Efeitos da suplementação dietética com cálcio sobre a plasticidade ontogenética decorrente do desmame precoce ou da exposição materna a nicotina na lactação

• Autor(a) principal: Nobre, Jessica Lopes
• Data de Publicação: 2011
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UERJ
• Texto Completo: http://www.bdtd.uerj.br/handle/1/12737
• topic: Calcium - metabolism; Lactation; Early weaning; Nicotine; Maternal exposure - adverse effects; Obesity - diet therapy; Metabolic programming; Cálcio - Metabolismo; Lactação; Desmame precoce; Nicotina; Exposição materna Efeitos adversos; Obesidade - Dietoterapia; Programação metabólica; CNPQ::CIENCIAS BIOLOGICAS::FISIOLOGIA::FISIOLOGIA DE ORGAOS E SISTEMAS::FISIOLOGIA ENDOCRINA

Calcium influences energy metabolism regulation and causes body weight loss. Since early weaning and maternal nicotine exposure during lactation programs for obesity, hyperleptinemia, insulin resistance and others endocrine dysfunctions, we studied the possible effect of dietary calcium supplementation on endocrine dysfunctions in these two experimental model of obesity: 1) Early Weaning (EW): lactating rats were involved with a bandage to interrupt the lactation during the last 3 days of standard lactation, and C (control) - dams whose pups had free access to milk during all lactation (21 days). 2) Maternal nicotine exposure (N): Two days after birth, it was implanted on the mothers, osmotic minipumps containing nicotine solution (6 mg/Kg/day, 14 days) or saline (C) in the same condition. At 120 days-old, all offspring received dietary calcium supplementation (10g of calcium carbonate/Kg of rat chow) or standard diet. Rats were killed at 180 days-old. Significant data were p<0.05. As expected, N and DP offspring showed higher visceral and total body fat mass, hyperleptinemia, hypothalamic leptin resistance and insulin resistance. In addition they presented higher serum 25-hydroxyvitamin D3. All these disturbances were corrected after calcium supplementation. Besides, adult EW offspring displayed hyperphagia and hypertriglyceridemia that was normalized with calcium therapy. Also, N offspring presented hypothyroidism, higher tyrosine hydroxylase expression and higher adrenal catecholamine content. Despite calcium treatment have normalized adrenal dysfunction, it did not reverse the hypothyroidism. So, dietary calcium supplementation seems to revert most of the metabolic syndrome parameters observed in our two developmental plasticity models. It is conceivable that the reduction in fat mass per se, induced by calcium therapy, is the main mechanism that improves all parameters. Because serum 25-hydroxyvitamin D3 levels were corrected by calcium supplementation in obese offspring, it is possible that the anti-obesity effect of calcium occurs through calcitriol action on the adipocyte.