The effects of phenobarbital, atropine, l-α-methyldopa, and DL-propranolol on dieldrin-induced hyperglycemia in the adult rat

Fox, Glyn R.; Virgo, Bruce B.

doi:10.1016/0041-008x(85)90239-x

Cited by 4 publications

(4 citation statements)

References 16 publications

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“…Hepatic gluconeogenic enzymes such as PEPCK1 are repressed in phenobarbital treated rodents but not in CAR knockout mice. , In addition, PXR activation has been reported to decrease both G6Pase and Pepck1 genes expression in mice, while G6Pase and Pepck1 genes were found to be down-regulated in transgenic mice bearing a constitutively activated mutant of hPXR . The effect of CAR and PXR on CPT1 gene expression has already been discussed (see section 2A).…”

Section: Effect Of Car and Pxr Activation On Glucose Metabolismmentioning

confidence: 96%

Xenoreceptors CAR and PXR Activation and Consequences on Lipid Metabolism, Glucose Homeostasis, and Inflammatory Response

et al. 2007

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Xenobiotic and drug metabolism and transport are managed by a large number of genes coordinately regulated by at least three nuclear receptors or xenosensors: aryl hydrocarbon receptor (AhR), constitutive androstane receptor (CAR, NR1I3), and pregnane X receptor (PXR, NR1I2). Initially characterized as xenosensors, it is now evident that CAR and PXR also trigger pleiotropic effects on liver function. Recent studies have shown the existence of crosstalk between xenosensors and other nuclear receptors or transcription factors controlling endogenous signaling pathways which regulate physiological functions. This review is focused on recent observations showing that activation of CAR and PXR alters lipid metabolism, glucose homeostasis, and inflammation by interfering with HNF4alpha, FoxO1, FoxA2, PGC1alpha, or NFkB p65. Such crosstalks explain clinical observations and provide molecular mechanisms allowing understanding how xenobiotics and drugs may affect physiological functions and provoke endocrine disruptions.

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Section: Effect Of Car and Pxr Activation On Glucose Metabolismmentioning

confidence: 96%

Xenoreceptors CAR and PXR Activation and Consequences on Lipid Metabolism, Glucose Homeostasis, and Inflammatory Response

et al. 2007

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“…Experiments with neuroactive agents in HEBD-treated adult rats have shown that the hyperglycemia results from increased output from the cholinergic and a-adrenergic systems of the CNS (Fox and Virgo 1985). The peripheral target is believed to be the pancreas which would respond by decreasing insulin secretion, thus decreasing glucose uptake and utilization, and increasing glucagon release, thus increasing gluconeogenesis and glycogenolysis.…”

Section: Discussionmentioning

confidence: 98%

“…These doses represent the age-specific, 24-h, LDS0 vdues as detenrnined in our laboratory. The determination of the LDS0 vdues for 10-and 60-day-old rats has been reported elsewhere (Fox and Virgo 1985). The LD50 value for the 5-day-old pup was calculated (Litchfield and Wilcoxon 1949) from the mortality caused by eight different doses of HEOD over the range of 5-75 mglkg.…”

Section: Methodsmentioning

confidence: 99%

“…1972;Kacew and Singha1 1973a: Kohli et al 1975). Hyperglyeemia is the most pronounced effect and in general, peak glucose levels are attained within 1-5 h after exposure (Kacew, Singhal, and Ling 1872;Fox and Virgo 1985). The hyperglycernia is generally considered to result from the actiwtion of hepatic and renal glareoaamgenic enzymes by the insecticide (Kacew, Singhal, Hrdina et id.…”

Section: Introductionmentioning

confidence: 97%

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Effects of dieldrin on hepatic carbohydrate metabolism in the suckling and adult rat

Fox¹,

Virgo²

1986

Can. J. Physiol. Pharmacol.

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Hepatic carbohydrate metabolism was studied in adult and suckling rats given age-specific LD50 doses of dieldrin po. These doses in 5-, 10-, and 60-day-old Wistar rats were 38, 28, and 63 mg/kg, respectively. Plasma glucose and free fatty acids (FFA), and hepatic glycogen, phosphoenolpyruvate carboxykinase (PEPCK), fructose-1,6-diphosphatase (FDP), and glucose-6-phosphatase (G6P) were measured 1 and 3 h after administration of the insecticide. Plasma glucose concentrations were elevated (17%) in some 5-day-old rats after 1 h and in all adults after 1 and 3 h (45 and 30%, respectively). Plasma FFA concentrations were decreased (9%) in the 5-day-old rat 1 h after dieldrin. Hepatic glycogen content was reduced in both 5- and 10-day-old pups at 1 hour (22 and 17%, respectively). Hepatic FDP activity was elevated in the 5-day-old rat at 1 h (17%) and was decreased (10%) in the 10-day-old rat at 3 h. Hepatic PEPCK activity was increased in adult animals by 30% 1 h after dieldrin. Furthermore, PEPCK activity was increased at 3 h in rats of all ages (76%, 5-day-old pup; 115%, 10-day-old pup; 56%, 60-day-old adult). Hepatic G6P activity was unaltered by dieldrin. Thus only the activity of hepatic PEPCK is consistently elevated by dieldrin exposure. However, this enhanced PEPCK activity is associated with dieldrin-induced hyperglycemia only in the adult rat.

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Relevance of hyperglycemia to dieldrin toxicity in suckling and adult rats

Fox

Virgo

1986

Toxicology

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The effects of phenobarbital, atropine, l-α-methyldopa, and DL-propranolol on dieldrin-induced hyperglycemia in the adult rat

Cited by 4 publications

References 16 publications

Xenoreceptors CAR and PXR Activation and Consequences on Lipid Metabolism, Glucose Homeostasis, and Inflammatory Response

Xenoreceptors CAR and PXR Activation and Consequences on Lipid Metabolism, Glucose Homeostasis, and Inflammatory Response

Effects of dieldrin on hepatic carbohydrate metabolism in the suckling and adult rat

Relevance of hyperglycemia to dieldrin toxicity in suckling and adult rats

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