Effect of Central Antileptin Antibody on the Onset of Female Rat Puberty
- PDF / 230,254 Bytes
- 5 Pages / 600.05 x 792 pts Page_size
- 65 Downloads / 170 Views
Research Article Effect of Central Antileptin Antibody on the Onset of Female Rat Puberty Ruimin Chen,1 Gail J. Mick,2, 3 Rongxian Xu,4 Daoxin Zheng,1 Yanfeng Fan,4 Xiangquan Lin,1 and Kenneth L. McCormick2 1 Department
of Endocrinology, Fuzhou Children’s Hospital of Fujian, Fuzhou 350005, China of Pediatric Endocrinology and Diabetes, University of Alabama at Birmingham, Birmingham, AL 35233, USA 3 Department of Pediatrics, University of Alabama at Birmingham, CPP 230, 1601 4th Avenue South, Birmingham, AL 35233, USA 4 Department of Nutrition and Maternal & Children Care School of Public Health, Fujian Medical University, Fuzhou 350004, China 2 Division
Correspondence should be addressed to Gail J. Mick, [email protected] Received 9 January 2009; Revised 4 July 2009; Accepted 29 July 2009 Recommended by David Zangen The effect of intracerebroventricular (ICV) antileptin antibody on the onset of puberty in the female rat and the relationship between serum leptin, luteinizing hormone (LH), and body weight were investigated. Antileptin antibody (group A) was infused ICV from days 23–36 in prepubertal female rats whereas the control (group B) received ICV goat immunoglobulin G (IgG). In the antileptin group, mean day of vaginal opening (VO) was postponed (day 34 versus day 30, P < .01 ). Body weight trended higher after 30 days in the antileptin group but not significantly. However, there was no difference in serum leptin and LH between the two groups on the day of VO. Serum leptin was relatively constant from day 23 through day 31 and did not correlate with LH (r = 0.14, P = .10). These studies demonstrate that central leptin promotes the onset of female rat puberty as evidenced by VO. Finally, central leptin impacts female rat pubertal onset in distinction from serum leptin and body weight. Copyright © 2009 Ruimin Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction It is well recognized that a requisite for the onset of human puberty is a healthy body composition, particularly a critical mass of body fat [1, 2]. Low body fat prevents or hinders the onset of puberty [3, 4]. For decades it has been proposed that a peripheral metabolic signal from adipose tissue oversees the onset of puberty. Leptin, an adipocyte hormone and product of the obese (ob) gene, may be a primary candidate signal molecule among other complex metabolic signals [1]. In humans, leptin correlates most significantly with BMI and body fat [5]. Numerous studies have inferred that leptin may regulate the hypothalamic-pituitary-gonadal axis. One indication that leptin is involved in centrally regulated maturation of the reproductive system was the discovery that ob/ob females are always sterile [6], and weight loss induced by dietary restriction fails to correct their sterility. Importantly, their fertility can be reversed by leptin treatment in both sexes [7, 8
Data Loading...
