Cholinergic regulation of hepatic tyrosine transaminase activity

Black, Ira B.; Reis, Donald J.

doi:10.1113/jphysiol.1971.sp009391

Cited by 41 publications

(4 citation statements)

References 22 publications

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“…These results suggest that the hypothalamic cholinergic influence on liver tyrosine aminotransferase is mediated largely by the cholinergic system in the LH-vagal pathway. Our results are consistent with the view of Black and Reis [62] that the vagal-cholinergic nerves are concerned in neural regulation of liver tyrosine aminotransferase.…”

Section: Hypothalamo-hepatic Relation In the Control Of Amino Acid Mesupporting

confidence: 93%

“…Black and Reis [62] showed that electrical stimulation of the vagus nerves or" administration of carbachol in adrenalectomized rats induces the activity of liver tyrosine aminotransferase (EC 2.6.1.5), an enzyme catalyzing the first reaction in the pathway by which tyrosine is finally degraded to acetoacetate and fumarate. As an extension of our previous studies [11][12][13][14] on chemical coding of the hypothalamic neurones in metabolic control, we have investigated the hypothalamic control of this hepatic enzyme by selectively stimulating the LH, a presumed parasympathetic centre [2,5,6], with different neurotransmitters.…”

Section: Hypothalamo-hepatic Relation In the Control Of Amino Acid Mementioning

confidence: 99%

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Central nervous system regulation of liver and adipose tissue metabolism

Shimazu

1981

Diabetologia

253

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Hypothalamic and autonomic nervous regulation of carbohydrate and amino acid metabolism in the liver and of lipid metabolism in adipose tissues is described. The direct neural mechanism underlying this regulation has been evaluated. Electrical stimulation of the ventromedial hypothalamic nucleus (VMH)-splanchnic nerve system causes glycogenolysis in the liver by rapid activation of glycogen phosphorylase, whereas electrical stimulation of the lateral hypothalamic nucleus (LH)-vagus nerve system promotes glycogenesis in the liver by activation of glycogen synthetase, through direct neural and neural-hormonal mechanisms. Studies on chemical coding of the hypothalamic neurones have revealed that norepinephrine-sensitive neurones in the VMH and acetylcholine-sensitive neurones in the LH are specifically involved in the regulation of liver phosphorylase and glycogen synthetase, respectively. Acetylcholine-sensitive neurones of the LH were also found to be concerned in regulation of hepatic tyrosine and aminotransferase activity, through intermediation of the cholinergic system in the LH-vagal pathway. Finally, it has been shown that the VMH acts as a regulatory centre for lipolysis in adipose tissues by modulating activation of the sympathetic nervous system. In addition, stimulation of the VMH enhanced lipogenesis in brown adipose tissue preferentially, probably through a mechanism mediated by sympathetic innervation of this tissue. The latter finding suggests that both the breakdown and resynthesis of triglycerides in brown adipose tissue, but not in white adipose tissue, are accelerated by stimulation of the VMH.

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Section: Hypothalamo-hepatic Relation In the Control Of Amino Acid Mesupporting

confidence: 93%

Section: Hypothalamo-hepatic Relation In the Control Of Amino Acid Mementioning

confidence: 99%

Central nervous system regulation of liver and adipose tissue metabolism

Shimazu

1981

Diabetologia

253

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“…There is some evidence that the autonomic nervous systems regulate enzyme synthesis, as reported for the appearance of circadian rhythmic changes in phosphoenolpyruvate carboxykinase in the liver of fed rats (27) and induction of tyrosine transaminase in rat liver (18). Moreover, alkaline phosphatase in rat atria has been reported to be induced by subcutaneous injection of isoprenaline (28).…”

Section: Discussionmentioning

confidence: 93%

Difference in the inductions of duodenal alkaline phosphatase by casein feeding and by starch feeding.

Ishikawa

Suzuki

Ono

et al. 1983

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryFeeding of starch or casein to rats that had been starved for 4 days resulted in marked increase in duodenal alkaline phosphatase activity in a few hours. In rats with a duodenal blind loop, the enzyme was induced by feeding starch, but not casein. Conditions leading to hyperglycemia, such as an intragastric adminis tration and an intravenous infusion of glucose, induced duodenal alkaline phosphatase to the same extent and in the same period as starch feeding. Subcutaneous injection of insulin alone did not induce the enzyme. In chemically sympathectomized rats, the enzyme was induced by starch feeding. In vagotomized or hexamethonium-treated rats, the enzyme was not induced by starch feeding or intragastric administration of glucose solution. On the contrary, subcutaneous injection of carbachol alone induced the enzyme. These results suggest that stimulation of the para sympathetic nervous system via hyperglycemia is important for induction of duodenal alkaline phosphatase by starch feeding. The mechanism of enzyme induction by casein feeding is still unknown. Key Words duodenal alkaline phosphatase, starch feeding, casein feed ing, hyperglycemia, sympathectomy, vagotomyIn rats, intestinal alkaline phosphatase is mainly localized in the brush border membrane (1), and its activity is highest in the duodenum, decreasing rapidly toward the ileum (2, 3). The enzyme is rapidly induced by protein (4-6) or carbohy drate (7) feeding in rats that have been starved for a few days.In the present study we examined whether direct contact of a nutrient with the small intestine was necessary for enzyme induction by using rats with a blind loop. We also examined whether the autonomic nervous system was involved in the enzyme induction.

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“…Especially, bilateral cervical vagotomies significantly suppress DNA synthesis in partially hepatectomized liver [14]. Cch also affects various liver metabolisms, such as biosynthesis of cholesterol [18], hepatic tyrosine aminotransferase [19], tyrosine transaminase [20], glycogen formation, and the activities of glycogen synthetase [21], phosphoenolpyruvate carboxykinase [22], glucokinase [22], and ornithine decarboxylase [14]. However, it is still obscure whether the Cch induces hepatocyte proliferation.…”

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confidence: 99%

Carbachol Induces Hepatocyte Proliferation, but Only in the Presence of Hepatic Nonparenchymal Cells

et al. 2007

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Vagal hyperactivity correlates with enhanced DNA synthesis and cell proliferation in the peripheral tissues of ventromedial hypothalamic (VMH)-lesioned rats. The infusion of an ACh receptor agonist, carbachol (Cch), induces rat duodenal and pancreatic cell proliferation to a degree comparable to the VMH lesions. Whereas the VMH lesions also induce the proliferation of hepatic cells, it is unclear whether Cch can also do this. Here we attempted to clarify the mechanism of hepatic cell proliferation induction by cholinergic stimulation. First, hepatic cell proliferation was examined in rats previously vagotomized and intraperitoneally administered with Cch via an osmotic minipump. Second, the sera from the Cch-infused rats were examined for a proliferative effect on isolated hepatic cells. And last, the effect of the presence of hepatic nonparenchymal cells (NPCs) on the proliferation of the cultured hepatocytes treated with Cch was investigated. Immunohistochemistry for proliferating cell nuclear antigen (PCNA) showed that the 3-day Cch infusion significantly increased the number of PCNA-immunoreactive cells in the liver. Moreover, the sera from the Cch-infused rats increased the number of PCNA-immunoreactive hepatocytes in culture. However, Cch alone did not induce proliferation in monocultured hepatocytes. When compared with the monoculture of hepatocytes, the coculture of those with hepatic NPCs resulted in enhanced PCNA immunoreactivity after a 4-day treatment with 3 mM Cch. These findings suggest that ACh induces hepatocyte proliferation, which is mediated by unidentified humoral factor(s) possibly secreted from hepatic NPCs, and that it also participates in liver hypertrophy in the VMH-lesioned animals.Key words: acetylcholine, cell proliferation, liver, autonomic nervous system, obesity.The mechanism of obesity formation is quite complex.Because the causal relation with a serious disease such as diabetes is suggested in obesity, diversified analyses of the mechanism of the obesity formation are needed. As for the cause, besides overeating and physical inactivity, inheritance, medicine, and the hypothalamus are possible reasons.Neural obesity is also called hypothalamic obesity and includes the obesity induced by the lesions of the ventromedial hypothalamus (VMH) [1]. The VMH is involved in the autonomic regulation of feeding, sugar metabolism in the liver, and endocrine secretion of the pancreas [2]. Feeding decreases if VMH is electrically stimulated, whereas it increases if VMH is injured. Moreover, feeding increases if the lateral hypothalamus (LH) is activated and reduces if LH is suppressed. The VMH and LH are reciprocally regulated to each other; therefore it has been thought for a long time that the primary cause of neural obesity induced by VMH lesions is an overeating from hunger.It was reported in the 1960s, however, that obesity developed even if overeating was controlled by a pair-feeding experiment. Enhanced insulin secretion, which may result in hyperinsulinemia, arises in VMH-lesio...

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Cholinergic regulation of hepatic tyrosine transaminase activity

Cited by 41 publications

References 22 publications

Central nervous system regulation of liver and adipose tissue metabolism

Central nervous system regulation of liver and adipose tissue metabolism

Difference in the inductions of duodenal alkaline phosphatase by casein feeding and by starch feeding.

Carbachol Induces Hepatocyte Proliferation, but Only in the Presence of Hepatic Nonparenchymal Cells

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