Abstract
Background: Type 2 diabetes (T2DM) has been associated with deficiencies in serum magnesium level, decreasing insulin sensitivity and glucose metabolism. Glycosylated hemoglobin (Hb1Ac) is a biomarker of glucose values within the half-life of the erythrocyte, that is, 3 months. Low circulating and intracellular magnesium levels can modify glucose metabolism and insulin sensitivity. Renal solute management is a parameter little used to estimate circulating and excreted concentrations of elements such as magnesium.
Objective: The purpose of this study was to assess and associated fractional excretion of magnesium (FEMg) and serum magnesium with metabolic parameters, especially Hb1Ac percent, in a group of well characterized subjects with T2DM and non-diabetics subjects (ND).
Methods: According to Hb1Ac, two groups were compared and associated with existing biochemical parameters, included Hb1Ac, fasting glucose, lipid profile, serum creatinine, serum magnesium and urinary creatinine for FEMg.
Results: HbA1c levels were explained by serum magnesium in 25%. Serum magnesium levels in the ND group were higher than in the T2DM group and this was a statistically significant difference. Serum magnesium ≤1.8 is a risk factor (OD 16.1; P=0.021) for an HbA1c ≥ 6.5%.
Conclusion: In this study, hypomagnesemia was a parameter strongly associated with the diagnosis and progression of T2DM, while FEMg showed no significant association.
Keywords: Hypomagnesaemia, Fractional excretion of magnesium, glycosylated hemoglobin, type 2 diabetes, risk factor, nondiabetic.
Current Diabetes Reviews
Title:Deranged Fractional Excretion of Magnesium and Serum Magnesium Levels in Relation to Retrograde Glycaemic Regulation in Patients with Type 2 Diabetes Mellitus
Volume: 17 Issue: 1
Author(s): Corvera A.C. Esmeralda, Pedroza E. David, Irais C. Maldonado, Sharara Núñez A. Ibrahim, Alcántar S. David, Martha A.Q. Escorza and Delgadillo G. Dealmy*
Affiliation:
- Departamento de Farmacologia, Facultad de Medicina U.T., Universidad Autonoma de Coahuila. Torreon, Coah.,Mexico
Keywords: Hypomagnesaemia, Fractional excretion of magnesium, glycosylated hemoglobin, type 2 diabetes, risk factor, nondiabetic.
Abstract:
Background: Type 2 diabetes (T2DM) has been associated with deficiencies in serum magnesium level, decreasing insulin sensitivity and glucose metabolism. Glycosylated hemoglobin (Hb1Ac) is a biomarker of glucose values within the half-life of the erythrocyte, that is, 3 months. Low circulating and intracellular magnesium levels can modify glucose metabolism and insulin sensitivity. Renal solute management is a parameter little used to estimate circulating and excreted concentrations of elements such as magnesium.
Objective: The purpose of this study was to assess and associated fractional excretion of magnesium (FEMg) and serum magnesium with metabolic parameters, especially Hb1Ac percent, in a group of well characterized subjects with T2DM and non-diabetics subjects (ND).
Methods: According to Hb1Ac, two groups were compared and associated with existing biochemical parameters, included Hb1Ac, fasting glucose, lipid profile, serum creatinine, serum magnesium and urinary creatinine for FEMg.
Results: HbA1c levels were explained by serum magnesium in 25%. Serum magnesium levels in the ND group were higher than in the T2DM group and this was a statistically significant difference. Serum magnesium ≤1.8 is a risk factor (OD 16.1; P=0.021) for an HbA1c ≥ 6.5%.
Conclusion: In this study, hypomagnesemia was a parameter strongly associated with the diagnosis and progression of T2DM, while FEMg showed no significant association.
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Esmeralda A.C. Corvera , David E. Pedroza , Maldonado C. Irais , Ibrahim Núñez A. Sharara , David S. Alcántar , Escorza A.Q. Martha and Dealmy G. Delgadillo *, Deranged Fractional Excretion of Magnesium and Serum Magnesium Levels in Relation to Retrograde Glycaemic Regulation in Patients with Type 2 Diabetes Mellitus, Current Diabetes Reviews 2021; 17 (1) . https://dx.doi.org/10.2174/1573399816666200714150434
DOI https://dx.doi.org/10.2174/1573399816666200714150434 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |

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