THE ESSENTIAL ROLE OF ZINC IN GROWTH

Zinc is known to play a relevant role in growth and development. The basic mechanisms of action of this trace element are intimately linked to the structure and action of countless enzymes involved in many different metabolic processes. In this respect, when zinc specifically acts on cartilage growth it is involved in multiple enzymatic reactions which make this a multifactorial event. Thus, we may divide the actions of zinc into three distinct types: 1) action on taste and smell acuity, appetite regulation, and food consumption and regulation; 2) action on DNA and RNA synthesis stimulating a) cell replication and differentiation of chondrocytes, osteoblasts and fibroblasts; b) cell transcription culminating in the synthesis of somatomedin-C (liver), alkaline phosphatase, collagen and osteocalcin (bone), and c) protein, carbohydrate and lipid metabolism, that is intimately related to the mechanisms of smell, taste, appetite, and food consumption and utilization; 3) action on hormonal mediation by participating in a) GH synthesis and secretion in somatomammotroph cells, b) the action of GH on liver somatomedin-C production, and c) somatomedin-C activation in bone cartilage. In addition to these multiple functions, zinc also interacts with other hormones somehow related to bone growth such as testosterone, thyroid hormones, insulin, and vitamin D-3.On the basis of the above considerations, we conclude that the integration of these mechanisms contributes to the perfect physiological functioning of bone. Tn the presence of zinc deficiency, this homeostasis is impaired, causing the weight-height deficiency detected in several species studied, the human species in particular.

Central nitrergic system regulation of neuroendocrine secretion, fluid intake and blood pressure induced by angiotensin-II

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

Previous studies demonstrated the inhibitory participation of serotonergic ( 5-HT) and oxytocinergic (OT) neurons on sodium appetite induced by peritoneal dialysis (PD) in rats. The activity of 5-HT neurons increases after PD- induced 2% NaCl intake and decreases after sodium depletion; however, the activity of the OT neurons appears only after PD-induced 2% NaCl intake. To discriminate whether the differential activations of the 5-HT and OT neurons in this model are a consequence of the sodium satiation process or are the result of stimulation caused by the entry to the body of a hypertonic sodium solution during sodium access, we analyzed the number of Fos-5-HT- and Fos-OT-immunoreactive neurons in the dorsal raphe nucleus and the paraventricular nucleus of the hypothalamus-supraoptic nucleus, respectively, after isotonic vs. hypertonic NaCl intake induced by PD. We also studied the OT plasma levels after PD- induced isotonic or hypertonic NaCl intake. Sodium intake induced by PD significantly increased the number of Fos-5- HT cells, independently of the concentration of NaCl consumed. In contrast, the number of Fos-OT neurons increased after hypertonic NaCl intake, in both depleted and nondepleted animals. The OT plasma levels significantly increased only in the PD- induced 2% NaCl intake group in relation to others, showing a synergic effect of both factors. In summary, 5-HT neurons were activated after body sodium status was reestablished, suggesting that this system is activated under conditions of satiety. In terms of the OT system, both OT neural activity and OT plasma levels were increased by the entry of hypertonic NaCl solution during sodium consumption, suggesting that this system is involved in the processing of hyperosmotic signals.