Remarkable residual alterations in responses to feeding regulatory challenges in Han/Wistar rats after recovery from the acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

“…It is important to note, however, that hypoglycemia and PEPCK inhibition do not appear to explain the mortality of TCDD-treated L-E rats [87], but they, and the stark rise of glucagon, may contribute to the development of the wasting syndrome, especially considering the anorexigenic effect of glucagon [19,27,39]. Hypoglycemia and a low hepatic glycogen level combined with low serum insulin but high glucagon and corticosterone levels might also explain, at least in part, the inability of TCDD-exposed rats to respond by eating to an acute energetic crisis caused by 2-deoxyglucose-elicited glucoprivation, and their enhanced susceptibility to hypoglycemia and lethality induced by exogenous insulin [77,90,91]. …”

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

“…It is important to note, however, that hypoglycemia and PEPCK inhibition do not appear to explain the mortality of TCDD-treated L-E rats [87], but they, and the stark rise of glucagon, may contribute to the development of the wasting syndrome, especially considering the anorexigenic effect of glucagon [19,27,39]. Hypoglycemia and a low hepatic glycogen level combined with low serum insulin but high glucagon and corticosterone levels might also explain, at least in part, the inability of TCDD-exposed rats to respond by eating to an acute energetic crisis caused by 2-deoxyglucose-elicited glucoprivation, and their enhanced susceptibility to hypoglycemia and lethality induced by exogenous insulin [77,90,91]. …”

Distribution of mRNAs encoding the arylhydrocarbon receptor, arylhydrocarbon receptor nuclear translocator, and arylhydrocarbon receptor nuclear translocator-2 in the rat brain and brainstem

“…Relatively little work has focused on the role of the AhR in the central nervous system; however, one of the hallmarks of TCDD toxicity is a wasting syndrome that is likely to be neurally based. This syndrome is characterized by hypophagia, weight loss (Peterson et al, 1984; Seefeld et al, 1984; Kelling et al, 1985; Christian et al, 1986), and a hypersensitivity to satiety signals (Pohjanvirta and Tuomisto, 1990). After animals resume eating, body weight stabilizes at a reduced level and is maintained by decreasing food intake (Seefeld et al, 1984; Pohjanvirta and Tuomisto, 1990).…”

“…This syndrome is characterized by hypophagia, weight loss (Peterson et al, 1984; Seefeld et al, 1984; Kelling et al, 1985; Christian et al, 1986), and a hypersensitivity to satiety signals (Pohjanvirta and Tuomisto, 1990). After animals resume eating, body weight stabilizes at a reduced level and is maintained by decreasing food intake (Seefeld et al, 1984; Pohjanvirta and Tuomisto, 1990). The neural network that regulates appetite is complex and seems to be controlled by interconnected brain regions that release anorexigenic and orexigenic signaling molecules.…”

“…Several lines of evidence support the idea that the AhR, ARNT, and/or ARNT2 mRNAs we and others have detected in the brain are translated into functional proteins that bind TCDD and induce the expression of cytochrome P450 1A1 and/or 1A2 genes. For example, the cortex, hypothalamus, and cerebellum all concentrate radiolabeled TCDD administered by peritoneal injection (Pohjanvirta et al, 1990). In addition, β‐naphthoflavone, an AhR ligand, increases the expression of CYP1A1 and CYP1A2 genes in the hypothalamus, cerebellum, and olfactory bulb of rats (Schilter and Omiecinski, 1993).…”

The Loss of Glucoprivic Feeding is an Early‐Stage Alteration in TCDD‐Treated Han/Wistar Rats

“…This glucoprivic feeding is an emergency response to inhibited cerebral glucose utilization (for a review, see Ritter 1986). However, the feeding response to 2DG was abolished and insulininduced eating was considerably attenuated in H/W rats treated with TCDD 2 to 3 months earlier (Pohjanvirta & Tuomisto 1990b).…”

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

“…It is important to note, however, that hypoglycemia and PEPCK inhibition do not appear to explain the mortality of TCDD-treated L-E rats [87], but they, and the stark rise of glucagon, may contribute to the development of the wasting syndrome, especially considering the anorexigenic effect of glucagon [19,27,39]. Hypoglycemia and a low hepatic glycogen level combined with low serum insulin but high glucagon and corticosterone levels might also explain, at least in part, the inability of TCDD-exposed rats to respond by eating to an acute energetic crisis caused by 2-deoxyglucose-elicited glucoprivation, and their enhanced susceptibility to hypoglycemia and lethality induced by exogenous insulin [77,90,91]. …”

Distribution of mRNAs encoding the arylhydrocarbon receptor, arylhydrocarbon receptor nuclear translocator, and arylhydrocarbon receptor nuclear translocator-2 in the rat brain and brainstem

“…Relatively little work has focused on the role of the AhR in the central nervous system; however, one of the hallmarks of TCDD toxicity is a wasting syndrome that is likely to be neurally based. This syndrome is characterized by hypophagia, weight loss (Peterson et al, 1984; Seefeld et al, 1984; Kelling et al, 1985; Christian et al, 1986), and a hypersensitivity to satiety signals (Pohjanvirta and Tuomisto, 1990). After animals resume eating, body weight stabilizes at a reduced level and is maintained by decreasing food intake (Seefeld et al, 1984; Pohjanvirta and Tuomisto, 1990).…”

“…This syndrome is characterized by hypophagia, weight loss (Peterson et al, 1984; Seefeld et al, 1984; Kelling et al, 1985; Christian et al, 1986), and a hypersensitivity to satiety signals (Pohjanvirta and Tuomisto, 1990). After animals resume eating, body weight stabilizes at a reduced level and is maintained by decreasing food intake (Seefeld et al, 1984; Pohjanvirta and Tuomisto, 1990). The neural network that regulates appetite is complex and seems to be controlled by interconnected brain regions that release anorexigenic and orexigenic signaling molecules.…”

“…Several lines of evidence support the idea that the AhR, ARNT, and/or ARNT2 mRNAs we and others have detected in the brain are translated into functional proteins that bind TCDD and induce the expression of cytochrome P450 1A1 and/or 1A2 genes. For example, the cortex, hypothalamus, and cerebellum all concentrate radiolabeled TCDD administered by peritoneal injection (Pohjanvirta et al, 1990). In addition, β‐naphthoflavone, an AhR ligand, increases the expression of CYP1A1 and CYP1A2 genes in the hypothalamus, cerebellum, and olfactory bulb of rats (Schilter and Omiecinski, 1993).…”

The Loss of Glucoprivic Feeding is an Early‐Stage Alteration in TCDD‐Treated Han/Wistar Rats

“…This glucoprivic feeding is an emergency response to inhibited cerebral glucose utilization (for a review, see Ritter 1986). However, the feeding response to 2DG was abolished and insulininduced eating was considerably attenuated in H/W rats treated with TCDD 2 to 3 months earlier (Pohjanvirta & Tuomisto 1990b).…”

Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

“…It is important to note, however, that hypoglycemia and PEPCK inhibition do not appear to explain the mortality of TCDD-treated L-E rats [87], but they, and the stark rise of glucagon, may contribute to the development of the wasting syndrome, especially considering the anorexigenic effect of glucagon [19,27,39]. Hypoglycemia and a low hepatic glycogen level combined with low serum insulin but high glucagon and corticosterone levels might also explain, at least in part, the inability of TCDD-exposed rats to respond by eating to an acute energetic crisis caused by 2-deoxyglucose-elicited glucoprivation, and their enhanced susceptibility to hypoglycemia and lethality induced by exogenous insulin [77,90,91]. …”

Distribution of mRNAs encoding the arylhydrocarbon receptor, arylhydrocarbon receptor nuclear translocator, and arylhydrocarbon receptor nuclear translocator-2 in the rat brain and brainstem

“…Relatively little work has focused on the role of the AhR in the central nervous system; however, one of the hallmarks of TCDD toxicity is a wasting syndrome that is likely to be neurally based. This syndrome is characterized by hypophagia, weight loss (Peterson et al, 1984; Seefeld et al, 1984; Kelling et al, 1985; Christian et al, 1986), and a hypersensitivity to satiety signals (Pohjanvirta and Tuomisto, 1990). After animals resume eating, body weight stabilizes at a reduced level and is maintained by decreasing food intake (Seefeld et al, 1984; Pohjanvirta and Tuomisto, 1990).…”

“…This syndrome is characterized by hypophagia, weight loss (Peterson et al, 1984; Seefeld et al, 1984; Kelling et al, 1985; Christian et al, 1986), and a hypersensitivity to satiety signals (Pohjanvirta and Tuomisto, 1990). After animals resume eating, body weight stabilizes at a reduced level and is maintained by decreasing food intake (Seefeld et al, 1984; Pohjanvirta and Tuomisto, 1990). The neural network that regulates appetite is complex and seems to be controlled by interconnected brain regions that release anorexigenic and orexigenic signaling molecules.…”

“…Several lines of evidence support the idea that the AhR, ARNT, and/or ARNT2 mRNAs we and others have detected in the brain are translated into functional proteins that bind TCDD and induce the expression of cytochrome P450 1A1 and/or 1A2 genes. For example, the cortex, hypothalamus, and cerebellum all concentrate radiolabeled TCDD administered by peritoneal injection (Pohjanvirta et al, 1990). In addition, β‐naphthoflavone, an AhR ligand, increases the expression of CYP1A1 and CYP1A2 genes in the hypothalamus, cerebellum, and olfactory bulb of rats (Schilter and Omiecinski, 1993).…”

The Loss of Glucoprivic Feeding is an Early‐Stage Alteration in TCDD‐Treated Han/Wistar Rats

“…This glucoprivic feeding is an emergency response to inhibited cerebral glucose utilization (for a review, see Ritter 1986). However, the feeding response to 2DG was abolished and insulininduced eating was considerably attenuated in H/W rats treated with TCDD 2 to 3 months earlier (Pohjanvirta & Tuomisto 1990b).…”