Searchable abstracts of presentations at key conferences in endocrinology
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195th Meeting of the Society for Endocrinology joint with Diabetes UK and the Growth Factor Group

Diabetes Strand

Lectures

ea0008ds1 | Lectures | SFE2004

Can we resurrect beta cell function? Insights from GLP-1

Matthews DR

The incretin access is the descriptive term behind the observed phenomenon that one can elicit more insulin secretion from oral glucose than from an equivalent intravenous stimulus. The major causes of this are two gut hormones GIP and GLP-1.GLP-1 is secreted in the intestine by the L cells and has effects at the beta cell, in the brain, and on gastric motility. At the beta cell it binds onto G protein receptors which activate the metabolic pathways rela...

ea0008ds2 | Lectures | SFE2004

New insights into the pathogenesis of diabetic kidney disease

Flyvbjerg A

At present, diabetic kidney disease affects about 15-25 % of all type 1 diabetic patients and 20-40 % of all patients with type 2 diabetes. The mechanisms underlying the development of diabetic kidney disease are extremely complex and not yet fully understood. Among many potential pathogenic mechanisms responsible for the progression in diabetic nephropathy, metabolic factors beyond blood glucose, e.g. advanced glycation end-products (AGEs), and growth factors/cytokines have b...

ea0008ds3 | Lectures | SFE2004

11β-hydroxysteroid dehydrogenase type 1: a cause of the metabolic syndrome and therapeutic target

Seckl J , Morton NM , Paterson J , Mullins JJ , Walker BR

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...