Yamamoto H, Nagai K, Nakagawa H
Institute for Protein Research, Osaka University, Japan.
Chronobiol Int. 1984;1(1):27-35. doi: 10.3109/07420528409059115.
Intracranial injection of D-mannitol (MA) or D-glucose (GL) caused photoperiodic hyperglycemia in rats; MA injection elicited hyperglycemia only in the light period, while GL injection induced it only in the dark period. To elucidate the mechanisms of these hyperglycemias, we examined the effect of the autonomic nervous system on them in rats under the L:D (12:12) condition. Propranolol, a beta-adrenergic blocker, and hexamethonium, a ganglion blocker, effectively inhibited hyperglycemia induced in either the light (MA) or dark (GL) period. In contrast, phenoxybenzamine, an alpha-adrenergic blocker, and atropine, a cholinergic blocker, inhibited hyperglycemia induced in the light period (MA), but not that induced in the dark period (GL). These findings suggest that alpha and beta-adrenergic and cholinergic mechanisms are involved in the hyperglycemia induced by MA in the light period, while only the beta-adrenergic mechanism is involved in the hyperglycemia induced by GL in the dark period.
向大鼠颅内注射D-甘露醇（MA）或D-葡萄糖（GL）会导致光周期高血糖；注射MA仅在光照期引发高血糖，而注射GL仅在黑暗期诱导高血糖。为阐明这些高血糖症的机制，我们在光照：黑暗（12:12）条件下研究了大鼠自主神经系统对其的影响。β-肾上腺素能阻滞剂普萘洛尔和神经节阻滞剂六甲铵有效抑制了在光照期（MA）或黑暗期（GL）诱导的高血糖。相比之下，α-肾上腺素能阻滞剂酚苄明和胆碱能阻滞剂阿托品抑制了光照期（MA）诱导的高血糖，但不抑制黑暗期（GL）诱导的高血糖。这些发现表明，α和β肾上腺素能及胆碱能机制参与了光照期MA诱导的高血糖，而仅β肾上腺素能机制参与了黑暗期GL诱导的高血糖。
