| Description |
Background: Epidemiological data associates low magnesium (Mg) intake with greater risk of metabolic syndrome/diabetes, and Mg status is often compromised in diabetic patients. It remains unclear whether low Mg consumption may exacerbate the metabolic disruptions that occur during diabetes. Objective: We hypothesized low dietary Mg during the development of diabetes would alter metabolic rate, and worsen glucose tolerance/insulin sensitivity. Methods: Three cohorts (n = 8 each) of 8-week-old TallyHo (TH) mice that develop Type 2 Diabetes by 16 weeks of age were fed special diets for 8 weeks. Group 1: TH + Low Mg diet (L-Mg, 100mg Mg Oxide/kg chow). Group 2: TH + Standard Mg diet (S-Mg, 500mg Mg Oxide/kg chow). Group 3: TH + High Mg diet (H-Mg, 1000mg Mg Bisglycinate/kg chow). Age-matched male C57BL/6J mice fed standard diets served as controls (Con, n = 8, 500mg Mg Oxide/kg chow). Results: Energy expenditure was lowest (p < 0.05) in L-Mg vs. all other groups. Insulin tolerance test (AUC, glucose mg/dL), indicated insulin resistance (p < 0.05) in L-Mg (12394 ± 2344) vs. Con (3866 ± 2344), and a trend (p = 0.052) indicating greater insulin resistance in S-Mg (10429 ± 2193) vs. Con. However, insulin tolerance was normalized in H-Mg (7838 ± 2344) vs. Con. QUICKI index indicated that all groups were insulin resistant (p < 0.05) compared to Con (0.585 ± 0.14). However, L-Mg (0.403 ± 0.15) had greater (p < 0.05) insulin resistance than S-Mg (0.462 ± 0.17) and H-Mg (0.454 ± 0.15). Insulin stimulated phosphorylation of hepatic insulin receptor was similar among all groups, whereas Akt phosphorylation was reduced (p < 0.05) in all diabetic mice regardless of Mg intake. Conclusions: Low dietary Mg intake reduces oxygen consumption and energy expenditure, and worsens insulin sensitivity in diabetic mice. Supplemental Mg can partially reduce fasting glucose and improve insulin tolerance, but could not be attributed to an improvement in hepatic insulin signaling. |
