FIG. 1.

Insulin-sensitizing activity of Mαα. A: GP were treated with Mαα as described in research design and methods. Fasting plasma glucose amounted to 112 ± 7 mg% and 108 ± 8 mg% in nontreated and Mαα-treated GP, respectively. Fasted GP were primed through the jugular vein cannula with Humulin R insulin in saline/0.2% BSA (fatty acid free), followed by constant infusion of 10–80 mU/kg BW/min for 180 min. Plasma glucose was monitored by Elite glucometer every 10 min and maintained by infusing a solution of 50% glucose in saline at a variable rate, up to 50 μL/min. M, the rate of infused glucose (mg/kg BW/min) required to maintain blood glucose under conditions of clamped hyperinsulinemia. M values for all nontreated animals (n = 7) were derived under hyperinsulinemic-euglycemic clamp conditions (plasma glucose 90–106 mg/dL, plasma insulin 20 ± 3 ng/mL). M values for Mαα-treated animals (n = 6) were derived under hyperinsulinemic-hypoglycemic clamp conditions (plasma glucose 67–87 mg/dL, plasma insulin 14 ± 3 ng/mL), as a result of robust increase in glucose uptake that could not be satisfied by maximal rates of glucose infusion (50 μL/min). Respective means are denoted by line (P < 0.05). B: Lactate/pyruvate-dependent glucose production (arbitrary units) induced by dexamethasone/8-(4-chlorophenylthio)-cAMP was determined in H4IIE cells as previously described (22), in the presence and absence of Mαα and insulin as indicated. Representative experiment in triplicates. Mean ± SE. *Significant as compared with nontreated cells (P < 0.05).