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Polycystic ovary syndrome （PCOS） is a reproductive endocrine disorder characterized by coexisting reproductive dysfunction and glucolipid metabolic disturbance， affecting 8%-13% of women of reproductive age and 3%-11% of adolescent females. Due to the highly heterogeneous clinical features， symptom-oriented individualized strategies are commonly adopted for the treatment of PCOS. Chronic low-grade inflammation is one of the core mechanisms for the occurrence of PCOS. Macrophages， as foundational cells of innate immunity， play an indispensable role in modulating systemic inflammatory responses. The imbalance of macrophage M1/M2 polarization is involved in chronic low-grade inflammation in PCOS via pathways such as activating pro-inflammatory responses， disrupting ovarian tissue repair， stimulating excessive synthesis of androgens， and promoting the occurrence of insulin resistance. Reshaping the phenotype of macrophages might serve as a potential therapeutic strategy for PCOS. Traditional Chinese medicine （TCM） holds that spleen deficiency and phlegm dampness is a crucial pathogenesis of PCOS. The spleen， being in charge of defensive function， plays a key role in ensuring normal physiological functions such as transportation and defense against external pathogen during the occurrence and development of PCOS. The imbalance of macrophage polarization resembles the transition from spleen being in charge of defensive function to spleen losing its defensive role in TCM. Therefore， this paper， for the first time， explores the deep connection between macrophage polarization and the pathogenesis of chronic low-grade inflammation in PCOS from the TCM theory of spleen being in charge of defensive function， providing theoretical support and new research directions for the treatment and drug research of PCOS.
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At present，many studies showed that food intolerance (FI) is one of the important factors for the occurrence and aggravation of irritable bowel syndrome (IBS). The FI in IBS patients is related to low grade inflammation of intestine. Fermentable oligo‑，di‑，monosaccharides and polyols (FODMAPs) diet can improve the symptoms of IBS and provide a new idea for exploring the pathogenesis and treatment of IBS. This article reviewed the advances in study on role of FI in pathogenesis of IBS.
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Some studies suggested that patients with irritable bowel syndrome (IBS) are more likely to develop inflammatory bowel disease (IBD) than the general population, which may lead to over-examination in some IBS patients. On the other hand, patients with IBD often have IBS-like symptoms, which may in turn lead to a delay diagnosis of IBD. Therefore, whole digestive tract examination must be carried out to exclude IBD in patients with IBS-like symptoms and having "high risk factors". The incidence of IBS increased in patients with IBD in remission. Such IBS in IBD patients should also be diagnosed and treated in time.
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Objective To investigate the effects of Lactobacillus rhamnosus GG (LGG) colonization in early life on intestinal barrier and intestinal development in offspring mice and its possible mechanism.Methods Six C57BL/6 pregnant mice with the same conception time of 6 weeks were selected and randomly divided into experiment group given 108 cfu/ml LGG live bacteria and control group given LGG inactivated bacteria by gavage from the 18th day of pregnancy until natural birth.The progeny mice in the two groups were continued to be gavaged with 107 cfu/ml of LGG live bacteria or LGG inactivated bacteria on days 1-5 of birth.The body weight changes of 3 week'progeny mice were recorded.The colonization of LGG bacteria in offspring mice was detected at 2nd and 3rd weeks.The mRNA of intestinal proinflammatory cytokines and tight junction molecules were evaluated by real-time PCR method.HE,immunohistochemistry,immunofluorescence staining and enzyme-linked immunosorbent assay were used to evaluate the intestinal barrier of 3-week old off spring mice.Results Compared with the control group,the progeny mice of the experiment group showed no significant difference in body weight at the first week,and the body weight increased at the second week and the third week [2ndweek:(3.790±0.240) g vs.(4.326±0.140) g,t=3.707,P=0.006;3rd week:(7.295±0.326) g vs.(8.040±0.370) g,t=3.130,P=0.011].LGG colonization can be detected only in the feces of progeny mice in the experiment group.Intestinal colonization can promote the growth of small intestine villi and colon crypt depth [jejunum:(320.000±22.514) μm vs.(265.100±15.611) μm,t=8.258,P＜0.001;ileum:(150.500±13.099) μm vs.(111.000±11.308) μm,t=9.958,P＜0.001;colon:(295.000±15.209) μm vs.(233.100±6.678) μm,t=9.129,P＜0.001].Compared with the control group,the number of goblet cells in the colonic crypt of the experiment group increased (11.62 ± 0.780 vs.35.24 ±1.370,t=15.000,P＜0.001),and the relative mRNA expression levels of pro-inflammatory factors as IFN-γ (1.280±0.232 vs.0.512±0.206,t=4.970,P=0.001),IL-6 (1.364±0.271 vs.0.941±0.215,t=2.452,P=0.040),IL-10 (1.341±0.320vs.0.744±0.294,t=2.762,P=0.025)andTNF-α (3.702±0.150 vs.2.581±0.500,t=2.553,P=0.034) in the experiment group decreased;the expression levels of the intimate tight junction molecules (Claudin3) (1.283±0.152 vs.1.881±0.172,t=4.932,P=0.001) and the atresia protein molecule (Occludin) (1.164±0.342 vs.0.812±0.224,t=3.67,P=0.016) significantly increased.Conclusion Early life LGG colonization protects the intestinal barrier by inhibiting lowgrade intestinal inflammation.This study will lay the experimental foundation for the supplementation of probiotics in early life so as to prevent intestinal diseases.
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Objective@#To investigate the efficacy of low dose and short-term oral rifaximin in patients with small intestinal bacterial overgrowth (SIBO) related irritable bowel syndrome (IBS).@*Methods@#From June 2017 to June 2018, at the Department of Gastroenterology of Huashan Hospital, Fudan University in Shanghai, a total of 37 patients with SIBO related IBS were sequentially enrolled and divided into three groups: diarrhea type, constipation type and mixed type. All the patients received rifaximin 200 mg each time, three times per day for 14 days. The clinical efficacy before and after treatment were compared by the scores of irritable bowel syndrome symptom severity scale (IBS-SSS) and irritable bowel syndrome associated quality of life (IBS-QoL). The efficacy of rifaximin on SIBO clearance and SIBO related chronic low-grade inflammation was evaluated by lactulose breath test (LBT) and exhaled nitric oxide (eNO). T test and variance analysis were used for statistical analysis.@*Results@#Among 39 patients with SIBO related IBS, 24 patients were diarrhea type, seven were constipation type and six were mixed type. Except one patient quitted the study because of chest tightness and palpitation, the IBS-SSS score of the left 36 patients before treatment was (250.83±55.10), and decreased to (151.11±33.96), and the difference was statistically significant (t=13.686, P<0.01). Before treatment the score of IBS-QoL was (28.03±16.16), and decreased to (14.39±9.31) after treatment, and the difference was statistically significant (t=6.867, P<0.01). There was no significant difference in IBS-SSS and IBS-QoL scores among the diarrhea type, constipation type and mixed type groups (all P>0.05). After treated by rifaximin, the negative conversion rate of SIBO was 52.8%(19/36). The negative conversion rate of hydrogen LBT was 54.5%(12/22) and among 11 methane LBT positive patients, six cases turned negative; and one of three patients with both positive hydrogen LBT and methane LBT turned negative. The negative conversion rate of eNO was 41.7%(15/36).@*Conclusions@#Low dose and short term rifaximin treatment can improve the severity of clinical symptoms and quality of life in SIBO-related IBS patients, and the efficacy is not related with the subtypes of IBS.
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Objective To investigate the efficacy of low dose and short-term oral rifaximin in patients with small intestinal bacterial overgrowth (SIBO)related irritable bowel syndrome (IBS). Methods From June 2017 to June 2018,at the Department of Gastroenterology of Huashan Hospital,Fudan University in Shanghai,a total of 37 patients with SIBO related IBS were sequentially enrolled and divided into three groups:diarrhea type,constipation type and mixed type. All the patients received rifaximin 200 mg each time,three times per day for 14 days. The clinical efficacy before and after treatment were compared by the scores of irritable bowel syndrome symptom severity scale (IBS-SSS)and irritable bowel syndrome associated quality of life (IBS-QoL). The efficacy of rifaximin on SIBO clearance and SIBO related chronic low-grade inflammation was evaluated by lactulose breath test (LBT)and exhaled nitric oxide (eNO). T test and variance analysis were used for statistical analysis. Results Among 39 patients with SIBO related IBS,24 patients were diarrhea type,seven were constipation type and six were mixed type. Except one patient quitted the study because of chest tightness and palpitation,the IBS-SSS score of the left 36 patients before treatment was (250. 83 ± 55. 10),and decreased to (151. 11 ± 33. 96),and the difference was statistically significant (t = 13. 686,P <0. 01). Before treatment the score of IBS-QoL was (28. 03 ± 16. 16),and decreased to (14. 39 ± 9. 31)after treatment,and the difference was statistically significant (t = 6. 867,P < 0. 01 ). There was no significant difference in IBS-SSS and IBS-QoL scores among the diarrhea type,constipation type and mixed type groups (all P > 0. 05). After treated by rifaximin,the negative conversion rate of SIBO was 52. 8％(19 / 36). The negative conversion rate of hydrogen LBT was 54. 5％(12 / 22)and among 11 methane LBT positive patients,six cases turned negative;and one of three patients with both positive hydrogen LBT and methane LBT turned negative. The negative conversion rate of eNO was 41. 7％ (15 / 36). Conclusions Low dose and short term rifaximin treatment can improve the severity of clinical symptoms and quality of life in SIBO-related IBS patients,and the efficacy is not related with the subtypes of IBS.
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Objective: To detect the expression of peroxisome proliferator-activated receptor (PPAR) in ovarian tissues of rats with chronic low-grade inflammation, and to explore the effect of PPAR-γ agonist rosiglitazone on ovarian dysfunction induced by chronic low-grade inflammation. Methods: A chronic low-grade inflammation model of rats was established by intraperitoneal injection of lipopolysaccharide (LPS). Two hundred rats were randomly assigned to control group (NS group) and chronic low-grade inflammation group (LPS group), and the rats were intraperitoneally injected with normal saline and LPS, respectively. The ovarian function of rats was assessed by detecting the serum levels of estradiol (E2), follicle stimulating hormone (FSH), luteinizing hormone (LH), and anti-Müllerian hormone (AMH) during different stages of the estrus cycle (proestrus, estrus, metestrus and diestrus). The protein expression levels of PPAR-α, PPAR-γ and PPAR-γ in ovarian tissues were detected using Western blotting. Eighty rats of each group were randomly divided into two subgroups, which were administered intragastrically by normal saline and rosiglitazone, respectively. Fourteen days after intragastric administration, the levels of proinflammatory cytokines, including interleukin (IL)-1β, IL-6 and tumor necrosis factor α (TNF-α), in ovarian tissues and ovarian function of rats in each subgroup were observed during different stages of the estrus cycle. Results: Compared with the NS group, during different stages of the estrus cycle, the serum levels of E2 and AMH of rats in the LPS group were significantly decreased (all P < 0.05), while the serum levels of FSH and LH were significantly increased (all P < 0.05). During different stages of the estrus cycle, the expression levels of PPAR-γ in ovarian tissues were significantly decreased in the LPS group compared with the NS group (all P < 0.05), while the expression levels of PPAR-α and PPAR-δ were not significantly different between the two groups (all P < 0.05). Compared with the intraperitoneal injection of LPS intragastric administration of normal saline subgroup, during different stages of the estrus cycle, the expression levels IL-1β, IL-6 and TNF-α in ovarian tissues of rats were significantly decreased in the intraperitoneal injection of LPS intragastric administration of rosiglitazone subgroup (all P < 0.05), the serum levels of E2 and AMH were significantly increased (all P < 0.05), and the serum levels of FSH and LH were significantly decreased (all P < 0.05). Conclusion: PPAR-γ agonist rosiglitazone can attenuate LPS-induced chronic low-grade inflammatory and improve ovarian function in rats.
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Objective@#To investigate the incidence of small intestinal bacterial overgrowth (SIBO) and systemic low-grade inflammation in patients with irritable bowel syndrome (IBS).@*Methods@#From June to October in 2017, 50 cases of IBS patients who met Rome Ⅳ criteria were consecutively collected at Outpatient Department of Gastroenterology of Shanghai Huashan Hospital. The incidence of SIBO was detected by hydrogen lactulose breath test (LBT) and methane LBT. The incidence of systemic low-grade inflammation in IBS patients was determined by fractional exhaled nitric oxide(FeNO) breath test. Chi-square test was used for statistical analysis.@*Results@#Among 50 IBS patients, the positive rate of FeNO was 70%(35/50), and the number of FeNO positive cases in diarrhea-predominant (n=28), constipation-predominant (n=14) and mix-type (n=8) IBS paitents was 18, 11 and six, respectively, and the difference was not statistically significant among three groups (χ2=1.020, P=0.600). The incidence rate of SIBO was 60% (30/50), with 20 cases (40%) being only positive for hydrogen LBT, seven cases (14%) being methane LBT, and three cases (6%) being both positive. The numbers of hydrogen LBT and methane LBT in diarrhea-predominant, constipation-predominant, and mix-type IBS patents were 17, three, three and two, six, two, respectively. There were statistically significant differences in positive rates of hydrogen LBT and methane LBT among three groups (χ2=6.076 and 6.392, both P<0.05). The positive rate of FeNO in IBS patients with SIBO was higher than that of IBS patients without SIBO (90%, 27/30 vs. 40%, 8/20), and the difference was statistically significant (χ2=14.286, P<0.01).@*Conclusions@#Combination of hydrogen LBT and methane LBT has a higher detection rate of SIBO than traditional single hydrogen LBT. There is a correlation between SIBO and systemic low-grade inflammation in IBS patients.
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A total of 108 subjects were enrolled in this study, including 21 healthy subjects(control group), 34 non-obese patients with polycystic ovary syndrome [PCOS1 group, body mass index(BMI)<25 kg/m2], 32 obese patients with PCOS(PCOS2 group, BMI≥25 kg/m2), and 21 simple obese patients whose age and BMI matched with PCOS2(OB group). BMI, waist-hip ratio(WHR), fasting plasma glucose(FPG), postprandial 2h plasma glucose(2hPG), HbA1C, fasting insulin(FINS), postprandial 2h insulin(2hINS), sex hormones, and lipid parameters were determined. The status of insulin resistance was assessed by homeostasis model assessment for insulin resistant index(HOMA-IR)and insulin sensitivity index(ISI). Levels of plasma galectin-3 and interleukin-6(IL-6)were detected by ELISA. The results showed that the plasma level of galectin-3 was significantly higher in PCOS group than those in control and OB groups(all P<0.05). Moreover, the level of galectin-3 was also higher in OB group compared with control group, while galectin-3 level in PCOS2 group was higher than that in PCOS1 group(all P<0.05). After adjusted by age, BMI, and WHR, correlation analysis showed that the level of galectin-3 was positively correlated with FPG, 2hPG, FINS, HOMA-IR, highly-sensitive C-reactive protein, and IL-6, while negatively correlated with ISI. A multiple linear regression analysis revealed that the plasma galectin-3 concentration was independently associated with IL-6, HOMA-IR, and BMI(all P<0.05). These data suggest that plasma galectin-3 is closely associated with glucose metabolism, chronic inflammation, and insulin resistance, which may be involved in the pathogenesis of PCOS. (Chin J Endocrinol Metab, 2018, 34: 578-582)
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Objective To investigate the incidence of small intestinal bacterial overgrowth (SIBO) and systemic low-grade inflammation in patients with irritable bowel syndrome (IBS ) .Methods From June to October in 2017 ,50 cases of IBS patients who met Rome Ⅳ criteria were consecutively collected at Outpatient Department of Gastroenterology of Shanghai Huashan Hospital .The incidence of SIBO was detected by hydrogen lactulose breath test (LBT) and methane LBT .The incidence of systemic low-grade inflammation in IBS patients was determined by fractional exhaled nitric oxide (FeNO) breath test .Chi-square test was used for statistical analysis .Results Among 50 IBS patients ,the positive rate of FeNO was 70％ (35/50) ,and the number of FeNO positive cases in diarrhea-predominant (n=28) ,constipation-predominant (n= 14) and mix-type (n= 8) IBS paitents was 18 ,11 and six ,respectively ,and the difference was not statistically significant among three groups (χ2=1 .020 ,P=0 .600) .The incidence rate of SIBO was 60％ (30/50) ,with 20 cases (40％ ) being only positive for hydrogen LBT ,seven cases (14％ ) being methane LBT ,and three cases (6％ ) being both positive .The numbers of hydrogen LBT and methane LBT in diarrhea-predominant ,constipation-predominant ,and mix-type IBS patents were 17 , three ,three and two ,six ,two ,respectively .There were statistically significant differences in positive rates of hydrogen LBT and methane LBT among three groups (χ2 =6 .076 and 6 .392 ,both P<0 .05) . The positive rate of FeNO in IBS patients with SIBO was higher than that of IBS patients without SIBO (90％ ,27/30 vs .40％ ,8/20) ,and the difference was statistically significant (χ2 =14 .286 ,P<0 .01) . Conclusions Combination of hydrogen LBT and methane LBT has a higher detection rate of SIBO than traditional single hydrogen LBT . There is a correlation between SIBO and systemic low-grade inflammation in IBS patients .
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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.
Resumo Introdução: O acúmulo de gordura visceral na obesidade está associado à produção excessiva de adipocinas pró-inflamatórias, o que contribui para o estado de inflamação crônica de baixo grau. A literatura também tem mostrado que a deficiência de minerais, em particular do magnésio, possui papel importante na patogênese desse distúrbio metabólico com repercussões clínicas relevantes. Objetivo: Trazer informações atualizadas sobre a participação da hipomagnesemia na inflamação crônica de baixo grau em indivíduos obesos. Método: Bases de dados Pubmed, SciELO, Lilacs e ScienceDirect, utilizando as palavras-chave: "obesity", "magnesium" e "low grade inflammation". Resultados: As evidências científicas sugerem que a deficiência de magnésio favorece a manifestação da inflamação crônica de baixo grau em indivíduos obesos. Conclusão: É evidente a participação do magnésio, por meio de reações bioquímicas e metabólicas, na proteção contra esse distúrbio metabólico presente na obesidade.
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Humans , Male , Metabolic Syndrome/etiology , Intra-Abdominal Fat/metabolism , Inflammation/etiology , Magnesium Deficiency/complications , Obesity/complications , Intra-Abdominal Fat/physiopathology , Adipokines/metabolism , Magnesium/administration & dosage , Magnesium Deficiency/physiopathology , Obesity/physiopathologyABSTRACT
AIM:To investigate the effect of growth hormone receptor(GHR) knockdown on nuclear factor-κB (NF-κB) activity and inflammatory cytokine production stimulated by growth hormone (GH) in 3T3-L1 adipocytes. METHODS:The specific siRNA for GHR was transfected into 3T3-L1 adipocytes to silence GHR expressions. The effects of GH on NF-κB activation and inflammatory cytokine production in 3T3-L1 adipocytes transfected with siRNA-GHR or siRNA-control were measured by dual-luciferase system analysis,real-time RT-PCR and ELISA. RESULTS:The protein expression of GHR was diminished after transfection with GHR specific siRNA. Dual-luciferase reporter system analysis re-vealed that GHR knockdown resulted in attenuation of GH-stimulated NF-κB activation in the 3T3-L1 adipocytes. GHR knockdown ameliorated the GH-induced production of inflammatory cytokines TNF-α,IL-1β,IL-6,MCP-1 and MIP-1α in the 3T3-L1 adipocytes. CONCLUSION:Knockdown of GHR might be efficacious to prevent GH-induced inflammatory re-sponses in the 3T3-L1 adipocytes.
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Objective To detect the changes of visceral sensitivity in rats presenting intestinal dysbacteriosis and the expressions of tight junction protein (ZO-1)and Toll-like receptor 4 (TLR4)so as to explore the effect of intestinal dysbacteriosis on visceral sensitivity and the possible mechanisms.Methods We randomly divided 30 male SD rats of SPF grade into normal control group (n = 12 )and dysbacteriosis group (n = 18 ).Rats in dysbacteriosis group were administered with lincomycin hydrochloride (300 mg/mL),1 mL each time per rat once a day for 7 consecutive days;those in normal control group were fed with the same amount of saline.On the eighth day,six rats were randomly selected from normal control group and dysbacteriosis group respectively to detect whether the model was successful.After the model was successfully constructed,the remaining 12 dysbacteriosis rats were randomly divided into the negative control group and the probiotics intervention group with 6 in each.Rats in the intervention group were given probiotic bifidobacterium triple viable capsules (Bifico)orally,one capsule with 1/3 mL of saline,1 mL each time per rat once a day for 7 consecutive days;those in the negative control group received the same amount of saline.On the eighth day,fresh feces was cultured for flora to detect visceral sensitivity by abdominal withdrawal reflex (AWR),the mRNA and protein expressions of ZO-1 and TLR4 in the colon,and the expression of serum inflammatory cytokines IL-10 and TNFα.Results The expression of ZO-1 in the colon was significantly lower in the rats of dysbacteriosis group than those in the control group,and the expression of TLR4 was also significantly increased.Correspondingly,the expression of pro-inflammatory factor TNFα in the serum of the rats in dysbacteriosis group was significantly increased,while that of anti-inflammatory factor IL-10 was significantly lower than in the control group (P <0.05).Furthermore,compared with dysbacteriosis group,the expression of ZO-1 was increased significantly and TLR4 was decreased in probiotics group in varying degrees. Similarly,the expression of TNFα was obviously lower while that of IL-10 in the serum was higher (P < 0.05 ). Conclusion Inhibiting the expression of ZO-1 and increasing the expression of TLR4,thus leading to chronic low-grade inflammation, may be one mechanism of visceral hypersensitivity caused by intestinal dysbacteriosis. Probiotics may restore the dysbacteriosis and thus improve visceral hypersensitivity.
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La inflamación puede definirse como una respuesta local al daño celular, que se caracteriza por aumento del flujo sanguíneo, vasodilatación capilar, infiltración de leucocitos y la producción local de mediadores de inflamación por parte del huésped. La inflamación es parte de la respuesta y es necesario el retorno a la homeostasis luego de daño producido por un agente infeccioso, daño físico o estrés metabólico. Cuando persiste el estímulo que dispara el proceso, la inflamación puede hacerse crónica y contribuir a la patogénesis de enfermedades como la diabetes mellitus tipo 2 y la hipertensión. En estas enfermedades, ácidos grasos saturados, lipoproteínas y agregados proteicos disparan la respuesta inmunitaria y producen inflamación, que al no poder ser fácilmente eliminados, perpetúan la respuesta y contribuyen con la persistencia de la enfermedad. Los patrones de consumo saludable se han asociado con bajas concentraciones de marcadores de inflamación. Entre los componentes de una dieta saludable el consumo de cereales integrales, pescado, frutas y verduras se asocian con menor inflamación. La vitamina C, E y los carotenoides disminuyen la concentración de marcadores de inflamación, mientras otros nutrientes como los lípidos, tienen efectos opuestos: los ácidos grasos saturados y los transmonosaturados son pro-inflamatorios, mientras que los ácidos grasos poliinsaturados, especialmente los de cadena larga, son antiinflamatorios. También se revisan los productos de glicosilación avanzada y su papel en la producción de inflamación de bajo grado(AU)
Inflammation could be defined as a local response to cell damage, characterized by increased blood flow, capillary vasodilation, leukocyte infiltration and local production of inflammation mediators by the host. Inflammation is part of the response and the return to homeostasis after an insult by a pathogen, physical damage or metabolic stress is also required. When the stimulus that triggers the response is not eliminated, inflammation could become chronic and contribute to the pathogenesis of diseases such as diabetes and hypertension. In these diseases saturated fatty acids, lipoproteins and protein aggregates trigger the immune response and produce inflammation. If they are not properly eliminated, the response is maintained and the disease continues. Healthy consumption patterns have been associated with low levels of inflammation markers. Some of the components identified as part of a healthy diet include whole grains, fish, fruits and vegetables. Vitamins C and E, as well as carotenoids, diminish the concentration of markers of inflammation, while other nutrients have opposite effects: saturated, as well as trans-monosaturated fatty acids are pro-inflammatory whereas polyunsaturated fatty acid, especially long chain, are anti-inflammatory. Advanced glycation end products and their role in inflammation are also reviewed(AU)
Subject(s)
Humans , Male , Female , Adipose Tissue , Metabolic Syndrome , Diabetes Mellitus , Diet/adverse effects , Food Hypersensitivity , Inflammation/etiology , Intestines/anatomy & histology , Cardiovascular Diseases , Diet, Food, and Nutrition , Immune System , Metabolic DiseasesABSTRACT
Irritable bowel syndrome (IBS) is one of the most prevalent functional disorders in Chile impacting on socio-economic development due to significantly impaired quality of life of the individual. It is characterised by abdominal discomfort associated with alterations in bowel habit and increased visceral hypersensitivity. One of the outstanding features of IBS is the presence of a bi-directional imbalance of gut-brain interactions, which can induce alterations in the intestinal immune response. IBS is characterised by increased intestinal mast cell activity associated with alterations of para-cellular permeability and activation of sensory nerve endings. The increased proximity of mast cell to colonic nerves is correlated with abdominal pain and increased visceral hypersensitivity of the patients. In spite of the well-described role of mast cell in the induction of mucosal inflammation, in IBS only a low-grade inflammation is observed. The present review discuses the possible immune-regulatory mechanisms that are involved in IBS pathophysiology.
El síndrome de intestino irritable (SII) es considerado uno de los trastornos funcionales más prevalente en Chile, que impacta el desarrollo socio-económico del país debido al deterioro de la calidad de vida de los individuos que lo portan. Es caracterizado por molestias abdominales asociadas a alteraciones en el hábito de defecación e hipersensibilidad visceral. Una de las características más destacadas en el SII es la presencia de un desequilibrio de las interacciones en el eje intestino-cerebro, el cual puede inducir alteraciones en la respuesta inmune intestinal. El SII es caracterizado por una aumentada actividad de los mastocitos en el intestino, asociada con alteraciones en la permeabilidad para-celular epitelial y la activación de terminaciones nerviosas en la mucosa intestinal. El aumento de la cercanía de los mastocitos a nervios colónicos está relacionado con el dolor abdominal y la hipersensibilidad visceral de los pacientes. Pese a que está muy bien descrito el papel del mastocito en la inducción de la inflamación en mucosas, en el SII se observa sólo un bajo-grado de inflamación. En la presente revisión se discute los posibles mecanismos regulatorios inmunes que están involucrados en la fisiopatología del SII.
Subject(s)
Humans , Irritable Bowel Syndrome/physiopathology , Irritable Bowel Syndrome/immunology , Colon/innervation , Hypersensitivity , Inflammation , Mast Cells/pathology , Nervous System/physiopathologyABSTRACT
Dos recientes estudios epidemiológicos de gran envergadura en los que participó Colombia, el INTERHEART y el INTERSTROKE, demostraron que en Latinoamérica en general y en Colombia en particular, el principal factor de riesgo para la presentación de infarto agudo del miocardio y accidente cerebro vascular isquémico y hemorrágico es la obesidad abdominal, a diferencia del resto del mundo donde el principal factor de riesgo fue el aumento en las concentraciones plasmáticas del colesterol total y del colesterol LDL, en el primer caso, y la hipertensión arterial, en el segundo. Estos datos dan soporte a la propuesta de que en Latinoamérica la transición rápida de los modelos económicos experimentados en los últimos años junto con la urbanización acelerada son la causa del explosivo aumento de la obesidad abdominal, la diabetes mellitus tipo 2 y las enfermedades cardio-cerebro-vasculares.
Two recent large-scale epidemiological studies, INTERHEART and INTERSTROKE in which Colombia took part, demonstrated that in Latin America in general and particularly in Colombia, the main risk factor for the presentation of acute myocardial infarction and ischemic, and hemorrhagic stroke was the abdominal obesity in contrast to the rest of the world where the main risk factor was increase in plasma concentrations of total cholesterol and LDL-cholesterol for myocardial infarction, and hypertension for stroke . These data give support to the proposal that in Latin America the rapid transition in economic models experienced in the last years together with the fast urbanization has led to an explosive increase in abdominal obesity, diabetes mellitus type 2, and cardiovascular and cerebrovascular diseases.
Subject(s)
Inflammation , Obesity, AbdominalABSTRACT
The authors analyze insulin resistance, the metabolic syndrome and endothelial dysfunction as consequence of a common antecedent, a low grade inflammation, indicating that in obesity there is a chronically activated inflammatory state of the adipose tissue. Furthermore, the inflammatory signaling is discussed according to the adipose tissue depot, visceral or subcutaneous.
Os autores analisam a resistência à insulina, a síndrome metabólica e a disfunção endotelial como consequência de um antecedente comum, a inflamação de baixo nível, o que mostra que a obesidade é um estado inflamatório cronicamente ativado do tecido adiposo. Discute-se, aqui, a sinalização inflamatória de acordo com a localização do tecido adiposo subcutâneo ou visceral.
Subject(s)
Animals , Humans , Adipose Tissue/physiology , Atherosclerosis/physiopathology , Insulin Resistance/physiology , Metabolic Syndrome/physiopathology , Obesity/physiopathology , Panniculitis/physiopathology , Adipokines/metabolism , Adipose Tissue/metabolism , Atherosclerosis/etiology , Endothelium, Vascular/metabolism , Inflammation Mediators/metabolism , Intra-Abdominal Fat/metabolism , Metabolic Syndrome/etiology , Obesity/complications , Obesity/metabolism , Panniculitis/metabolism , Subcutaneous Fat/metabolismABSTRACT
Obesity has been a world-wide growing health problem in children and adolescents,insulin resistance plays a pivotal role in the pathogenesis of obesity-associated complications,the mechanism is still unknown.There is growing evidence that obesity is associated with low-grade inflammation in youth.The onset of low-grade inflammation in obesity may be associated with the inflammatory cytokine secreted by adipose tissue,local Monocyte/Macrophage system and role of oxidative stress.The study of inflammatory cytokines in pathogenesis of obesity and insulin resistance will help to develop new treatment strategies to prevent obesity and obesity-associated complications.
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Objective To investigate the association between microalbuminuria (MA) and high-sensitive C-reactive protein in essential hypertensive subjects. Methods Urinary albumin excretion rate (UAER)and the concentrations of high-sensitive C-reactive protein(hs-CRP) were measured. One hundred and eight patients with hypertension were divided into 2 groups: normoalbuminuria and microalbuminuria group. concentrations of hs-CRP was compared between the two groups , and the association between MA and hs-CRP was evaluated.Results Patients with microalbuminuria were significantly characterized by higher systolic blood pressure (SBP) ,pulse pressure(PP) ,circulating fibrinogen and hs-CRP. Evaluation of bivariate correlation indicated that UAER was positively correlated with SBP , PP , body mass index (BMI) ,Serum creatinine (SCr), fibrinogen and hs-CRP. Multivariate regression analysis demonstrated PP, SCr and hs-CRP were independent risks associated with UAER.Conclusions Microalbuminuria is a sensitive marker in essential hypertensive subjects with early renal injury .hs-CRP is an independent risk associated with UAER ,which suggests that inflammation correlate with early renal injury in essential hypertension.
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AIM: To explore the anti-low-grade-inflammation mechanisms of Shenqi Compound Recipe(SQCR) in GK rats. METHODS: Specefic pathogen free(SPF) GK rats were divided randomly according to blood glucose level into four groups:Model,Ramipril,SQCR low dosage,SQCR high dosage group and normal Wistar rats(normal control group).GK rats were injected N-?-nitrol-L-arginine methyl ester(L-NAME) intra-peritoneally and took high-fat diet and Wistar rats were injected saline intra-peritoneally and took common diet freely,respectively.In the experiment periods,each group was administrated correspondent substance respectively for 32 days.Serum concentrations of C reactive protein(CRP) and adiponectin were determined by ELISA.Adiponectin mRNA expressions in white adiposed tissue were measured by real time reverse transcriptase PCR. RESULTS:Concentrations of CRP all decreased(P