Publication: Gut Microbiota Composition in Prediabetes and Newly Diagnosed Type 2 Diabetes: A Systematic Review of Observational Studies
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Date
2022
Journal Title
Journal ISSN
Volume Title
Publisher
Frontiers Media S.A.
Abstract
Evidence of gut microbiota involvement in regulating glucose metabolism and type 2 diabetes mellitus (T2DM) progression is accumulating. The understanding of microbial dysbiosis and specific alterations of gut microbiota composition that occur during the early stages of glucose intolerance, unperturbed by anti-diabetic medications, is especially essential. Hence, this systematic review was conducted to summarise the existing evidence related to microbiota composition and diversity in individuals with prediabetes (preDM) and individuals newly diagnosed with T2DM (newDM) in comparison to individuals with normal glucose tolerance (nonDM). A systematic search of the PubMed, MEDLINE and CINAHL databases were conducted from inception to February 2021 supplemented with manual searches of the list of references. The primary keywords of “type 2 diabetes”, “prediabetes”, “newly-diagnosed” and “gut microbiota” were used. Observational studies that conducted analysis of the gut microbiota of respondents with preDM and newDM were included. The quality of the studies was assessed using the modified Newcastle-Ottawa scale by independent reviewers. A total of 18 studies (5,489 participants) were included. Low gut microbial diversity was generally observed in preDM and newDM when compared to nonDM. Differences in gut microbiota composition between the disease groups and nonDM were inconsistent across the included studies. Four out of the 18 studies found increased abundance of phylum Firmicutes along with decreased abundance of Bacteroidetes in newDM. At the genus/species levels, decreased abundance of Faecalibacterium prausnitzii, Roseburia, Dialister, Flavonifractor, Alistipes, Haemophilus and Akkermansia muciniphila and increased abundance of Lactobacillus, Streptococcus, Escherichia, Veillonella and Collinsella were observed in the disease groups in at least two studies. Lactobacillus was also found to positively correlate with fasting plasma glucose (FPG), HbA1c and/or homeostatic assessment of insulin resistance (HOMA-IR) in four studies. This renders a need for further investigations on the species/strain-specific role of endogenously present Lactobacillus in glucose regulation mechanism and T2DM disease progression. Differences in dietary intake caused significant variation in specific bacterial abundances. More studies are needed to establish more consistent associations, between clinical biomarkers or dietary intake and specific gut bacterial composition in prediabetes and early T2DM.
Description
Volume 12
Keywords
gut microbiota, type 2 diabetes, prediabetes, 16S rRNA sequencing, systematic review
Citation
Letchumanan G, Abdullah N, Marlini M, Baharom N, Lawley B, Omar MR, Mohideen FBS, Addnan FH, Nur Fariha MM, Ismail Z and Pathmanathan SG (2022) Gut Microbiota Composition in Prediabetes and Newly Diagnosed Type 2 Diabetes: A Systematic Review of Observational Studies. Front. Cell. Infect. Microbiol. 12:943427. doi: 10.3389/fcimb.2022.943427
URI
https://www.frontiersin.org/articles/10.3389/fcimb.2022.943427/full
https://www.scopus.com/record/display.uri?eid=2-s2.0-85136866717&origin=resultslist&sort=plf-f&src=s&sid=afbb30fec47e68324a407a39afdba60b&sot=b&sdt=b&s=TITLE-ABS-KEY%28%22+Gut+Microbiota+Composition+in+Prediabetes+and+Newly+Diagnosed+Type+2+Diabetes%3A+A+Systematic+Review+of+Observational+Studies%22%29&sl=124&sessionSearchId=afbb30fec47e68324a407a39afdba60b
https://oarep.usim.edu.my/handle/123456789/10506
https://www.scopus.com/record/display.uri?eid=2-s2.0-85136866717&origin=resultslist&sort=plf-f&src=s&sid=afbb30fec47e68324a407a39afdba60b&sot=b&sdt=b&s=TITLE-ABS-KEY%28%22+Gut+Microbiota+Composition+in+Prediabetes+and+Newly+Diagnosed+Type+2+Diabetes%3A+A+Systematic+Review+of+Observational+Studies%22%29&sl=124&sessionSearchId=afbb30fec47e68324a407a39afdba60b
https://oarep.usim.edu.my/handle/123456789/10506