Publications by authors named "Iryna Liauchonak"

4 Publications

  • Page 1 of 1

Non-Nutritive Sweeteners and Their Implications on the Development of Metabolic Syndrome.

Nutrients 2019 Mar 16;11(3). Epub 2019 Mar 16.

Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON K7L 3N6, Canada.

Individuals widely use non-nutritive sweeteners (NNS) in attempts to lower their overall daily caloric intake, lose weight, and sustain a healthy diet. There are insufficient scientific data that support the safety of consuming NNS. However, recent studies have suggested that NNS consumption can induce gut microbiota dysbiosis and promote glucose intolerance in healthy individuals that may result in the development of type 2 diabetes mellitus (T2DM). This sequence of events may result in changes in the gut microbiota composition through microRNA (miRNA)-mediated changes. The mechanism(s) by which miRNAs alter gene expression of different bacterial species provides a link between the consumption of NNS and the development of metabolic changes. Another potential mechanism that connects NNS to metabolic changes is the molecular crosstalk between the insulin receptor (IR) and G protein-coupled receptors (GPCRs). Here, we aim to highlight the role of NNS in obesity and discuss IR-GPCR crosstalk and miRNA-mediated changes, in the manipulation of the gut microbiota composition and T2DM pathogenesis.
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http://dx.doi.org/10.3390/nu11030644DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6471792PMC
March 2019

Diagnostic value of hysteroscopy in abnormal uterine bleeding.

Can Fam Physician 2018 06;64(6):442-444

Student in the Graduate Diploma and Professional Master in Medical Sciences program in the School of Medicine at Queen's University in Kingston, Ont.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5999244PMC
June 2018

The Biased G-Protein-Coupled Receptor Agonism Bridges the Gap between the Insulin Receptor and the Metabolic Syndrome.

Int J Mol Sci 2018 Feb 17;19(2). Epub 2018 Feb 17.

Department of Biomedical and Molecular Science, Queen's University, Kingston, ON K7L 3N6, Canada.

Insulin signaling, as mediated through the insulin receptor (IR), plays a critical role in metabolism. Aberrations in this signaling cascade lead to several pathologies, the majority of which are classified under the umbrella term "metabolic syndrome". Although many of these pathologies are associated with insulin resistance, the exact mechanisms are not well understood. One area of current interest is the possibility of G-protein-coupled receptors (GPCRs) influencing or regulating IR signaling. This concept is particularly significant, because GPCRs have been shown to participate in cross-talk with the IR. More importantly, GPCR signaling has also been shown to preferentially regulate specific downstream signaling targets through GPCR agonist bias. A novel study recently demonstrated that this GPCR-biased agonism influences the activity of the IR without the presence of insulin. Although GPCR-IR cross-talk has previously been established, the notion that GPCRs can regulate the activation of the IR is particularly significant in relation to metabolic syndrome and other pathologies that develop as a result of alterations in IR signaling. As such, we aim to provide an overview of the physiological and pathophysiological roles of the IR within metabolic syndrome and its related pathologies, including cardiovascular health, gut microflora composition, gastrointestinal tract functioning, polycystic ovarian syndrome, pancreatic cancer, and neurodegenerative disorders. Furthermore, we propose that the GPCR-biased agonism may perhaps mediate some of the downstream signaling effects that further exacerbate these diseases for which the mechanisms are currently not well understood.
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http://dx.doi.org/10.3390/ijms19020575DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855797PMC
February 2018

Human orf: Atypical rash in an urban medical practice.

Can Fam Physician 2017 10;63(10):769-771

Instructor at Pharma-Medical Science College of Canada in Toronto.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5638474PMC
October 2017
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