Abstract
Decreased growth hormone (GH) function in obese patients might contribute to associated metabolic abnormalities. This study aimed to investigate the effect of leptin, GH and periods of leptin sensitivity or/and insensitivity on the expression of the SOCS-3 gene in the ovine pituitary and to examine the influence of centrally administered leptin on GH release in sheep. Our first experiment investigated the periods of leptin resistance and leptin sensitivity, which are known as the long day (LD) and the short day (SD) periods, respectively, using ewes that were surgically fitted with third ventricular cannulae. The ewes were assigned randomly to one of three treatments and were centrally infused at 0, 1 and 2 h, beginning at sunset. The treatments consisted of central infusions of either Ringer-Locke buffer or leptin (0.5 or 1.0 μg/kg body weight (BW), respectively). Our next experiment examined the pituitaries isolated from ewes decapitated in either May or November. The explants were treated with control or GH (100 or 300 ng/ml) or leptin (50 or 100 ng/ml)—containing media and incubated for one of four different time intervals. The in vivo experiments demonstrated variable effects of leptin on GH release depending on the period of leptin sensitivity/ insensitivity. The in vitro experiments demonstrated that leptin significantly influenced the expression of the SOCS-3 gene during that SD compared to that during the LD. During the SD, we observed that significantly low or high doses of GH affected the expression of SOCS-3. These results indicated a strong correlation between leptin or GH and SOCS-3, which might explain leptin resistance and the associated perturbations in GH signaling.
Highlights
Hyperinsulinemia, hypoadiponectinemia and leptin resistance associated with obesity can suppress the secretion of growth hormone (GH), which results in increased fat accumulation that might represent an important factor in the pathogenesis of obesity [1]
Exogenous leptin did not induce the expression of the suppressor of cytokine signaling-3 (SOCS-3) gene in db/db mice, which lack leptin receptors. These results suggested that suppressor of cytokine signaling (SOCS)-3, which can act as a potent inhibitor of leptin signaling, blocks leptin-induced signal transduction and might represent a potential mediator of the leptin resistance that occurs in obesity [37]
The effects of the hormone have been detected as early as 30 minutes after its administration. These results indicate a significant correlation between leptin and SOCS-3 expression, which might explain the phenomenon of leptin resistance
Summary
Hyperinsulinemia, hypoadiponectinemia and leptin resistance associated with obesity can suppress the secretion of growth hormone (GH), which results in increased fat accumulation that might represent an important factor in the pathogenesis of obesity [1]. GH is an anabolic hormone that exhibits important functions in the regulation of somatic growth, either directly or indirectly via effectors such as insulin-like growth factor-1 (IGF-1). Another facet of the biological effects elicited by GH includes its ability to modulate metabolism and energy homeostasis [2]. Local GH resistance within the adipose tissue might further mediate fat accumulation, exacerbating the pathogenesis of obesity [4]. The expression of leptin receptor mRNA has been detected within the anterior pituitary gland and the hypothalamus by RT-PCR [9], and leptin appears to exhibit an important role in the control of GH release [7,10,11]
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