In this study, we compared the effects of low molecular weight (LMW) chitosan (MW: 25,000-50,000), high molecular weight (HMW) chitosan (MW: 500,000-1000,000) and chitin on ethanol-induced gastric mucosal injury and on the healing of acetic acid-induced gastric ulcers in rats. Oral administration of LMW chitosan (250, 500 and 1000 mg/kg) dose-dependently prevented ethanol-induced gastric mucosal injury. Repeated oral administration of LMW chitosan (100, 200 and 400 mg/kg twice daily) also dose-dependently accelerated the gastric ulcer healing. However, the effects of HMW chitosan and chitin on the gastric mucosal injury formation and the gastric ulcer healing were less potent than those of LMW chitosan. LMW chitosan (250 and 500 mg/kg, orally) was ineffective in inhibiting gastric acid secretion in pylorus-ligated rats, although it had a weak acid-neutralizing action. LMW-chitosan (250, 500 and 1000 mg/kg orally) dose-dependently prevented the decrease in gastric mucus content induced by ethanol. These results indicate that of the three compounds, LMW chitosan has the most potent gastric cytoprotective and ulcer healing-promoting actions. In addition, gastric mucus-increasing action of LMW-chitosan may be, at least in part, related to the anti-ulcer effect of this compound.

Abstract. The present study was conducted to investigate whether goat fetal myoblasts with no inherent adipogenic potential can be induced to transdifferentiate into adipocytes. Goat fetal myoblasts were transiently transfected by the adipogenic transcription factors, peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer-binding protein-α (C/EBPα). Both PPARγ and C/EBPα were capable of inducing adipogenic transdifferentiation as indicated by the appearance of mature adipocytes when the transfected cells were cultured in adipogenic differentiation medium (ADM). Ectopic expression of PPARγ induced endogenous C/EBPα expression and vice versa only when the cells were cultured in ADM. Removal of troglitazone, a PPARγ agonist, from the ADM resulted in a dramatic decline in the number of adipocytes, indicating that PPARγ stimulation is necessary to induce adipogenic transdifferentiation of goat fetal myoblasts. These results demonstrate for the first time that primary cultured myoblasts can be transdifferentiated into adipocytes. Key words: Adipogenesis, CCAAT/enhancer binding protein-α (C/EBPα), Goat, Myoblast, Peroxisome proliferator activating receptor-γ (PPARγ), Transdifferentiation (J. Reprod. Dev. 53: [563][564][565][566][567][568][569][570][571][572] 2007) o r m a t i o n o f s k e l e t a l m u s c l e d u r i n g development begins with the progeny of skeletal muscle cells, termed myoblasts. Proliferative myoblasts withdraw from the cell cycle and terminally differentiate to form myotubes that eventually mature into contracting muscle fibers [ 1 ] . T h i s p r o c e s s , t e r m e d m y o g e n e s i s , i s characterized by sequential expression of myogenic regulatory factors (MRFs) comprising Myf-5, MyoD, myogenin, and MRF4. Amongst these MRFs, the MyoD and Myf-5 expressions are required for specification of myogenic lineage and are detected in proliferative myoblasts, while myogenin is required for late myogenesis and is expressed in terminally differentiated myotubes [1]. In addition to these MRFs, several markers are utilized for identification of myogenic cells. Pax7 is a marker for myoblasts [1], and desmin is expressed in both myoblasts and myotubes [2,3]. Sarcomeric myosin heavy chain, which is required for the contracting properties of skeletal muscle, is expressed after myotubes are formed [1,3].Both peroxisome proliferator activating receptor-γ (PPARγ) and CCAAT/enhancer binding protein-α (C/EBPα) are key regulatory transcription factors t h a t p r o m o t e f a t c e l l f o r m a t i o n , t e r m e d adipogenesis [4][5][6]. Terminal differentiation of preadipocytes to adipocytes is believed to be under the control of PPARγ and C/EBPα [4][5][6], and it has been accepted that once activated, PPARγ and C/

ABSTRACT. Skeletal muscle contains several progenitor/stem cells with myogenicity as well as adipogenicity such as satellite cells. Our previous study demonstrated that forced expression of PPARγ is sufficient to induce transdifferentiation of predetermined myoblasts in vitro. In the present study, we examined whether introduction of PPARγ gene could induce adipogenesis of satellite cells in vivo. A plasmid vector containing enhanced green fluorescent protein (EGFP) or PPARγ gene was introduced into rat tibialis anterior muscle by electroporation. Histological analyses revealed that electroporation induces degenerative/regenerative response in skeletal muscle, including activation of satellite cells. When EGFP gene was introduced, newly formed myotubes resulted from fusion of activated satellite cells, showed EGFP expression, indicating that electroporation could transfect satellite cells with exogenously introduced gene. Gene transfer of PPARγ resulted in an increase of PPARγ-positive mononucleated cells on day 3 after electroporation but failed to induce adipogenesis thereafter. These results suggested that, in addition to an expression of PPARγ, niches that support adipogenesis are required for satellite cells to enter adipogenesis in vivo.