2007
DOI: 10.1016/j.tox.2007.01.004
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Mechanisms of inhibited liver tissue repair in toxicant challenged type 2 diabetic rats

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Cited by 8 publications
(3 citation statements)
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References 51 publications
(96 reference statements)
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“…Cyclin D has been shown to be critical in preceding hepatocytes through the G1 restriction point. The synthesis stimulation of this cyclin involves several intermediates, like ERK1/2 and p38 MAPK (Sawant et al, 2007). TA and CT are two of the most frequently used chemical models to study the interplay between repair and injury in hepatotoxicity.…”
Section: Discussionmentioning
confidence: 99%
“…Cyclin D has been shown to be critical in preceding hepatocytes through the G1 restriction point. The synthesis stimulation of this cyclin involves several intermediates, like ERK1/2 and p38 MAPK (Sawant et al, 2007). TA and CT are two of the most frequently used chemical models to study the interplay between repair and injury in hepatotoxicity.…”
Section: Discussionmentioning
confidence: 99%
“…Three possible mechanisms are reported to increase sensitivity of liver necrosis in diabetic animals as compared to non-diabetic animals [19] : (1) Weakning of compensatory liver cell division following hepatotoxicants like TA, and associated liver injury (2) Decreased IL-6 and ERK1/2 MAPK and increased TGF毬1 expression (3) decreased cyclin D1 expression, and lowering of p-pRB, resulted in inhibiting G0/G1 to S-phase clearance of hepatocytes and liver tissue repair. Hepatoprotective effect of FE in the present study might be medicated through these mechanisms.…”
Section: Discussionmentioning
confidence: 99%
“…Continued depletion of ATP levels might result in the inhibition of tissue repair, increased progression of liver injury, hepatic failure and mortality in fructose-fed rats. In addition, the formation of advanced glycation end products (AGEs) due to high intracellular glucose might alter the liver function, cell proliferation and tissue repair (Sawant et al, 2007). Various observations have given rise to the proposal that the regenerative ability of liver could be diminished due to fat accumulation or steatosis (Yang et al, 2001).…”
Section: Discussionmentioning
confidence: 99%