We examined the effect of dietary oils with different fatty acid compositions on the growth of visceral adipose tissue in rats. Rats were fed for 4 mo starting at weaning a basal diet containing (12 g/100 g diet) perilla oil rich in (n-3) polyunsaturated fatty acids (PUFA), safflower oil rich in (n-6) PUFA, olive oil rich in monounsaturated fatty acid, or beef tallow rich in saturated fatty acids. The amount of food consumed and body weight gain did not differ among the four dietary groups. The weight of the epididymal fat pad and the serum triglyceride concentration in perilla oil-fed rats were significantly lower (P < 0.05) than those of olive oil- and beef tallow-fed groups. The product of [(volume of individual adipocytes) x (number of adipocytes in epididymal fat pad)], which presumably represents total adipocyte volume in the fat pad, was significantly lower (P < 0.05) in perilla oil-fed rats than in beef tallow- and olive oil-fed groups. Expression of the late genes of adipocyte differentiation, peroxisome proliferator-activated receptor alpha, adipocyte P2 and adipsin, was significantly (P < 0. 05) down-regulated in epididymal fat tissue of rats that had been fed perilla oil rather than beef tallow or olive oil, whereas expression of the early gene, lipoprotein lipase, was not significantly affected. Greater levels (P < 0.05) of (n-3) PUFA in the membrane phospholipid fraction of the fat tissue were observed in perilla oil-fed rats than in the other dietary groups. These results suggest that perilla oil or (n-3) PUFA prevents excessive growth of adipose tissue in rats at least in part by suppressing the late phase of adipocyte differentiation.
Liver stellate cells (SCs) play central roles in both the storage of retinol and the development of liver fibrosis. The present study is aimed to understand the mechanism by which retinoic acid (RA, an active metabolite of retinol) enhances hepatic fibrosis in rats. We tested the effect of 9-cis-RA on several aspects in vitro rat SC cultures, including the activity of cellular plasminogen activator (PA), messenger RNA (mRNA), and protein levels of transforming growth factor-beta (TGF-beta) mRNA level of type-I procollagen, and the activity of type-I collagenase. Employing the rat liver fibrosis model produced by porcine serum, we also estimated the effect of oral administration of a stable RA analog on the progression of the fibrosis, as well as on hepatic TGF-beta contents. In vitro SC cultures, 9-cis-RA enhanced cellular PA and plasmin levels thereby induced plasmin-mediated activation of latent TGF-beta. Active TGF-beta generated self-stimulated its synthesis as well as that of collagen and suppressed the production of collagenase in an autocrine manner. In in vivo rat models, an RA analog accelerated the porcine serum-induced fibrosis by enhancing TGF-beta contents and, thus, collagen levels in the liver, although the RA analog alone was not fibrogenic. These results suggest that RA exacerbated liver fibrosis, at least in part, by inducing the activation and production of latent TGF-beta in liver SCs.
occurs during hepatic fibrosis and cirrhosis. 1,2,5 TGF-b stim-SEE EDITORIAL ON PAGE 1067 ulates SCs to transform into myofibroblast-like cells, enhances their production of extracellular matrix proteins, [1][2][3][4] Liver stellate cells (SCs) play central roles in both the stor-and alters the degradation of the extracellular matrix. 1,6 TGFage of retinol and the development of liver fibrosis. The pres-b suppresses the growth and function of hepatocytes, at least ent study is aimed to understand the mechanism by which in part, by down-regulating the production of hepatocyte retinoic acid (RA, an active metabolite of retinol) enhances growth factor in SCs. 7 hepatic fibrosis in rats. We tested the effect of 9-cis-RA on Three subtypes of TGF-b (TGF-b 1 , -b 2 , and -b 3 ), whose several aspects in vitro rat SC cultures, including the activity biological properties are nearly identical, are found in mamof cellular plasminogen activator (PA), messenger RNA malians. 8 TGF-bs are synthesized and secreted in a biologi-(mRNA), and protein levels of transforming growth factor-b cally latent form (latent TGF-b: 235-280 kd) which must be (TGF-b) mRNA level of type-I procollagen, and the activity activated before it can bind to receptors and perform biologiof type-I collagenase. Employing the rat liver fibrosis model cal activities. 8,9 Latent TGF-b 1 consists of the following three produced by porcine serum, we also estimated the effect of components: the active TGF-b 1 homodimer, the paired TGForal administration of a stable RA analog on the progression b 1 propeptide (also known as the latency-associated peptide), of the fibrosis, as well as on hepatic TGF-b contents. In vitro and the latent TGF-b 1 binding protein. The 25-kd homodi-SC cultures, 9-cis-RA enhanced cellular PA and plasmin levels meric active TGF-b is noncovalently associated with latencythereby induced plasmin-mediated activation of latent TGF-associated peptide (75 kd), and latency-associated peptide, b. Active TGF-b generated self-stimulated its synthesis as in turn, is disulfide-bonded to latent TGF-b 1 binding protein well as that of collagen and suppressed the production of (range, 135-180 kd). Activation releases the 25-kd TGF-b collagenase in an autocrine manner. In in vivo rat models, an molecule from the large complex. In vitro, the latent TGF-b RA analog accelerated the porcine serum-induced fibrosis by can be activated through physical means, such as transient enhancing TGF-b contents and, thus, collagen levels in the acidification (pH 3), which disrupts the noncovalent interacliver, although the RA analog alone was not fibrogenic. These tions between TGF-b and latency-associated peptide, 8,10 or results suggest that RA exacerbated liver fibrosis, at least in by proteases, especially plasmin, which may cleave latencypart, by inducing the activation and production of latent TGF-associated peptide within its amino-terminal region and reb in liver SCs. (HEPATOLOGY 1997;26:913-921.) lease active TGF-b. 10 Plasmin-mediated activation also occur...
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