(1) Background: Magnesium deficiency is usually associated with type 2 diabetes mellitus (T2DM). Individuals living with T2DM with hypomagnesemia show a more rapid disease progression and have an increased risk for diabetes complications. (2) Methods: This is a cross-sectional and descriptive study in the National Institute of Nutrition and Food Technology of Tunis in Tunisia, including all adult outpatients (≥18 years old) with a diagnosis of T2DM from 1 September 2018 to 31 August 2019. The aim of this study was to evaluate the prevalence of plasmatic magnesium deficiency in a Tunisian population of T2DM and to study the relationship between magnesium status and intake, glycemic control and long-term diabetes-related complications. (3) Results: Among the 101 T2DM outpatients, 13 (12.9%) presented with a plasmatic magnesium deficiency. The mean age was 56 ± 7.9 years with a female predominance (62%, n = 63). The mean of the plasmatic magnesium level was 0.79 ± 0.11 mmol/L (0.5–1.1), and the mean of 24 h urinary magnesium excretion was 87.8 ± 53.8 mg/24 h [4.8–486.2]. HbA1c was significantly higher in the plasmatic magnesium deficiency group than the normal magnesium status group (10% ± 1.3 vs. 8.3% ± 1.9; p = 0.04), with a significant difference in participants with a poor glycemic control (HbA1c > 7%) (100%, n = 13/13 vs. 53%, n = 47/88; p = 0.001). A weak negative relationship was also found between plasmatic magnesium and HbA1c (r = −0.2, p = 0.03). Peripheral artery disease was more commonly described in individuals with low plasmatic magnesium levels than in individuals with normal levels (39%, n = 5 vs. 0%, n = 0; p < 0.001). The mean plasmatic magnesium level in participants without diabetic nephropathy and also peripheral artery disease was significantly higher compared to individuals with each long-term diabetes-related complication (0.8 mmol/L ± 0.1 vs. 0.71 mmol/L ± 0.07; p = 0.006) and (0.8 mmol/L ± 0.1 vs. 0.6 mmol/L ± 0.08; p < 0.001), respectively. (4) Conclusions: Hypomagnesemia was identified in individuals with T2DM, causing poor glycemic control and contributing to the development and progression of diabetes-related microvascular and macrovascular complications.

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