Magnesium deficiency enhances basal glucose disposal in the rat
Lowney, P.; Hannon, T.S.; Baron, A.D.
American Journal of Physiology 268(5 Pt 1): E925-E931
1995
ISSN/ISBN: 0002-9513 PMID: 7762647 Document Number: 444064
To investigate the contribution of hepatic and peripheral tissues to the enhanced glucose disposal rate (K-g) observed in magnesium (Mg)-deficient rats, euglycemic-hyperinsulinemic clamps were performed with continuous infusion of (3-3H)glucose and three insulin infusion rates, 1, 8, and 16 mu-U cntdot kg-1 cntdot min-1. Moderately Mg-deficient (Mg-, 4.2 mu-M Mg/g diet) and Mg-adequate (Mg+, 16.7 mu-M Mg/g diet) Sprague-Dawley rats were studied after 3 wk of dietary treatment. Growth, fasting glucose, and insulin concentrations were not affected by dietary treatment. Basal hepatic glucose output (HGO) and glucose disposal (R-d) were increased by 24% in Mg- rats (P lt 0.001). After 1 mu-U insulin cntdot kg-1 cntdot min-1 infusion, R-d and the glucose infusion rate that maintained euglycemia were significantly increased in Mg- rats by 24 and 46%, respectively. However, when the increase in R-d above baseline was examined, no significant differences were observed. Therefore, the increased basal glucose disposal observed in Mg- rats may be mediated by noninsulin-dependent mechanisms. Insulin suppression of HGO during 1 mu-U insulin cntdot kg-1 cntdot min-1 infusion was greater in Mg- rats (43%) compared with Mg+ rats (27%, P lt 0.05). In conclusion, the increased K-g observed in Mg- rats is likely to be caused by an increase in noninsulin-mediated glucose uptake and an enhancement of hepatic insulin sensitivity.