Physiology experiment: Rats treated with ACTH and Dexamethasone

Point of experiment was to see physiological role and influence of ACTH and Dexamethasone on adrenal gland via cholesterol extracted from gland. And we invested glucose level in blood after treatment.

Cholesterol results were as expected, Dex treated animals had the highest amount of cholesterol in glands, then control group, at the and ACTH group.

But we have the problem with glucose reading. DEX treated group is OK, they have higher than control glucose level.
ACTH treated should have higher glucose level in blood than control group, but they have almost the same glucose concentration.

Now my problem: we have to explain this unusual result. But we have to explain it from physiological point of view, I mean we have to give physiological reasons for this unexpected result. Even dough it was probably mistake done during experiment.

Can you help me with probable reasons for this. Professor sad that we should try to find science papers that explains this result for glucose, and than quote them in our paper. But no luck, we've found none. Please help, THANK YOU!

p.s. I was thinking that ACTH treatment was to late to induce corticosteroids release in to blood or there was to little time for corticosteroids to induce glucose release in to the blood. But I can't back up this idea with some science paper. We've treated them 3h before sacrifice with 6µg ACTH.

Glucose results: [Broken]

p.s.s.:bugeye: :bugeye: you don't allow tags, strange, they are useful, and especially could be useful for biology forum
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Was it a single injection of ACTH or Dex that you gave? And how did you administer it? In other words, intraperitoneal, intravenous, subcutaneous, etc.?

Have you taken into account the half life of each "drug" in circulation?
Here are some references that can help with that:
Lopez FJ, Negro-Vilar A. Estimation of endogenous adrenocorticotropin half-life using pulsatility patterns: a physiological approach to the evaluation of secretory episodes. Endocrinology. 1988 Aug;123(2):740-6.

Matsuyama H, Ruhmann-Wennhold A, Johnson LR, Nelson DH. Disappearance rates of exogenous and endogenous ACTH from rat plasma measured by
bioassay and radioimmunoassay. Metabolism. 1972 Jan;21(1):30-5.

Cook DM, Greer MA, Kendall JW. The half-life of endogenous immunoreactive ACTH in rat plasma. Proc Soc Exp Biol Med. 1972 Mar;139(3):972-4.

Also, have you thought about feedback mechanisms?

(And we don't allow img tags here because they can be easily abused, but you can upload attachments instead - those are moderated so they don't appear until approved by a mentor.)
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1. Thank you Moonbear, thank you very much, your references helped me, especially one about adrenocorticotropin half-life (in my textbook the value is 25min, in those papers about 7minutes)

Treatment was: ACTH, 6IU (30µg) intramuscular 3h before sacrificing the animals.
Dex, administered intraperitoneal, 1mg/kg, twice, 24h and 1h before sacrificing.

Well my guesses haven't changed, I'm still thinking that time period form ACTH administration till sacrificing was too long to observe noticeable effects on blood glucose level.
And I'm thinking that maybe control group had elevated ACTH/corticosterone levels, thus higher glicemia (and masking ACTH higher glicemia), because of stress (they have spent more time in lab than other groups before sacrificing).

And i'm going crazy because all works I've found about corticosterone half/life are from 60's, or 70's, and not available, not even abstracts. Or they require subscription (money) :(:(.

Again, thank you Moonbear :)

p.s. how do you search for articles ?

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