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A role for central postsynaptic alpha 2-adrenoceptors in glucoregulation.
1Department of Chemical Pathology, St. Vincent's Hospital, Sydney, N.S.W., Australia.
Brain Research
|October 25, 1991
Summary
Clonidine causes high blood sugar by acting on postsynaptic alpha 2-adrenoceptors in the brain. These receptors play a key role in regulating glucose levels, influencing how the body manages blood sugar.
Area of Science:
- Neuroendocrinology
- Pharmacology
- Metabolic Regulation
Background:
- Central and peripheral administration of clonidine, an alpha 2-adrenoceptor agonist, induces significant hyperglycemia in rats.
- The precise mechanism, whether central (pre- or postsynaptic alpha 2-adrenoceptors) or peripheral, remains unclear.
Purpose of the Study:
- To investigate the role of central alpha 2-adrenoceptors in clonidine-induced hyperglycemia.
- To elucidate the involvement of presynaptic and postsynaptic alpha 2-adrenoceptors in glucoregulation.
Main Methods:
- Computerized mass spectrometry was used to quantify noradrenaline (NA) and its metabolite 3,4-dihydroxyphenylglycol (DHPG) in the medial basal hypothalamus.
- Rats were treated with clonidine, yohimbine (alpha 2-antagonist), guanethidine (noradrenergic blocker), and 2-deoxy-D-glucose (2-DG).
Main Results:
- Guanethidine partially inhibited the hyperglycemic response to clonidine, suggesting a central component.
- Clonidine reduced the hypothalamic DHPG/NA ratio, indicating presynaptic alpha 2-adrenoceptor agonism and inhibition of NA release.
- Postsynaptic alpha 2-adrenoceptor stimulation by clonidine was implicated in glucose release.
- Yohimbine increased the DHPG/NA ratio (presynaptic stimulation) but blocked 2-DG-induced hyperglycemia, suggesting antagonism of postsynaptic alpha 2-adrenoceptors involved in hepatic glucose output.
Conclusions:
- Postsynaptic alpha 2-adrenoceptors play a significant role in the central regulation of glucose metabolism.
- These findings highlight the critical involvement of postsynaptic alpha 2-adrenoceptors in mediating hepatic glucose output and overall glucoregulation.