2026-09-22T12:25:22Zhttps://wakespace.lib.wfu.edu/server/oai/request

oai:null:10339/149112026-09-18T12:40:09Zcom_10339_14934col_10339_38132

Fairfield, Heather 2009-08-03T14:40:28Z 2010-06-18T19:00:00Z 2009-08-03T14:40:28Z 2010-06-18T19:00:00Z 2009-08-03T14:40:28Z https://wakespace.lib.wfu.edu/handle/10339/14911 Leptin, the hormone product of the Obese (Ob) gene, is secreted from adipocytes to communicate energy status, reduce food consumption and increase metabolism of fat stores. Interestingly, females have higher leptin levels than males in humans, rodents, and other mammals, even when adjusted for fat mass. We therefore tested whether the hormones estrogens and androgens control leptin synthesis in cultured cells. A mouse adipocyte cell line (3T3-L1) was treated with 17β-estradiol and dihydrotestosterone and RNA was harvested for analysis by qRT-PCR. Media extracts were also collected for leptin ELISA. The present study suggests a weak stimulation of Obese mRNA accumulation by estrogen that parallels the accumulation of Resistin mRNA, a known estrogen responsive gene. In contrast, dihydrotestosterone strongly reduces the Ob mRNA levels in 3T3-L1 adipocytes with effects detected at 0.1 nM, with maximal and significant effects at 10 nM following 12 hours of treatment. The DHT effect is accentuated if Ob mRNA accumulation is normalized relative to mRNA of the adipocytes differentiation marker, PPARγ. Treatment with estrogen and androgen receptor antagonists prevent estrogen enhanced Ob message accumulation and DHT decreased Ob mRNA levels, respectively. No differences in leptin secretion from 3T3-L1 cells were detected 12 hours after DHT treatment. en_US Wake Forest University leptin estrogen dihydrotestosterone The role of sex steroids in the regulation of the Obese gene and leptin secretion Thesis Release the entire work for access only to the Wake Forest University system for one year from the date below. After one year, release the entire work for access worldwide. Johnson, Erik C. Muday, Gloria K. Browne, Carole L. Biology open.access