Text Box: LEPTIN AND 11 BETA HYDROXYSTERIOD DEHYDROGENASE EXPRESSION IN FEMALE RATS ADIPOSE TISSUE TREATED WITH GLYCYRRHETIC ACID FROM NEONATAL PERIOD Man Yi1, Xindong Xue1, Kelun Wei 1, T. Nakanishi2, Y. Nakagawa2, T. Ohzeki2 1Pediatric department of 2nd Hospital of China Medical University, China 2Pediatric Department of Hamamatsu University School of Medicine, Japan Objective: Glycyrrhetic Acid (GCA) is an inhibitor of 11 beta Hydroxysteriod Dehydrogenase (11beta HSD). In order to explore the relationship of obesity and type 2 diabetes, GCA was administrated to the female SD rats from neonatal period to 9 months old. Leptin and 11 beta Hydroxysteriod dehydrogenase expression were analyzed. Material & Methods: Nineteen rats were divided into 3 groups. Group A received GCA from birth and group B from 4 weeks old and group C was normal control. Oral Glucose Tolerance Test was done at 9 months old. Plasma HA1c levels were also measured. Body weighs were recorded twice a week for nine months. Northern Blotting Assay was used to analyze the expression of leptin and 11beta HSD in rats adipose tissue. Results: 1. Body weitht: At one month there are no significant different between any groups. At six months old and nine months old, the body weight of GCA treated group increased significantly than group C. 2. OGTT & HA1c results: In group A and group B the OGTT was abnormal and HA1c levels were higher than the group C. 3. There was no significant difference between groups in the leptin expression of adipose tissue. 4. 11beta HSD RNA expression could be detected in SD female rats adipose tissue. In treated group it expressed higher. Conclusions: Oral GCA administration in rats from neonatal period can cause the rats obesity and type 2 diabetes.in adulthood; Glucocorticoids may play a role on the development of obesity. It is suggested that Leptin resistance existed in adipose tissue of GCA treat rats. GCA could not inhibit the adipose tissue 11beta HSD1 expression and this might be the main reason for the rats central obesity. 1868