inulin fed mice showed a more beneficial microbial taxa profile than those mice that were control fed. Control mice showed higher levels of dimethylglycine, choline, creatine and the polyamine spermine. Higher levels of spermine, specifically, correlate to higher levels of the Proteobacteria which has been implicated in GI disorders. E4 inulin fed mice showed higher levels of bile acids, short chain fatty acids and metabolites involved in energy, increased levels of tryptophan metabolites and robust increases in sphingomyelins. Specifically in E4 inulin fed mice we saw increases in certain genera of bacteria, all of which have been implicated in being beneficial to the composition of the microbiome and producing one or more of the above mentioned metabolites. Conclusions We believe the disparities of microbial metabolite production between E4 inulin fed mice and E4 control fed mice can be attributed to differences in certain taxa that produce these metabolites, and that higher levels of these taxa are due to the dietary intervention of inulin. Despite the APOE4 allele increasing one's risk for certain diseases, we believe that beneficially modulating the gut microbiota may be one way to enhance host metabolism and decrease disease risk over time. Funding Sources NIH/NIDDK T323048107792, NIH/NIA R01AG054459, NIEHS/NIH P42ES007380. Supporting Tables, Images and/or Graphs

scholarly journals Cartilage-gut-microbiome axis: a new paradigm for novel therapeutic opportunities in osteoarthritis

RMD Open ◽  
2019 ◽  
Vol 5 (2) ◽  
pp. e001037 ◽  
Author(s):  
Jean-Marie Berthelot ◽  
Jérémie Sellam ◽  
Yves Maugars ◽  
Francis Berenbaum
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
Cartilage Degradation ◽  
Low Grade ◽  
New Paradigm ◽  
Healthy Human ◽  
Human Cartilage ◽  
Intact Cartilage ◽  
Low Grade Inflammation

DNA of gut microbiota can be found in synovium of osteoarthritis and rheumatoid arthritis. This finding could result from the translocation of still alive bacteria from gut to joints through blood, since the diversified dormant microbiota of healthy human blood can be transiently resuscitated in vitro. The recent finding of gut microbiome in human cartilage, which differed between osteoarthritis and controls, suggests that a similar trafficking of dead or alive bacteria from gut microbiota physiologically occurs between gut and epiphysial bone marrow. Subchondral microbiota could enhance cartilage healing and transform components of deep cartilage matrix in metabolites with immunosuppressive properties. The differences of microbiome observed between hip and knee cartilage, either in osteoarthritis or controls, might be the counterpart of subtle differences in chondrocyte metabolism, themselves in line with differences in DNA methylation according to joints. Although bacteria theoretically cannot reach chondrocytes from the surface of intact cartilage, some bacteria enter the vascular channels of the epiphysial growth cartilage in young animals, whereas others can infect chondrocytes in vitro. In osteoarthritis, the early osteochondral plate angiogenesis may further enhance the ability of microbiota to locate close to the deeper layers of cartilage, and this might lead to focal dysbiosis, low-grade inflammation, cartilage degradation, epigenetic changes in chondrocytes and worsening of osteoarthritis. More studies on cartilage across different ethnic groups, weights, and according to age, are needed, to confirm the silent presence of gut microbiota close to human cartilage and better understand its physiologic and pathogenic significance.

The effects of a low-fat, plant-based dietary intervention on body weight, metabolism, and insulin sensitivity

2005 ◽  
Vol 118 (9) ◽  
pp. 991-997 ◽  
Author(s):  
Neal D. Barnard ◽  
Anthony R. Scialli ◽  
Gabrielle Turner-McGrievy ◽  
Amy J. Lanou ◽  
Jolie Glass
Keyword(s):  
Body Weight ◽  
Insulin Sensitivity ◽  
Dietary Intervention ◽  
Low Fat

scholarly journals Lifestyle-related determinants of inflammation in adolescence

2007 ◽  
Vol 98 (S1) ◽  
pp. S116-S120 ◽  
Author(s):  
Julia Wärnberg ◽  
Esther Nova ◽  
Javier Romeo ◽  
Luís A. Moreno ◽  
Michael Sjöström ◽  
...  
Keyword(s):  
Physical Activity ◽  
Inflammatory Markers ◽  
Large Scale ◽  
Dietary Habits ◽  
Epidemiological Studies ◽  
Low Grade ◽  
Inflammatory Processes ◽  
Young Subjects ◽  
Low Grade Inflammation ◽  
Apparently Healthy

Inflammatory processes are involved in the pathogenesis of the most common chronic non-communicable diseases and may also play an important initiating role in their development. Only recently have inflammatory markers been included in epidemiological studies focusing on nutritional status, body composition and physical activity. We are just starting to understand how different lifestyles can determine basal levels of inflammatory biomarkers in early ages. This review aims to summarise what is known about the relationships between lifestyle-related determinants (focusing on overweight, physical activity and dietary habits) and inflammatory markers in apparently healthy young populations. Obesity is the most widely studied determinant. Several large-scale studies have now demonstrated that healthy young subjects with more body fat or higher BMI have moderately higher concentrations of inflammatory markers than their leaner peers, supporting the idea that obesity should be considered as a state of chronic low-grade inflammation. Less data is available to allow us to elucidate how physical activity/fitness or dietary patterns may have a direct effect on inflammation in apparently healthy, disease-free young populations.

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