CLARIFICATION OF CONTROL MECHANISM OF NONSHIVERING THERMOGENESIS BY ANALYSIS OF GENE INFORMATION AND INTRACELLULAR SIGNAL TRANSDACTION SYSTEM

Brown adipose tissue(BAT)，the major site of nonshivering thermogenesis，plays important roles in metabolic temperature regulation。The present study was done to clarify the role of glucagon and its control mechanism on BAT function，and the following results were obtained.(1)In Ca-treated rat，noradrenaline(NA)-induced increases in T I D2 BAT I D2 and T I D2 col i D2 were small as compared to control rat.While T I D 2 tail D 2 was increased in Ca-treated rat，but decreased in control by NA.It is suggested that Ca suppresses NA-induced thermogenesis in BAT as well as constriction of peripheral blood vessels.The effects of glucagon were not different between Ca-treated rat and control one.(2)Food intake of the inbred heat-tolerant，as well as cold-tolerant，FOK rat did not differ from that of Std：Wistar rat in both warm-acclimated and cold-acclimated conditions.(3)In cold-acclimated Frat，NA-induced increase in oxygen consumption was larger than those of control strains.Glucagon-induced increase in Tcol was also larger in FOK rat.(4)Plasma glucagon levels after acute cold exposure were higher in both warm-acclimated and cold-acclimated FOK rat than control strains.(5)EC I D 250个D 2 of BAT to glucagon was smaller in FOK rat as compared to Std：Wistar one.(6)Inositol-triphosphate(IP D 23个D_-(6)Inositol-triphosphate(IP D 23i D D 2)increased yoxen consumtion of trantriphosphate(IP I-23i-D_2)increased yoxen contion of R-S-D-D-R-D-D-D 2 increr-R-S-D-D-R-D-R-D-2 increased-R-S-S-D-2-1。(6)Inositol-triphosphate(IP)The signal of short form PRL-receptor mRNA was stronger than that of long form one，and this signal was stronger in neonatal BAT than adult‘s one.These result suggest that glucagon plays an important role in enhansment of nonshivering thermogenesis of the inbred heat-tolerant，as well as cold-tolerant，FOK rat，and that glucagon stimulates BAT mogenic activity via IP I D 23E D 2-Ca-tolerant，FOK rat，and that glucagon stimulates BAT mogenic activity via IP D 23e D 2-Ca-tolerant，D1rothiute，and this signal of short form。

Brown adipose tissue (BAT), the major site of nonshivering thermogenesis, plays important roles in metabolic temperature regulation. The present study was done to clarify the role of glucagon and its control mechanism on BAT function, and the following results were obtained.(1) In Ca-treated rat, noradrenaline (NA)-induced increases in TィイD2BATィエD2 and TィイD2colィエD2 were small as compared to control rat. While TィイD2tailィエD2 was increased in Ca-treated rat, but decreased in control by NA. It is suggested that Ca suppresses NA-induced thermogenesis in BAT as well as constriction of peripheral blood vessels. The effects of glucagon were not different between Ca-treated rat and control one.(2) Food intake of the inbred heat-tolerant, as well as cold-tolerant, FOK rat did not differ from that of Std : Wistar rat in both warm-acclimated and cold-acclimated conditions.(3) In cold-acclimated FOK rat, NA-induced increase in oxygen consumption was larger than those of control strains. Glucagon-induced increase in Tcol was also larger in FOK rat.(4) Plasma glucagon levels after acute cold exposure were higher in both warm-acclimated and cold-acclimated FOK rat than control strains.(5) ECィイD250ィエD2 of BAT to glucagon was smaller in FOK rat as compared to Std : Wistar one.(6) Inositol-triphosphate(IPィイD23ィエD2) increased oxygen consumption of BAT of neonatal rat dose-dependently.(7) Prolactin (PRL) treatment decreased the thermogenic response of BAT to glucagon.(8) PCR analysis demonstrated signals of PRL-receptor mRNA in BAT. The signal of short form PRL-receptor mRNA was stronger than that of long form one, and this signal was stronger in neonatal BAT than adult's one.These result suggest that glucagon plays an important role in enhansment of nonshivering thermogenesis of the inbred heat-tolerant, as well as cold-tolerant, FOK rat, and that glucagon stimulates BAT thermogenic activity via IPィイD23ィエD2-CaィイD12+ィエD1 route and this route is inhibitedly regulated by PRL.