RESUMO
Purpose: The aim of this study was to assess the impact of Ramadan intermittent fasting on metabolic and inflammatory profiles in type 2 diabetic patients (T2D). Methods: It was a prospective study including 55 T2D patients treated with oral hypoglycemic drugs, who intended to observe Ramadan fasting in 2019. All participants underwent a questionnaire, a physical examination, laboratory investigations, and a cardiovascular risk assessment using the Framingham score before Ramadan (T0), immediately after Ramadan (T1), and two months after Ramadan (T2). Results: The mean age of participants was 54.5 ± 10.1 years. The number of fasted days was 29.3 ± 2.3 days. The mean total daily calorie intake decreased significantly by 19% during Ramadan (p < 10-3). A significant decrease in weight (79.8 ± 12.9 vs 78.4 ± 13.3 kg, p = 0.003), body mass index (29.8 ± 5.4 vs 29.2 ± 5.4 kg/m2, p = 0.004), waist circumference (98.2 ± 9.6 vs 96.3 ± 10.2 cm, p = 0.015), fat body mass (24.3 ± 9.4 vs 23.5 ± 9.7 kg, p = 0.043) was observed at T1. The weight loss was significantly correlated with the number of fasting days (r = 0.348, p = 0.009) and was maintained at T2. Serum fructosamine increased at T1 (303.6 ± 46 vs 333.49 ± 59.49 µmol/L, p < 10-3) and returned to its baseline levels at T2. A significant decrease in insulin (9.7 ± 5.5 vs 7.98 ± 5.05 mIU/L, p = 0.043), fibrinogen (3.7 ± 0.8 vs 3.4 ± 0.6 g/L, p = 0.003), and hs-CRP (4.8 ± 5.7 vs 3.7 ± 4.5 mg/L, p = 0.058) levels was observed at T1. Homocysteine level was significantly higher after Ramadan (12.2 ± 6.2 vs 13.5 ± 6.4 µmol/L, p = 0.001). However, no significant changes were found in blood pressure, fasting blood glucose, HOMA-IR, uric acid, lipids, and white blood cells count. The mean Framingham score decreased insignificantly after Ramadan. Conclusions: Ramadan fasting in T2D patients seems to have a favorable impact on anthropometric parameters and inflammatory profile. However, it may cause a transient worsening of glycemic control.
RESUMO
(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.
