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Background: Glucocorticoid excess promotes visceral obesity and cardiovascular disease. Ligand availability to the glucocorticoid receptor is controlled by isoforms of 11β-hydroxysteroid dehydrogenase (11β-HSD) which converts endogenous cortisone to active cortisol. Aim: To evaluate the expression and activity of 11β-HSD1 in subcutaneous adipose tissue (SC) and visceral adipose tissue (VAT) in prepubertal children with normal weight. Methods: Fourteen patients (11 female/3 male) with a mean age of 6.9 ± 0.9 years and a body mass index (BMI) of 17.4 ± 0.61 underwent elective open abdominal surgery. Results: Expression of 11β-HSD1 mRNA in SC and VAT was similar (0.8 ± 0.15 vs. 0.61 ± 0.12 AU). The activity of this enzyme in SC was significantly lower compared to VAT (1.42 ± 0.39 vs. 2.79 ± 0.61 ng cortisol/g tissue/24 h, p < 0.05). In addition, we observed a significant direct correlation with the expression of 11β-HSD1 in VAT adipose tissue with the patient’s BMI (r = 0.825, p = 0.002). Conclusions: This correlation together with the increased activity of this enzyme in visceral adipose tissue might contribute to decreased hepatic insulin sensitivity due to increased portal cortisol when BMI increases. These observations appear to be particularly important in children born with low birth weight who develop rapid early weight gain.

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Age-associated memory impairment (AAMI) is a clinical entity which was originally described to define memory problems linked to normal aging. Apolipoprotein E and ACE genes have both been associated with cognitive impairment in aging and dementia. The purpose of this study was to investigate memory and executive functions in AAMI according to the genetic background. We found that subjects carrying the Apo E epsilon4 allele exhibit lower memory performance on tests of both declarative and procedural memory. We did not find differences on frontal lobe tests. These findings give further support to the hypothesis concerning a genetic susceptibility for cognitive impairment in aging.