Liu I M, Niu C S, Chi T C, Kuo D H, Cheng J T
Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, Taiwan.
Neuroscience. 1999;92(3):1137-42. doi: 10.1016/s0306-4522(99)00068-8.
Exposure to a cold environment may increase the activity of the sympathetic nervous system inducing an elevation of plasma norepinephrine and may result in hyperglycemia. In the present study, we found that a hypoglycemic effect was produced in streptozotocin-induced diabetic rats after cold-exposure at 4 degrees C for 1 h. In addition to the blockade of this hypoglycemic effect by guanethidine (a ganglion-blocking agent) and prazosin (an alpha1-adrenoceptor antagonist), an increase of plasma norepinephrine was also observed in streptozotocin-induced diabetic rats receiving this cold-stress. Participation of sympathetic hyperactivity can thus be considered. Furthermore, naloxone, in a dose (0.5 mg/kg, i.p.) sufficient to block opioid receptors, reversed this hypoglycemia. Also, an increase of plasma beta-endorphin-like immunoreactivity was observed in streptozotocin-induced diabetic rats receiving this cold-stress. Intravenous injection of beta-endorphin into streptozotocin-induced diabetic rats produced a lowering of plasma glucose. Administration of methoxamine at a dose sufficient to activate the alpha1-adrenoceptors produced hypoglycemia and a similar increase of plasma beta-endorphin-like immunoreactivity in streptozotocin-induced diabetic rats. However, plasma beta-endorphin-like immunoreactivity level was not modified by similar treatment with methoxamine or cold-stress in normoglycemic rats. Therefore, beta-endorphin appears to be responsible for the induction of hypoglycemic effects in streptozotocin-induced diabetic rats after cold exposure which is different to the response in normal rats.
暴露于寒冷环境可能会增加交感神经系统的活性，导致血浆去甲肾上腺素升高，并可能导致血糖升高。在本研究中，我们发现链脲佐菌素诱导的糖尿病大鼠在4℃冷暴露1小时后会产生低血糖效应。除了胍乙啶（一种神经节阻断剂）和哌唑嗪（一种α1肾上腺素能受体拮抗剂）可阻断这种低血糖效应外，接受这种冷应激的链脲佐菌素诱导的糖尿病大鼠血浆去甲肾上腺素也会增加。因此，可以认为交感神经活动亢进参与其中。此外，纳洛酮以足以阻断阿片受体的剂量（0.5mg/kg，腹腔注射）可逆转这种低血糖。同样，接受这种冷应激的链脲佐菌素诱导的糖尿病大鼠血浆β-内啡肽样免疫反应性增加。向链脲佐菌素诱导的糖尿病大鼠静脉注射β-内啡肽可降低血糖。以足以激活α1肾上腺素能受体的剂量给予甲氧明可导致链脲佐菌素诱导的糖尿病大鼠低血糖，并使血浆β-内啡肽样免疫反应性出现类似增加。然而，正常血糖大鼠用甲氧明或冷应激进行类似处理后，血浆β-内啡肽样免疫反应性水平未发生改变。因此，β-内啡肽似乎是链脲佐菌素诱导的糖尿病大鼠冷暴露后低血糖效应的诱导原因，这与正常大鼠的反应不同。
