Table 2.

Plasma glucose and ACTH concentrations in rats 30 min after intravenous injections of saline, insulin, or 2-DG

Treatment	Glucose (mm)				ACTH (pg/ml)
	0 min	30 min	n	30 min versus 0 min	0 min	30 min	n	30 min versus 0 min	Insulin versus 2-DG
Sham lesioned
Saline	5.09 ± 0.40	4.99 ± 0.35	8	ns	116.6 ± 14.0	114.8 ± 9.2	5	ns
Insulin	5.00 ± 0.72	2.10 ± 0.19	8	p < 0.0001	111.7 ± 3.5	258.0 ± 41.8	7	p < 0.01
2-DG	5.78 ± 0.19	17.97 ± 0.48	5	p < 0.0001	113.0 ± 5.9	479.7 ± 26.6	6	p < 0.001	p < 0.002
Lesioned
Insulin	5.6 ± 0.28	1.99 ± 0.11	13	p < 0.0001	112.0 ± 5.2	152.3 ± 13.3	6	ns
2-DG	5.84 ± 0.25	15.06 ± 0.27	7	p < 0.0001	92.3 ± 5.8	194.0 ± 26.4	3	ns	ns

Rats were given an injection of either a mouse anti-dopamine-β-hydroxylase-serum conjugated to saporin aimed at the PVH to lesion catecholaminergic afferents (Lesioned), or an equal volume of nonspecific mIgG-saporin (Sham lesioned).

Both insulin and 2-DG generated appropriate and significant glycemic responses 30 min later, irrespective of whether the catecholaminergic projections to the PVH were present or not. Saline injections had no effect. Insulin or 2-DG injections in sham-lesioned rats generated robust ACTH secretory responses, with the response to 2-DG being significantly greater than the response to insulin. In lesioned rats, these secretory responses were blunted to the extent that they were no longer significantly different from sham lesioned rats. Insulin and 2-DG therefore provide increasingly strong activation signals to the secretory mechanisms in CRH neuroendocrine neurons, and catecholamine neurons that innervate the PVH are required for full ACTH secretory responses to insulin and 2-DG injections.