Bromocriptine improves glucose tolerance in obese mice via central dopamine D2 receptor-independent mechanism
Fig 2
Acute effects of bromocriptine on blood glucose levels via an
α2-adrenergic receptor-dependent mechanism. (A-B) Blood glucose levels just after the injection of bromocriptine (BC, 10 mg/kg, i.p.) or vehicle (Veh, 10% ethanol) in 4-month-old C57BL/6J mice under 2-h (A) and 16-h fasting conditions (B). n = 5 per group. (C-I) Effects of a pretreatment with autonomic nervous system (ANS)-blocking agents on the acute glucose-elevating effects of BC in C57BL/6J mice (2–3 months old). (C) Experimental procedures. (D-I) Effects of a pretreatment with hexamethonium (D, HEX), a cocktail of phenoxybenzamine and propranolol (E, POB+PRO), prazosin (F, PZS), yohimbine (G, YHB), propranolol alone (H), atropine (I, ATR), or saline (Sal) on blood glucose levels in mice treated with BC or vehicle under 2-h fasting conditions. n = 4–5 per group. (J) Effects of BC on the expression levels of gluconeogenesis markers (Pepck and G6pase mRNAs) and ER stress marker (Chop mRNA) in the livers of C57BL/6J mice (8 weeks old) fed ad libitum. Liver tissues were isolated 1 h after the injection of BC (10 mg/kg, i.p.) or vehicle at ZT14. n = 6–7 per group. Values are expressed as the means ± S.D. Significant differences in panels A, B, and J were examined by the Student’s t-test: * p < 0.05 and **p < 0.01. Significant differences in panels D-I were assessed by a two-way ANOVA with Tukey’s test: †p < 0.05 and ††p < 0.01 (saline + vehicle treatment vs. saline + BC treatment), #p < 0.05 and ##p < 0.01 (saline + BC treatment vs. blocker + BC treatment), §§p < 0.01 (blocker + vehicle treatment vs. blocker + BC treatment), ap < 0.05 and aap < 0.01 (saline + vehicle treatment vs. blocker + BC treatment), and bp < 0.05 and bbp < 0.01 (saline + BC treatment vs. blocker + vehicle treatment).