Endocrine Abstracts

The Metabolic Syndrome (insulin resistance, hyperglycaemia, dyslipidaemia, hypertension) amplified by visceral obesity resembles Cushing's but plasma cortisol levels are not usually elevated. To explain this paradox altered tissue sensitivity to glucocorticoids has been invoked. 11b-hydroxysteroid dehydrogenase type 1 (11b-HSD1) reactivates cortisone to cortisol, thus amplifying local glucocorticoid action. An adipose-selective increase in 11b-HSD1 may underlie the Metabolic S...

11beta-Hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) is a key enzyme which amplifies intracellular levels of active glucocorticoids within specific tissues, including the brain. The hippocampus highly expresses both corticosteroid receptors and 11beta-HSD-1, making it a prime target for glucocorticoid actions. This brain region plays an important role in fear/anxiety behaviours and learning and memory. We examined the anxiety-related behaviours (elevated plus maze and ope...

5beta-Reductase is a key glucocorticoid metabolising enzyme. In humans, urinary steroid metabolite profiles suggest an inverse relationship between 5beta-reductase and 11beta-hydroxysteroid dehydrogenase (11HSD1) in obesity and congenital deficiency of 11HSDs. Indeed in the obese Zucker rat hepatic 11HSD1 is decreased and 5beta-reductase increased. Here we use animal models with well characterised alterations in 11HSD1 to explore the link between these enzymes.11HSD1 was m...

Metabolic Syndrome (visceral obesity, insulin resistance, type2 diabetes) resembles Cushing's syndrome, but lacks elevated circulating cortisol levels. This has engendered the hypothesis that excessive local glucocorticoid regeneration, resulting from elevated adipose 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) underlies the Metabolic Syndrome. We report that 11beta-HSD-1 nullizygosity (11beta-HSD-1-/-) reduced intra-adipose corticosterone levels and i...

Most SGA infants show rapid catch-up growth in the first year of life such that height is in the normal range by 2 years. However, around 10% fail to catch-up and remain short. This latter group generally presents to specialist growth clinics at school age. Earlier identification would facilitate monitoring of growth and timely intervention.A 3-year, prospective population-based study was undertaken to determine the feasibility of identifying SGA babies ...