## Abstract The involvement of the mitochondrial permeability transition pore (PTP) in the responses of mitochondria from adjuvant‐induced arthritic rats to Ca^2+^ addition was investigated. The respiratory activity, the Ca^2+^‐induced osmotic swelling and the electrophoretic ^45^Ca^2+^ uptake were
Gluconeogenesis in the liver of arthritic rats
✍ Scribed by Zélio Fedatto Júnior; Emy Luiza Ishii-Iwamoto; Ciomar Bersani Amado; Geraldo E. Vicentini; Ângelo D'Urso Panerari; Adelar Bracht; Ana Maria Kelmer-Bracht
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 118 KB
- Volume
- 17
- Category
- Article
- ISSN
- 0263-6484
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✦ Synopsis
The gluconeogenic response in the liver from rats with chronic arthritis to various substrates and the eects of glucagon were investigated. The experimental technique used was the isolated liver perfusion. Hepatic gluconeogenesis in arthritic rats was generally lower than in normal rats. The dierence between normal and arthritic rats depended on the gluconeogenic substrate. In the absence of glucagon the following sequence of decreasing dierences was found: alanine (À71 . 8 per cent) % glutamine (À71 . 7 per cent) 4 pyruvate (À60 per cent) 4 lactate pyruvate (À44 . 9 per cent) 4 xylitol (n.s. non-signi®cant) % glycerol (n.s.). For most substrates glucagon increased hepatic gluconeogenesis in both normal and arthritic rats. The dierence between normal and arthritic rats, however, tended to diminish, as revealed by the data of the following sequence: alanine (À48 . 9 per cent) % pyruvate (À47 . 6 per cent) 4 glutamine (À33 . 8 per cent) 4 glycerol (n.s.) % lactate pyruvate (n.s.) % xylitol (n.s.). The causes for the reduced hepatic gluconeogenesis in arthritic rats are probably related to: (a) lower activities of key enzymes catalyzing most probably steps preceding phosphoenolpyruvate (e.g. phosphoenolpyruvate carboxykinase, pyruvate carboxylase, etc.); (b) a reduced availability of reducing equivalents in the cytosol; (c) speci®c dierences in the situations induced by hormones or by the individual substrates. Since glycaemia is almost normal in chronically arthritic rats, it seems that lower gluconeogenesis is actually adapted to the speci®c needs of these animals.
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