Hepatic metabolism of meal-fed rats: Studies in vivo and in the isolated perfused liver

Bazotte, Roberto Barbosa; Constantin, Jorgete; Hell, Naomi Shinomiya; Bracht, Adelar

doi:10.1016/0031-9384(90)90308-q

Cited by 21 publications

(19 citation statements)

References 23 publications

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“…They showed that meal-fed training increases the activity of hepatic glycogen synthase. This result might provide an explanation for previous findings of increased hepatic glycogen accumulation and resistance to catabolism [2,3] in meal-fed trained rats. Their results also indicated that the hepatic generation of glucose from amino acids is not affected by meal-fed training.…”

supporting

confidence: 51%

Biomedical Vignette

2001

Journal of Biomedical Science

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supporting

confidence: 51%

Biomedical Vignette

2001

Journal of Biomedical Science

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“…1, rats with type 1 diabetes contained high levels of hepatic glycogen after a 24 h fast, with a diabetes1/control ratio equal to 18.7. It should be noted that the relatively high levels of hepatic glycogen in 24 h fasted diabetes1 rats, 55.8 µmol g −1 , were actually much lower than the maximal levels normally attained by the normal fed rats which may reach values as high as 330 µmol g −1 (Bazotte et al, 1990). Rats with diabetes type 2 also presented higher hepatic glycogen levels, namely 8.2 µmol g −1 , but the diabetes2/control ratio was only 2.76.…”

Section: Treatment Of Datamentioning

confidence: 84%

Glycogen levels and energy status of the liver of fasting rats with diabetes types 1 and 2

Oliveira

Amado

Martini

et al. 2007

Braz. arch. biol. technol.

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Glycogen levels and the energy status of livers from fasting rats with diabetes types 1 and 2 were measured. After a 24 h fast, the hepatic glycogen levels of rats with diabetes1 and diabetes2 were, 18.7 and 2.6 times higher, respectively, than those of livers from the normal rats. In diabetes1 rats, the glycogen levels decreased when the fasting period was extended to 48 and 72 h. The opposite occurred with the control and diabetes2 rats. Consistently, glucose release by the perfused livers from diabetes1 rats was considerably higher during at least 60 minutes after initiating perfusion. The hepatic ATP content of diabetes1 rats was similar to that of the control rats; in diabetes2 rats, the hepatic ATP content was increased. It could be concluded that regulation of glycogen deposition and degradation in rats with diabetes1 differed markedly from that of rats with diabetes2 which, in turn, behaved similarly to normal healthy rats.

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“…1 to 3 reveal, the production of all these metabolites was relatively low with the exception of urea. The low basal rates of lactate, pyruvate and glucose release are due to the low glycogen levels in fasted rats (Bazotte et al 1990). Oxygen uptake, however, was relatively high before alanine infusion due to the oxidation of endogenous fatty acids Fig.…”

Section: Resultsmentioning

confidence: 99%

Low Doses of Tumour Necrosis Factor α and Interleukin 1β Diminish Hepatic Gluconeogenesis from Alanine in vivo

Kelmer-Bracht

Broetto-Biazon

Sá‐Nakanishi

et al. 2006

Basic Clin Pharma Tox

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Previous reports have attributed a stimulating action on hepatic gluconeogenesis to tumour necrosis factor a (TNFa) administered to rats at high doses (250 mg/kg). However, in adjuvant-induced arthritic rats, which present TNFa and other interleukins in the circulation, hepatic gluconeogenesis is diminished. The same occurs in some types of experimental cancer models as, for example, rats bearing the Walker-256 tumour. The present work represents an attempt of reproducing in rats gluconeogenesis inhibition by interleukins using low instead of high doses of both TNFa and interleukin 1b (IL1b). TNFa and IL1b at doses of up to 10 mg/kg were given endovenously to rats and, after six hours, gluconeogenesis from alanine and several related parameters were evaluated in the isolated haemoglobin-free perfused rat liver. Livers from rats injected with TNFa and IL1b, either alone or in combination, presented diminished gluconeogenesis. The degrees of inhibition caused by TNFaπIL1b, TNFa and IL1b were, respectively, 48.5, 38.8 and 30.4%. TNFa also diminished oxygen uptake. No action on urea and ammonia production was found. Possibly, both TNFa and IL1b contribute to the decreased rates of hepatic gluconeogenesis that were found in rats with arthritis, sepsis and some kinds of cancer, but not to the decreased rates of ureagenesis.

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Hepatic metabolism of meal-fed rats: Studies in vivo and in the isolated perfused liver

Cited by 21 publications

References 23 publications

Biomedical Vignette

Biomedical Vignette

Glycogen levels and energy status of the liver of fasting rats with diabetes types 1 and 2

Low Doses of Tumour Necrosis Factor α and Interleukin 1β Diminish Hepatic Gluconeogenesis from Alanine in vivo

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