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Young Ju Park  (Park YJ) 2 Articles
Effect of Leptin on Alteration of beta-cell Mass in Rat Pancreas.
Seong Bin Hong, Yu Mi Han, Young Ju Park, Yun Joo Oe, Sung Ki Kim, Yoe Joo Kim, Moon Suk Nam, Yong Seong Kim, In Sun Park
Korean Diabetes J. 2002;26(4):253-264.   Published online August 1, 2002
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BACKGROUND
Diabetes mellitus can occur when insulin secretion and action are inadequate in relation to blood glucose level. Several experiments recently reported that leptin and pancreatic beta-cells have functional axis to interact each other. The present study was aimed to investigate the role of leptin on regulation of beta-cell mass during neonatal period when they show a dynamic growth. METHOD: Leptin was injected intraperitoneally to rat neonates for 7 days from the second day after birth. Using the pancreas of the rat pups, immunohistochemical stain, in-situ hybridization and northern blot for insulin were done for analysis of beta-cell mass as well as for insulin synthesis and secretion. In addition, PCNA (proliferating cell nuclear antigen) was examined to assess the effect of leptin on islet cell proliferation. RESULT: 1) The weight gain and blood glucose levels showed no significant difference between leptin injected groups (0.1 mg/kg, 0.5 mg/kg) and control one. 2) The weights of pancreas were not different between both group. 3) Pancreatic islets of rat who received leptin 0.5 mg/kg were reduced in area and number than those of normal pups. They also showed the decreased beta-cell number per islet compared with control as well as leptin 0.1 mg/kg injected groups (59+/-49 vs 47+/-31 vs 31+/-21 per islet, p<0.05). 4) The beta-cell mass of rat who received leptin 0.5 mg/kg decreased but there was no significant difference. 5) The mRNA expressions of insulin were not different among control, leptin 0.1 mg/kg and leptin 0.5 mg/kg group. 6) The expression of PCNA as a proliferation marker showed no difference between control and leptin injected group. CONCLUSION: These results reflected that leptin negatively regulated neonatal islet cell growth occurring in normal rat pups, and resulted to relative decrease of beta-cell number compared to the untreated control. We, therefore, suggest that leptin may play the important role in beta-cell mass during neonatal period.
Serum Proinsulin, Proinsulin/Total Insulin Ratio and Insulin Resistance in Elderly-onset Type 2 Diabetes.
Yoon Ju Oh, Young Ju Park, Young Wan Kim, Sung Ki Kim, Seong Bin Hong, Yoe Joo Kim, Mi Rim Kim, Moon Suk Nam, Yong Seong Kim
Korean Diabetes J. 2001;25(2):113-124.   Published online April 1, 2001
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AbstractAbstract PDF
BACKGROUND
It is well known that the concentration of serum proinsulin and the ratio of proinsulin/total insulin (P/I) are elevated in type 2 diabetes. Proinsulin is produced by the ribosome in pancreatic beta cells, undergoes maturation in Golgi body and exists in the form of secretory granules. Immature granules possess disproportionately large amount of proinsulin. When there is increased demand of insulin caused by diabetes, higher level of proinsulin is secreted from immature granules of dysfunctioning beta cells. Thus, the elevated concentration of proinsulin and the increased ratio of P/I are considered to be the markers of pancreatic dysfunction and predictors for the future development of diabetes. The elderly-onset type 2 diabetes is also thought to develop due to both dysfunction of insulin secretion by impaired beta cell with aging and increased insulin resistance in peripheral tissue due to less muscle mass and more fat. However, it is still controversial as to which mechanism is predominant in the development of type 2 diabetes. METHODS: We measured the levels of fasting blood glucose, serum proinsulin and specific human insulin by using radioimmunoassay kit, and calculated the P/I ratio and insulin sensitivity index in normal adults (40or=60, n=35) and also in the newly-diagnosed elderly type 2 diabetes (age>or=60, n=24). RESULTS: The concentration of serum proinsulin and the ratio of P/I in normal adults over age 40 were 7.70+/-6.08 pmol/L and 0.13+/-0.10, respectively. The concentration of proinsulin in the normal adult, normal elderly and elderly diabetes group were 6.50+/-3.71, 11.17+/-8.30 and 16.75+/-11.68 pmol/L. The differences among three groups were statistically significant (p= 0.0001). The P/I ratios for each of the three groups were 0.11+/-0.05, 0.17+/-0.12 and 0.16+/-0.08 (p=0.0004). P/I ratios in the elderly control and elderly diabetes were higher than that of the normal adult group. Insulin sensitivity index (ISI, 10,000/(basal glucose X basal insulin)) of elderly diabetes (1.19+/-0.89) was lower when compared with the indices of other groups (40or=60 control; 2.27+/-1.11, p=0.0001). CONCLUSION: Although the age-related reduction of pancreatic insulin secretory function attributes to the pathogenesis of old-age onset type 2 diabetes, it appears that the decreased insulin sensitivity may serve as more important factor in the development of the disease.

Diabetes Metab J : Diabetes & Metabolism Journal