Hu Y, Purushotham K R, Wang P, Dawson R, Humphreys-Beher M G
Department of Oral Biology and Pharmacodynamics, University of Florida, Gainesville 32610.
Am J Physiol. 1994 Mar;266(3 Pt 1):G433-43. doi: 10.1152/ajpgi.1994.266.3.G433.
The nonobese diabetic (NOD) mouse is subject to autoimmune disease-associated lymphocytic attack on the salivary glands with a corresponding loss of exocrine function. Downregulation of stimulus response to the beta-adrenoceptor agonist, isoproterenol, appears to be related to a decline in beta-adrenergic receptor density, changes in the level of intracellular second messenger signaling component adenosine 3',5'-cyclic monophosphate, and protein kinase A activity. An autoantibody to the beta 1-adrenergic receptor present in the sera of diabetic NOD mice may be involved in the reduced agonist response by virtue of its ability to retard dihydroalprenolol radioligand binding to receptors in the membranes of salivary glands from control mice and recognition of purified beta 1-adrenergic receptor by immunoblotting techniques.
非肥胖型糖尿病（NOD）小鼠易患自身免疫性疾病，其唾液腺会受到淋巴细胞攻击，相应地外分泌功能丧失。对β-肾上腺素能受体激动剂异丙肾上腺素的刺激反应下调，似乎与β-肾上腺素能受体密度下降、细胞内第二信使信号转导成分3',5'-环磷酸腺苷水平变化以及蛋白激酶A活性有关。糖尿病NOD小鼠血清中存在的β1-肾上腺素能受体自身抗体，可能因其能够抑制二氢阿普洛尔放射性配体与对照小鼠唾液腺细胞膜上受体的结合，以及通过免疫印迹技术识别纯化的β1-肾上腺素能受体，从而参与了激动剂反应的降低。
