Dong Mei Jia | PubMed Health

PubMed2004

Early decrease in serum IV-7S levels during IFN treatment predicts anti-fibrogenic effect in nonresponders with chronic hepatitis C.

BACKGROUND: We evaluated whether early changes in serum levels of fibrogenic markers during interferon (IFN) treatment can predict long-term anti-fibrogenic effects in patients with chronic hepatitis C (CHC). METHODS: We retrospectively examined the serum levels of N-terminal peptide of type III procollagen (P-III-NP) and 7S domain of type IV collagen (IV-7S) in 56 patients with CHC who were revealed to be IFN-nonresponders. We measured these markers before (T0) and 1 month (T1) after the commencement of IFN therapy, at the end of 24 weeks' IFN therapy (T24), and 1 year (T24-1) and more than 2 years (T24-2) after the cessation of IFN therapy. We also measured these markers twice, at intervals of more than 2 years, in 43 IFN-untreated patients with CHC as controls. RESULTS: In nonresponders, both P-III-NP and IV-7S levels at T24-2 were significantly decreased compared with those at T0. P-III-NP levels at T1 were significantly decreased compared with those at T0, and remained at significantly low levels until the end of the observation period. IV-7S levels at T1 were not significantly different from those at T0. In patients whose IV-7S levels at T24-2 were decreased compared with those at T0, IV-7S levels at T1 were significantly lower than those at T0. In patients whose IV-7S levels at T24-2 were elevated or unchanged compared with those at T0, IV-7S levels at T1 were significantly higher than those at T0. In untreated patients, both P-III-NP and IV-7S levels at more than 2 years after the initial time were significantly increased compared with those at the initial time. CONCLUSIONS: An early decrease in IV-7S levels after IFN treatment is a useful indicator of anti-fibrogenic effects in nonresponders.

Adult↗

PubMed2002

Troglitazone stimulates pancreatic growth in normal rats.

INTRODUCTION: Peroxisome proliferator-activated receptors (PPARs) are a family of ligand-activated nuclear transcription factors belonging to the nuclear hormone receptors. Troglitazone, a specific ligand for PPAR-gamma is shown to regulate not only lipids and glucose metabolism, but also cell cycle, differentiation, and apoptosis. AIM: To examine the effect of chronic oral administration of troglitazone on the age-related changes of insulin resistance, plasma CCK levels, and pancreatic growth in normal rats. METHODOLOGY: A troglitazone-rich diet (0.2%) was given from 12 to 28 weeks of age or from 12 or 28 weeks of age to 72 weeks of age. RESULTS: Fasting serum glucose concentrations in control rats increased progressively with age, which was almost completely prevented by troglitazone treatment. Serum insulin concentrations and pancreatic insulin content in the control rat markedly increased at 28 weeks of age but decreased at 72 weeks of age. These parameters in troglitazone-treated rats remained at nearly the same concentrations at all ages. Insulin concentration relative to DNA in the control rats increased with age, whereas in the troglitazone-treated rats it remained at nearly the same concentrations throughout the observation periods and was significantly lower than that in the controls. Insulin resistance in control rats showed a great increase at 72 weeks of age, whereas it was nearly the same at all ages in troglitazone-treated rats and was significantly lower than those in the control rats. Plasma cholecystokinin concentrations in control rats slightly but insignificantly increased with age, whereas pancreatic weight decreased age-dependently when corrected for body weight. Although troglitazone treatment appeared to decrease plasma cholecystokinin concentrations compared with those in the control rats, it significantly increased pancreatic weight and prevented age-dependent decrease. Troglitazone treatment significantly increased pancreatic protein and DNA contents, but the protein per DNA ratio, an indicator of cellular size, remained at nearly the same concentrations at all ages. The contour of the islets in the control rats at 72 weeks of age was somewhat irregular with structural disarrangement and fibrosis. Moreover, the islets were separated into small sections (cluster) by fibrosis. Troglitazone treatment prevented or reversed these age-related changes of the islets to those in rats at 12 weeks of age. CONCLUSION: Our results indicate that troglitazone stimulates pancreatic growth in the normal rat not only by reducing insulin resistance and improving glucose metabolism, but also by suppressing fibrosis of the islets.

Aging↗