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Effect of resistant starch type 2 on inflammatory mediators: A systematic review and meta-analysis of randomized controlled trials
•Resistance starch type II passes to the large intestine in undigested form and can be fermented by gut microbiota.•Colonic fermentation of resistance starch improves the growth of some useful bacterial.•A meta-analysis conducted on randomized clinical trials which assessed resistance starch effect...
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Published in: | Complementary therapies in medicine 2021-01, Vol.56, p.102597-102597, Article 102597 |
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description | •Resistance starch type II passes to the large intestine in undigested form and can be fermented by gut microbiota.•Colonic fermentation of resistance starch improves the growth of some useful bacterial.•A meta-analysis conducted on randomized clinical trials which assessed resistance starch effect on inflammatory mediators.•Eight randomized clinical trials included in systematic review and meta-analysis.•The overall effect illustrated no significant change in serum levels of c-reactive protein (CRP), interlukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in intervention group compared with the control group.
Inflammation is the main cause in the development of chronic diseases. The enhancement of pro-inflammatory factors, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hs-CRP) is the main risk factor in chronic diseases. Resistant starch type 2 (RS2) is non-gelatinized granules which their enzymatic hydrolysis is very low. RS2 might be able to reduce inflammatory mediators, therefore; our aim for this study was indicating RS2 effects on inflammatory mediators such as IL-6, TNF-a, and CRP among healthy and unhealthy subjects.
Articles which assessed RS2 effect on IL-6, TNF-α, and hs-CRP were found by advanced search methods. Electronic databases including Google scholar, ISI web of science, SCOPUS, and PubMed, were searched up to October 2019. Treatment effect was the mean difference between changes in serum levels of inflammatory biomarkers in each arm of the clinical trials. To pool the effect of resistant starch on inflammatory biomarkers, we used random effects model.
We included eight articles in systematic review and meta-analysis. The overall effect illustrated no significant change in serum levels of hs-CRP, IL-6, and TNF-α in intervention group compared with the control group (WMD: -7.18 pg/mL, 95% CI: −27.80, 13.45; P = 0.495, I2 = 100.0%, WMD: -0.003 pg/mL, 95% CI: −0.07, 0.06; P = 0.919, I2 = 98.1%, WMD: -0.003 pg/mL, 95% CI: −0.004, -0.001; P < 0.0001, I2 = 98.0% respectively).
In conclusion, we found that RS2 could not reduce inflammatory mediators, but we still need more RCTs with longer intervention duration, higher dose, and studies in different countries. |
doi_str_mv | 10.1016/j.ctim.2020.102597 |
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Inflammation is the main cause in the development of chronic diseases. The enhancement of pro-inflammatory factors, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hs-CRP) is the main risk factor in chronic diseases. Resistant starch type 2 (RS2) is non-gelatinized granules which their enzymatic hydrolysis is very low. RS2 might be able to reduce inflammatory mediators, therefore; our aim for this study was indicating RS2 effects on inflammatory mediators such as IL-6, TNF-a, and CRP among healthy and unhealthy subjects.
Articles which assessed RS2 effect on IL-6, TNF-α, and hs-CRP were found by advanced search methods. Electronic databases including Google scholar, ISI web of science, SCOPUS, and PubMed, were searched up to October 2019. Treatment effect was the mean difference between changes in serum levels of inflammatory biomarkers in each arm of the clinical trials. To pool the effect of resistant starch on inflammatory biomarkers, we used random effects model.
We included eight articles in systematic review and meta-analysis. The overall effect illustrated no significant change in serum levels of hs-CRP, IL-6, and TNF-α in intervention group compared with the control group (WMD: -7.18 pg/mL, 95% CI: −27.80, 13.45; P = 0.495, I2 = 100.0%, WMD: -0.003 pg/mL, 95% CI: −0.07, 0.06; P = 0.919, I2 = 98.1%, WMD: -0.003 pg/mL, 95% CI: −0.004, -0.001; P < 0.0001, I2 = 98.0% respectively).
In conclusion, we found that RS2 could not reduce inflammatory mediators, but we still need more RCTs with longer intervention duration, higher dose, and studies in different countries.</description><identifier>ISSN: 0965-2299</identifier><identifier>EISSN: 1873-6963</identifier><identifier>DOI: 10.1016/j.ctim.2020.102597</identifier><identifier>PMID: 33197672</identifier><language>eng</language><publisher>Scotland: Elsevier Ltd</publisher><subject>Biomarkers ; C-reactive protein ; C-reactive protein (CRP) ; Chronic illnesses ; Citation management software ; Clinical trials ; Cytokines ; Diabetes ; Dietary fiber ; Fermentation ; Health risks ; Inflammation ; Interleukin 6 ; Interleukin-6 (IL-6) ; Interleukins ; Intervention ; Kinases ; Meta-analysis ; Microbiota ; Proteins ; Resistance factors ; Resistant starch ; Risk analysis ; Risk factors ; Search engines ; Serum levels ; Starch ; Statistical analysis ; Systematic review ; Tumor necrosis factor-alpha (TNF-a) ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Complementary therapies in medicine, 2021-01, Vol.56, p.102597-102597, Article 102597</ispartof><rights>2020 Elsevier Ltd</rights><rights>Copyright © 2020 Elsevier Ltd. All rights reserved.</rights><rights>2020. Elsevier Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-25a07c99b2e93b3ba4db801da31ac71cfe5d7ab94af055919e254b7e3fd8d9f73</citedby><cites>FETCH-LOGICAL-c494t-25a07c99b2e93b3ba4db801da31ac71cfe5d7ab94af055919e254b7e3fd8d9f73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33197672$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Haghighatdoost, Fahimeh</creatorcontrib><creatorcontrib>Gholami, Ali</creatorcontrib><creatorcontrib>Hariri, Mitra</creatorcontrib><title>Effect of resistant starch type 2 on inflammatory mediators: A systematic review and meta-analysis of randomized controlled trials</title><title>Complementary therapies in medicine</title><addtitle>Complement Ther Med</addtitle><description>•Resistance starch type II passes to the large intestine in undigested form and can be fermented by gut microbiota.•Colonic fermentation of resistance starch improves the growth of some useful bacterial.•A meta-analysis conducted on randomized clinical trials which assessed resistance starch effect on inflammatory mediators.•Eight randomized clinical trials included in systematic review and meta-analysis.•The overall effect illustrated no significant change in serum levels of c-reactive protein (CRP), interlukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in intervention group compared with the control group.
Inflammation is the main cause in the development of chronic diseases. The enhancement of pro-inflammatory factors, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hs-CRP) is the main risk factor in chronic diseases. Resistant starch type 2 (RS2) is non-gelatinized granules which their enzymatic hydrolysis is very low. RS2 might be able to reduce inflammatory mediators, therefore; our aim for this study was indicating RS2 effects on inflammatory mediators such as IL-6, TNF-a, and CRP among healthy and unhealthy subjects.
Articles which assessed RS2 effect on IL-6, TNF-α, and hs-CRP were found by advanced search methods. Electronic databases including Google scholar, ISI web of science, SCOPUS, and PubMed, were searched up to October 2019. Treatment effect was the mean difference between changes in serum levels of inflammatory biomarkers in each arm of the clinical trials. To pool the effect of resistant starch on inflammatory biomarkers, we used random effects model.
We included eight articles in systematic review and meta-analysis. The overall effect illustrated no significant change in serum levels of hs-CRP, IL-6, and TNF-α in intervention group compared with the control group (WMD: -7.18 pg/mL, 95% CI: −27.80, 13.45; P = 0.495, I2 = 100.0%, WMD: -0.003 pg/mL, 95% CI: −0.07, 0.06; P = 0.919, I2 = 98.1%, WMD: -0.003 pg/mL, 95% CI: −0.004, -0.001; P < 0.0001, I2 = 98.0% respectively).
In conclusion, we found that RS2 could not reduce inflammatory mediators, but we still need more RCTs with longer intervention duration, higher dose, and studies in different countries.</description><subject>Biomarkers</subject><subject>C-reactive protein</subject><subject>C-reactive protein (CRP)</subject><subject>Chronic illnesses</subject><subject>Citation management software</subject><subject>Clinical trials</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Dietary fiber</subject><subject>Fermentation</subject><subject>Health risks</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukin-6 (IL-6)</subject><subject>Interleukins</subject><subject>Intervention</subject><subject>Kinases</subject><subject>Meta-analysis</subject><subject>Microbiota</subject><subject>Proteins</subject><subject>Resistance factors</subject><subject>Resistant starch</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Search engines</subject><subject>Serum levels</subject><subject>Starch</subject><subject>Statistical analysis</subject><subject>Systematic review</subject><subject>Tumor necrosis factor-alpha (TNF-a)</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis 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Med</addtitle><date>2021-01</date><risdate>2021</risdate><volume>56</volume><spage>102597</spage><epage>102597</epage><pages>102597-102597</pages><artnum>102597</artnum><issn>0965-2299</issn><eissn>1873-6963</eissn><abstract>•Resistance starch type II passes to the large intestine in undigested form and can be fermented by gut microbiota.•Colonic fermentation of resistance starch improves the growth of some useful bacterial.•A meta-analysis conducted on randomized clinical trials which assessed resistance starch effect on inflammatory mediators.•Eight randomized clinical trials included in systematic review and meta-analysis.•The overall effect illustrated no significant change in serum levels of c-reactive protein (CRP), interlukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in intervention group compared with the control group.
Inflammation is the main cause in the development of chronic diseases. The enhancement of pro-inflammatory factors, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hs-CRP) is the main risk factor in chronic diseases. Resistant starch type 2 (RS2) is non-gelatinized granules which their enzymatic hydrolysis is very low. RS2 might be able to reduce inflammatory mediators, therefore; our aim for this study was indicating RS2 effects on inflammatory mediators such as IL-6, TNF-a, and CRP among healthy and unhealthy subjects.
Articles which assessed RS2 effect on IL-6, TNF-α, and hs-CRP were found by advanced search methods. Electronic databases including Google scholar, ISI web of science, SCOPUS, and PubMed, were searched up to October 2019. Treatment effect was the mean difference between changes in serum levels of inflammatory biomarkers in each arm of the clinical trials. To pool the effect of resistant starch on inflammatory biomarkers, we used random effects model.
We included eight articles in systematic review and meta-analysis. The overall effect illustrated no significant change in serum levels of hs-CRP, IL-6, and TNF-α in intervention group compared with the control group (WMD: -7.18 pg/mL, 95% CI: −27.80, 13.45; P = 0.495, I2 = 100.0%, WMD: -0.003 pg/mL, 95% CI: −0.07, 0.06; P = 0.919, I2 = 98.1%, WMD: -0.003 pg/mL, 95% CI: −0.004, -0.001; P < 0.0001, I2 = 98.0% respectively).
In conclusion, we found that RS2 could not reduce inflammatory mediators, but we still need more RCTs with longer intervention duration, higher dose, and studies in different countries.</abstract><cop>Scotland</cop><pub>Elsevier Ltd</pub><pmid>33197672</pmid><doi>10.1016/j.ctim.2020.102597</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biomarkers C-reactive protein C-reactive protein (CRP) Chronic illnesses Citation management software Clinical trials Cytokines Diabetes Dietary fiber Fermentation Health risks Inflammation Interleukin 6 Interleukin-6 (IL-6) Interleukins Intervention Kinases Meta-analysis Microbiota Proteins Resistance factors Resistant starch Risk analysis Risk factors Search engines Serum levels Starch Statistical analysis Systematic review Tumor necrosis factor-alpha (TNF-a) Tumor necrosis factor-TNF Tumor necrosis factor-α |
title | Effect of resistant starch type 2 on inflammatory mediators: A systematic review and meta-analysis of randomized controlled trials |
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