Chronic ritodrine treatment induces refractoriness of glucose-lowering β2 adrenoceptor signal in female mice

Effects of β3-adrenoceptor activation on expression of pancreatic adrenoceptors and angiotensin II receptors in ApoE−/− mice

“…Furthermore, hyperinsulinemia can suppress β 3 -adrenoceptor gene transcription (Hadri et al, 1997). Chronic β 3 -adrenoceptor activation decreased glucose and insulin levels and increased intracellular cAMP level, finally resulting in increased levels of transcription factors involved in β 2 -adrenoceptor expression (Guettier et al, 2009;Tsuchiya et al, 2012). While β 3 -adrenoceptor could resist receptor down-regulation induced by longterm agonist stimulation, and the up-regulation of β 3 -adrenoceptor could increase its sensitivity to β 3 -adrenoceptor agonist (Coman et al, 2009).…”

Spinal β-adrenergic receptors’ activation increases the blood glucose level in mice

“…In addition, isoprenaline (a β-adrenergic receptors agonist) shows hyperglycemia and provokes a considerable elevation of insulin, and propranolol (a β-adrenergic receptor antagonist) partially and temporarily inhibits the secretion of insulin (Loubatieres et al 1971 ; John et al 1990 ). Furthermore, ritodrine (a β 2 -adrenergic receptor agonist) decreases glucose concentration and increases blood insulin level under fasting condition (Tsuchiya et al 2012 ). A recent study has reported that β-adrenergic receptors are up-regulated in the skeletal muscle in the streptozotocin-induced diabetic model (Xavier et al 2012 ).…”