Effect of Physical Exercise on Bone Density and Remodeling in Egyptian Type 1 Diabetic Osteopenic Adolescents

<p>Abstract</p> <p>Background</p> <p>The study was planned to assess effect of physical exercise on bone remodeling in type I diabetics with osteopenia.</p> <p>Methods</p> <p>Twenty-four type I diabetes mellitus (DM1) with osteopenia (10 females and 14 males) were compared to thirty-eight age- and sex-matched healthy control individuals (20 females and 18 males) for biochemical and radiologic parameters of bone mass. Laboratory investigations included serum and urinary calcium, inorganic phosphorus, alkaline phosphatase, and serum "procollagen type 1 N-terminal propeptide (P1NP). Bone densitometry was assessed at neck femur using Dual Energy X-ray Absorptiometry (DEXA). Serum P1NP and DEXA were reevaluated after a planned exercise program.</p> <p>Results</p> <p>Patients and controls were comparable with respect to serum as well as urinary biochemical parameters of bone mass namely; calcium, phosphorus and total serum alkaline phosphatase. Osteopenic DM1 patients displayed lower mean serum P1NP than control group (20.11 ± 6.72 ugdL versus 64.96 ± 34.89 ugdL; p < 0.05). A significant correlation was observed between BMD and degree of glycemic control reflected by serum glycated hemoglobin (r = -0.44, p, 0.030). Bone densitometry correlated with serum P1NP (r = -0.508, p, 0.011). After a planned regular exercise for 3 months, serum P1NP and BMD levels increased with percentage change of 40.88 ± 31.73 and 3.36 ± 2.94, respectively. Five patients resumed normal densitometry and they were all males.</p> <p>Conclusion</p> <p>Diabetic osteopenic patients displayed lower serum levels of procollagen type 1 N-terminal propeptide which reflects poor bone formation. A 3-months planned exercise program was associated with improvement of bone densitometry and significant increment of serum P1NP.</p

Metabolismo do cálcio na fenilcetonúria Calcium metabolism in phenilke

A Fenilcetonúria é um erro inato do metabolismo do aminoácido fenilalanina. O tratamento é essencialmente dietético e envolve uma restrição severa no consumo de alimentos contendo aminoácido fenilalanina. Embora a alimentação seja complementada com fórmulas a fim de suprir as necessidades de vitaminas, minerais e aminoácidos essenciais, carências nutricionais ainda ocorrem. Isto se deve, principalmente, à restrição de fontes protéicas, que acarreta deficiência na ingestão de diversos nutrientes, dentre eles o cálcio. O cálcio possui importante relação com a formação mineral óssea. Estudos recentes demonstram que portadores de fenilcetonúria apresentam freqüentemente osteopenia e fraturas, sendo a maior incidência em crianças acima de 8 anos de idade. O rápido aumento da estatura, a dieta deficiente em cálcio e níveis de aminoácido fenilalanina elevados têm sido descritos como os principais fatores para a aquisição de massa óssea inadequada. A suplementação de cálcio em crianças saudáveis mostrou um efeito positivo sobre a aquisição de massa óssea na fase da pré-puberdade. Assim, torna-se relevante compreender a necessidade da suplementação de cálcio em pacientes fenilcetonúria, a fim de favorecer o desenvolvimento ósseo esperado.<br>Phenylketonuria is an inborn error of the metabolism of the amino acid phenylalanine. The treatment is essentially dietetic and involves a severe restriction in the consumption of foods containing aminoacid phenylalanine. Although the diet is complemented with supplements in order to meet the vitamin, mineral and essential amino acid requirements, nutritional deficiencies still occur. This is mainly due to restricting the consumption of protein sources, which results in low intake of several nutrients, including calcium. Calcium is strongly related to bone mineral formation. Recent studies have demonstrated that patients with phenylketonuria often present osteopenia and fractures, the greatest incidence being in children older than 8 years. Rapid growth, a calcium-deficient diet and elevated aminoacid phenylalanine plasma levels have been described as the principal factors responsible for inadequate bone formation. It has been shown that calcium-supplementation in healthy children had a positive effect on bone mass acquisition during prepuberty. Therefore, it is pertinent to understand the need of calcium-supplementation in phenylketonuria in order to promote full bone development