Kate Phuong-Nguyen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Kate Phuong-Nguyen has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- Bryony A. McNeill
Centre for Research in Assessment and Digital Learning (CRADLE), Deakin University, Melbourne, Australia
1 shared publication - Dat Da Ly
School of Medicine, The Institute for Mental and Physical Health and Clinical Translation, Deakin University, Geelong, VIC 3216, Australia
1 shared publication - Kathryn Aston-Mourney
School of Medicine, The Institute for Mental and Physical Health and Clinical Translation, Deakin University, Geelong, VIC 3216, Australia
1 shared publication - Leni R. Rivera
School of Medicine, Institute for Mental and Physical Health and Clinical Translation, Deakin University, Geelong, VIC 3220, Australia
1 shared publication - Trang T. T. Truong
Deakin Institute for Mental and Physical Health and Clinical Translation (Deakin IMPACT), School of Medicine, Deakin University, Australia
1 shared publication
Latest Publications
- Open Access
- 12 July 2026
- Published by MDPI AG in Biomolecules
- Vol. 16 (7) , 1017
Maternal Metformin Exposure Induces Gut Microbial Shifts in Non-Diabetic Dams and Sex-Stratified Changes in Mouse Offspring
Beyond being one of the most widely prescribed medications for type 2 diabetes, metformin has been increasingly used during pregnancy for gestational diabetes and polyendocrine metabolic ovarian syndrome. While it is considered safe for pregnancy and lactation, metformin is known to induce gut microbial changes in non-pregnant individuals with type 2 diabetes, and maternal and offspring microbial alterations are known to influence offspring development. Therefore, understanding whether metformin drives microbiota changes beyond the confounding effects of maternal hyperglycaemia holds significant implications for maternal–foetal health. In this study, non-diabetic C57BL/6 mouse dams received either control or metformin treatment (5 mg/mL) in drinking water during pregnancy and lactation. Microbial profiling from faecal samples of dams at gestational day 15 and offspring at 6 weeks of age was analysed using 16S rRNA sequencing and an R-based pipeline. Metformin positively restructured dominant taxa associated with healthy pregnancy in dams, while inducing broad taxonomic changes in males and Bacteroidetes-dominant shifts in female offspring. Overall, maternal metformin treatment promoted short-chain fatty acid-producing taxa while suppressing potentially opportunistic bacteria, without compromising community richness. Further studies are required to elucidate the functional mechanisms underlying these shifts and their long-term implications for maternal–foetal health.
- 12 July 2026
- Published by MDPI AG in Biomolecules
- Vol. 16 (7) , 1017
Open AccessMaternal Metformin Exposure Induces Gut Microbial Shifts in Non-Diabetic Dams and Sex-Stratified Changes in Mouse Offspring
Beyond being one of the most widely prescribed medications for type 2 diabetes, metformin has been increasingly used during pregnancy for gestational diabetes and polyendocrine metabolic ovarian syndrome. While it is considered safe for pregnancy and lactation, metformin is known to induce gut microbial changes in non-pregnant individuals with type 2 diabetes, and maternal and offspring microbial alterations are known to influence offspring development. Therefore, understanding whether metformin drives microbiota changes beyond the confounding effects of maternal hyperglycaemia holds significant implications for maternal–foetal health. In this study, non-diabetic C57BL/6 mouse dams received either control or metformin treatment (5 mg/mL) in drinking water during pregnancy and lactation. Microbial profiling from faecal samples of dams at gestational day 15 and offspring at 6 weeks of age was analysed using 16S rRNA sequencing and an R-based pipeline. Metformin positively restructured dominant taxa associated with healthy pregnancy in dams, while inducing broad taxonomic changes in males and Bacteroidetes-dominant shifts in female offspring. Overall, maternal metformin treatment promoted short-chain fatty acid-producing taxa while suppressing potentially opportunistic bacteria, without compromising community richness. Further studies are required to elucidate the functional mechanisms underlying these shifts and their long-term implications for maternal–foetal health.