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. 2013 Dec 31;306(7):R457–R469. doi: 10.1152/ajpregu.00151.2013

Fig. 1.

Fig. 1.

Effects of caudal fourth ventricular (CV4) infusion of l-lactate on blood glucose levels, hypoglycemic hyperphagia, and glucagon and corticosteorne secretion during insulin-induced hypoglycemia in male rats. A, C, and D depict mean values ± SE (n = 5/group) for blood glucose (mg/dl), plasma glucagon (ng/ml), and plasma corticosterone (ng/ml), respectively, at +2 h after continuous infusion with artificial cerebrospinal fluid (aCSF) or l-lactate (25 μM·2.0 μl−1·h−1) between −10 min and +120 min, and subcutaneous injection of saline (SAL) or neutral protamine Hagedorn insulin (INS; 12.5 U/kg body wt sc) at time 0 (t0). B shows mean grams of consumed food ± SE for n = 5 rats/group between t0 and +120 min after initiation of above treatments. Treatment groups are presented as follows: aCSF + SAL, aCSF + INS, l-lactate + INS. *P < 0.05 vs. aCSF + SAL; **P < 0.05 vs. aCSF + INS. The data show that INS significantly reduced blood glucose and that this decrement was enhanced by concomitant hindbrain lactate infusion in INS-injected rats. INS-induced hypoglycemia stimulated food intake, a response that was abolished by hindbrain lactate administration. Plasma glucagon and corticosterone levels were elevated during hypoglycemia and were not further modified at the time point examined by hindbrain lactate repletion.