By Michael C. Henson, V. Daniel Castracane
The isolation of leptin in 1994 and its characterization as an element influencing urge for food, strength stability, and adiposity, instantly thrust the polypeptide into the quickly becoming physique of literature situated at the body structure of weight problems. The starting to be medical expertise of weight problems as an enormous health and wellbeing hazard in built societies dovetailed completely with any of a couple of roles that leptin could play during this abenant physiological situation. nearly neglected amidst the thrill generated through early leptin courses was once the advice that the "fat hormone" may additionally keep watch over a variety of platforms and occasions very important to copy, together with pubertal improvement, gonadal endocrinology, fettility, and being pregnant. spotting this capability, a comparatively small cadre of researchers started to study leptin particularly as a reproductive hormone, therefore making a new and fertile box of research. curiosity during this region has seeing that won momentum and an elevated variety of members have now made major contributions to our figuring out of many leptin-related mechanisms which are correct to reproductive biology. Leptin and replica is the 1st significant quantity to in particular tackle leptin as a reproductive hormone and heavily examines the advances made within the few minutes in view that this box of curiosity built. Preeminent researchers ti'om some of the subdisciplines operating inside this quarter current a welcomed compendium of the wealth of similar literature and voice novel interpretations of cun'ent advances.
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Extra info for Leptin and Reproduction
Example text
Arcuate neurons bearing OblOb receptors may project to the median eminence to the tanycytelportal capillary junction. Leptin would either combine with its receptors on the terminals that transmit information to the cell bodies in the AN or diffuse to the AN to combine with its receptors on the perikarya of AN neurons. , 1997), we postulate that leptin causes a decrease in NPY release. Because NPY inhibited LH release in intact and castrated male rats (Reznikov and McCann, 1993), we hypothesize that NPY decreases the release of LHRH by inhibiting the noradrenergic neurons which mediate pulsatile release of LHRH.
Energy intake and utilization vary during development in rats. J. , 129, 1593-1596. , Cunningham, M. , McClain, M. , Clifton, D. , and Steiner, R. A. (2000). Galanin-like peptide (GALP) is a target for regulation by leptin in the hypothalamus of the rat. Endocrinology, 141, 2703-2706. , and Suda, T. (1999). Temporal profiles of interleukin-lbeta, interleukin-6, and tumor necrosis factor-alpha in the plasma and hypothalamic paraventricular nucleus after intravenous or intraperitoneal administration of lipopolysaccharide in the rat: estimation by push-pull perfusion.
Surprisingly, ketamine anesthesia, either alone or in the presence of LPS, provoked a rebound in plasma leptin levels after 120 min that reached concentrations similar to or even greater than those present in the LPS-treated rats. We hypothesize that this rebound may be caused by decreased negative feedback of the depressed plasma leptin concentrations during anesthesia, which at the termination of anesthesia act centrally to stimulate leptin release. To further understand the possible role of the sympathetic nervous system in the LPS-induced leptin release, we studied the effects of a-adrenergic and J3-adrenergic agonists and antagonists on the response to LPS.