Journal of Yeungnam Medical Science

Eung Chan Jang

2 Articles

The Effect of Long Chain N-3 Polyunsaturated Fatty Acids on Development of Collagen-induced Arthritis in Rats.: Kyung Ho Shin, Se Dong Kim, Hwan Jin Jeon, Eung Chan Jang, Suck Kang Lee; Yeungnam Univ J Med. 2002;19(1):39-48. Published online June 30, 2002; DOI: https://doi.org/10.12701/yujm.2002.19.1.39

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Abstract PDF: BACKGROUND
The treatment of rheumatoid arthritis still depend on conserve therapy in major. Recent studies report that n-3 polyunsaturated fatty acids(PUFA) could modulate the incidence and progress of arthritis. The purpose of this study was to investigate the effects of n-3 PUFA on the development of collagen-induced arthritis in rats. MATERIALS AND METHODS: Female Louvain rats were used for this experiment. Rats were randomly assigned into either normal(n=8) or collagen-immunized groups, and collagen immunized groups were divided into control(n=8, normal diet) and n-3 PUFA(n=8, 5% n-3 PUFA in diet) groups. One week after feeding n-3 PUFA to rats, they were immunized with type II collagen emulsified in incomplete Freund's adjuvant into tail and back. Development of arthritis was confirmed by x-ray and microscopic examination. RESULTS: Incidence of arthritis at the 5th week after immunization was 38% in control and 0% in n-3 PUFA. Rats with arthritis showed edema in hind paws and inflammation in synovial membrane of the knee joint. Plasma glucose and insulin were not changed by both of immunization and diet. Plasma triglycerides and cholesterol concentrations were decreased by n-3 PUFA. CONCLUSION: n-3 PUFA may prevent or treat collagen-induced arthritis in rats. Further studies are needed for action mechanism of it.

Effect of Age on Glucose Metabolism of Skeletal Muscle in Rats.: Eung Chan Jang, Woon Ki Youn, Suck Kang Lee; Yeungnam Univ J Med. 2001;18(1):94-100. Published online June 30, 2001; DOI: https://doi.org/10.12701/yujm.2001.18.1.94

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BACKGROUND
It is doubtful that aging causes deteriorated glucose metabolism and insulin resistance of skeletal muscle. Some researchers had different results about it. So we have studied the mechanism responsible for the abnormal glucose tolerance associated with aging in rapidly growing and matured rats. MATERIALS AND METHODS: Animals were used S.D. rats. Growing rats were 7 weeks old (BW: 160-190 gm) and matured rats were 28 weeks old (BW: 420-525 gm). RESULTS: Fasting blood glucose and plasma insulin levels were significantly elevated in matured rat compared with growing rats. And during oral glucose tolerance test the glucose level was also significantly elevated in matured rats. These results confirmed an insulin resistant state of aging. Insulin levels at 30 minutes of oral glucose tolerance test was significantly elevated in growing rat. But at 120 minutes it was maintained at higher level in matured rats than in growing rats. It suggested the possibility of increased insulin secretion by initial stimulation of beta-cells in growing rats, and increased secretion and decreased catabolic rate of insulin in matured rats. Glucose uptake rate of soleus muscle in matured rats was lower than that of growing rats, but the difference was not statistically significant. The dose(insulin)- responsive (glucose uptake) curve of soleus muscle was only slightly deviated to the right side. CONCLUSION: Glucose metabolism of rat skeletal muscle was worsened by aging. The data of glucose uptake experiments suggested the possibility of insulin resistance of skeletal muscle in matured rats, but the mechanism of insulin resistance of skeletal muscle need further studies.

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