ABSTRACT
Mammalian reproductive axis is regulated by the combination of three fundamental tissues of neuroendocrine system including hypothalamus, hypophysis and gonads. In recent years, pineal gland has been included in this axis. The aim of the present study was to investigate the effect of 12L (Light):12D (Dark) photoperiod and melatonin administration (0.5 mg/kg/day; subcutaneously) on testicular volume and cellular parameters of testis at the pinealectomized (PE) rats. For this aim, twelve adult rats were firstly pinealectomized and then divided into two groups as GI and GII randomly. The GI rats served as control group and received only normal saline, whereas GII rats were the melatonin administered group. It was found that the total testicular volume, diameter and epithelial height of seminiferous tubules and number and nuclear diameter of the interstitial cells of the testes were increased in the GII. However, increase in the interstitial cell number was not found statistically significant among groups. In conclusion, it was observed that the 12L:12D photoperiod and doses of melatonin given increased the investigated parameters in PE rats.
El eje reproductivo de los mamíferos está regulado por la combinación de tres tejidos fundamentales del sistema neuroendocrino, incluyendo el hipotálamo, hipófisis y las gónadas. En los últimos años, la glándula pineal se ha incluido en este eje. El objetivo fue investigar el efecto del fotoperíodo 12L (Luz):12O (oscuridad) y la administración de melatonina (0,5 mg/kg/día, vía subcutánea) sobre el volumen testicular y los parámetros celulares del testículo en ratas pinealectomizadas (RP). Doce ratas adultas fueron pinealectomizadas y divididas en dos grupos, GI y GII de manera aleatoria. Las ratas del GI sirvieron como grupo de control y recibieron sólo solución salina normal, mientras que a las ratas del GII se les administró melatonina. Se encontró que el volumen total, diámetro y altura del epitelio de los túbulos seminíferos de los testículos, y el número y diámetro nuclear de las células intersticiales se incrementaron en el GII. Sin embargo, el aumento en el número de las células intersticiales no fue significativo entre los grupos. En conclusión, se observó que el fotoperíodo 12L:12O y la dosis administrada de melatonina aumentan los parámetros investigados en RP.
Subject(s)
Animals , Rats , Melatonin/administration & dosage , Photoperiod , Testis , Pineal Gland/surgery , Rats, WistarABSTRACT
BACKGROUND: There is a growing recognition that the adipose tissue is an endocrine organ that secretes signaling molecules such as adiponectin and resistin. The peroxisome proliferator activated receptor γ (PPARγ) is expressed in high levels in the adipose tissue. Thiazolidinediones are selective PPARγ agonists with insulin-sensitizing properties. It has been postulated that thiazolidinediones such as rosiglitazone exert their pharmacodynamic effects in part through modulation of resistin (implicated in insulin resistance) and adiponectin (an insulin-sensitizing molecule) expression subsequent to activation of PPARγ. There are conflicting data, however, on the biological direction in which resistin expression is modulated by PPARγ agonists and whether an increase in adiponectin expression can occur in the face of an upregulation of resistin. METHODS: Using the murine 3T3-L1 adipocytes as a model, we evaluated the changes in resistin and adiponectin gene expression after vehicle, rosiglitazone (10 μmol/L, a PPARγ agonist), GW9662 (5 μmol/L, a selective PPARγ antagonist) or GW662 and rosiglitazone co-treatment.RESULTS: In comparison to vehicle treatment, rosiglitazone increased the average adiponectin and resistin mRNA expression by 1.66- and 1.55-fold, respectively (P＜0.05). Importantly, GW9662 also upregulated adiponectin expression (by 1.57-fold, P＜0.05) but did not influence resistin expression (P＞0.05). Co-treatment with rosiglitazone and GW9662 maintained the adiponectin upregulation (1.87-fold increase from vehicle, P＜0.05) while attenuating resistin upregulation (1.31-fold increase from vehicle, P＜0.05) induced by rosiglitazone alone (1.55-fold increase from vehicle, P＜0.05). CONCLUSION: This study presents new evidence that adiponectin transcript is upregulated with both a PPARγ agonist (rosiglitazone) and antagonist (GW9662), while GW9662 co-treatment does not block rosiglitazone-induced adiponectin upregulation. These data collectively suggest that biological mechanisms independent from PPARγ may underlie thiazolidinedione pharmacodynamics on adiponectin expression. Moreover, increased adiponectin expression by GW9662, in the absence of an upregulation of resistin expression, lends further support on the emerging clinical potential of PPARγ antagonists in treatment of insulin resistance. Decreased resistin expression may not be crucial for the insulin-sensitizing effect of rosiglitazone. These findings may serve as a foundation for future dose-ranging and time-course studies of thiazolidinedione pharmacodynamics on adipocytokine expression in human adipocytes.