ABSTRACT
The gut microbiota (GM) plays a vital role in human health, with increasing evidence linking its imbalance to chronic kidney disease and end-stage kidney disease. Although the exact methods underlying kidney-GM crosstalk are not fully understood, interventions targeting GM were made and lay in three aspects: diagnostic, predictive, and therapeutic interventions. While these interventions show promising results in reducing uremic toxins and inflammation, challenges remain in the form of patient-specific GM variability, potential side effects, and safety concerns. Our understanding of GMs role in kidney disease is still evolving, necessitating further research to elucidate the causal relationship and mechanistic interactions. Personalized interventions focusing on specific GM signatures could enhance patient outcomes. However, comprehensive clinical trials are needed to validate these approaches' safety, efficacy, and feasibility.
ABSTRACT
Research was performed on a group of 30 patients with non-insulin-dependent diabetes mellitus (NIDDM), who never received antidiabetic medication before, and on a group of 17 healthy adults. The patients were administered treatment with metformin, 1,000 mg/day. Plasmatic and urinary concentration of magnesium have been measured, copper and zinc along with the concentrations of glucose, HDL, LDL, cholesterol, tryglicerides, HbA1c, and total erythrocyte magnesium, in advance and after 3 months of treatment. Data showed significant differences in the NIDDM group vs the control group: for plasma magnesium-1.95 ± 0.19 vs 2.20 ± 0.18 mg/dl, p < 0.001; urine magnesium-237.28 ± 34.51 vs 126.25 ± 38.22 mg/24 h, p < 0.001; erythrocyte magnesium-5.09 ± 0.63 vs 6.38 ± 0.75 mg/dl, p < 0.001; plasma zinc-67.56 ± 6.21 vs 98.41 ± 20.47 µg/dl, p < 0.001; urine zinc-1,347.54 ± 158.24 vs 851.65 ± 209.75 µg/24 h, p < 0.001; plasma copper-111.91 ± 20.98 vs 96.33 ± 8.56 µg/dl, p < 0.001; and urine copper-51.70 ± 23.79 vs 36.00 ± 11.70 µg/24 h, p < 0.05. Treatment with metformin for 3 months modified significant erythrocyte magnesium-5.75 ± 0.61 vs 5.09 ± 0.63 mg/dl, p < 0.001 and urine magnesium-198.27 ± 27.07 vs 237.28 ± 34.51 mg/24 h, p < 0.001, whereas it did not modify significant the plasmatic and urinary concentration of the other cations. The erythrocyte magnesium concentration was inversely correlated with HbA1c (r = -0.438, p = 0.015). The plasma level of copper was positively correlated with HbA1c (r = 0.517, p < 0.003), tryglicerides (r = 0.534, p < 0.003), and cholesterol (r = 0.440, p < 0.05), and the plasma level of zinc was inversely correlated with glycemia (r = -0.399, p = 0.029). Our data show a significant action of metformin therapy, by increasing the total intraerythrocyte magnesium concentration and decreasing the urinary magnesium elimination, positively correlated with the decrease of glycemia and HbA1c in NIDDM patients.
