Unveiling contrasts in microbiota response: A1c control improves dysbiosis in low-A1c T2DM, but fails in high-A1c cases—a key to metabolic memory?
Authors' conclusion
Despite a notable A1c outcome, G2 could not restore its MB. This seeming resistance to change, leading to a persistent inflammation component found in G2, might be part of the "metabolic memory" in T2DM.
Study context
- Population
- Patients with uncontrolled T2DM undergoing intensive glycaemic control aiming for ≥1% A1c reduction
- Participants
- 18 vs 13
- Exposure
- Intensive glycaemic control in T2DM with A1c <9% vs A1c >9%
- G1n = 18
- G2n = 13
- Outcome
- Gut microbiota response to intensive glycaemic control
- Follow-up
- Baseline, 6 and 12 months
Main finding
As reported in the abstract
Gut microbiota changes
- G1: decrease in Erysipelotrichaceae_UCG_003 and Mollicutes order (linked to metabolic syndrome)
- G2: increase in proinflammatory Megasphaera and Acidaminococcus; only one beneficial genus, butyrate-producer Phascolarctobacterium, increased
Observational data: associations, not effects.
Further findings
| Outcome | G1 | G2 |
|---|---|---|
| Average A1c reduction | average 1.1% | 3.13% |
Original publication
Unveiling contrasts in microbiota response: A1c control improves dysbiosis in low-A1c T2DM, but fails in high-A1c cases—a key to metabolic memory? BMJ Open Diabetes Res Care. Published 27 June 2024. doi:10.
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