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) ( 1 , 2 ). Insulin resistance with total, visceral, and hepatic adiposity is thought to be a major driver of such early maturation ( 3 , 4 ). Non-classical congenital adrenal hyperplasia or heterozygous carriers of 21-hydroxylase deficiency can
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have an unfavorable lipid partition profile with increased intra-abdominal lipid deposition and, therefore, higher waist circumference, liver/muscle fat deposition, and insulin resistance ( 28 ). There are no sufficient data about the influence of
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. Different studies have described alterations of the cortisol clearence, half-life of free cortisol, and insulin resistance leading to a reduction of the treatment efficacy due to an increased androgen secretion in pubertal children ( 24 , 25 , 26 ). The
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. The relationship between serum phosphate levels with childhood obesity and insulin resistance . Journal of Pediatric Endocrinology and Metabolism 2011 81 – 83 . ( https://doi.org/10.1515/jpem.2011.116 ) 10 Håglin L. Hypophosphatemia: cause
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β-cell function, insulin resistance, glycemia, and type 2 diabetes in finnish men . Journal of Clinical Endocrinology and Metabolism 2017 102 443 – 450 . ( https://doi.org/10.1210/jc.2016-2933 ). 9 Yuan Y Zhou B Wang S Ma J Dong F
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regarding adverse lipid profile and higher insulin resistance. Benefits of rhGH in childhood were manifested by increased TBMC, BMD LS, Z-sc LS, and Z-sc FN, tendency to increased LBM and parallel Fat% reduction in TP. Upon reaching the final height