Searchable abstracts of presentations at key conferences in endocrinology

ea0011s9 | Psychological determinants of metabolic risk | ECE2006

Rhabdomyolysis and other adverse effects of statins: what happens when we inhibit HMG CoA reductase

Law M

HMG CoA reductase, the rate-limiting enzyme in the mevalonate pathway, is 14 steps away from cholesterol synthesis. Statins dramatically reduce the serum concentration of LDL cholesterol by inhibiting this enzyme, but may similarly lower the concentration of many other compounds in the pathway, including ubiquinone (possibly the mechanism of statin-induced rhabdomyolysis though the evidence is far from conclusive). Certain drugs are important co-factors in statin-induced rhabd...

ea0011s10 | Embryonic stem cells | ECE2006

Stem cells: regeneration in type 1 diabetes

Trucco M

Type 1 diabetes (T1D) is an autoimmune disease, the clinical onset of which most frequently presents in children and adolescents who are genetically predisposed. T1D is characterized by a T-cell mediated, specific, insulin-producing beta cell destruction. The well-differentiated and specialized islet beta cells seem to physiologically retain the ability to compensate for the cells lost by reproducing themselves, while undifferentiated cell sources may help in generating new on...

ea0011s40 | Stromal cell-matrix interactions | ECE2006

Cell-adhesion molecules and osteoclast function

Helfrich M

Bone is a dynamic tissue, maintained and repaired by the actions of, osteoclasts, osteoblasts and osteocytes, together with a variety of bone marrow cells, stromal cells and endothelium. Osteoblasts lay down bone and this is subsequently remodelled by osteoclasts. Osteocytes act mainly as mechanosensors. Osteoclasts are of haemopoietic origin, whereas osteoblasts are derived from mesenchymal stem cells. During cell differentiation and in mature cells, cell adhesion molecules a...

ea0010s5 | New frontiers in thyroid cancer | SFE2005

Introduction - chernobyl irradiation and thyroid cancer

Sheppard M

In April 1986, the explosion at the Chernobyl nuclear power plant resulted in widespread radioactive contamination in southern Belarus, northern Ukraine and southern Russia. The main radiation dose was to the thyroid and came from exposure to I131 from drinking contaminated milk. A substantial increase in thyroid cancer incidence in children was observed as early as 5 years after the accident. The first report in 1992 described 114 cases of thyroid cancer in childre...

ea0010s25 | Bone breaking diseases | SFE2005

Parathyroid disease

Davies M

Parathyroid hormone(PTH) is released by the parathyroid glands to regulate the concentration of ionised calcium in extracellular fluid.Any change in ionised calcium is followed by reciprocal changes in PTH secretion. PTH acts on the kidney to increase the renal tubular reabsorption of calcium and to increase the synthesis of the hormonal metabolite of vitamin D which enhances the intestinal absorption of calcium. Prolonged PTH secretion increases calcium release from bone as a...

ea0010s28 | Bone breaking diseases | SFE2005

Switching on dead bones

Miller M

The treatment of growth hormone deficiency (GHD) with growth hormone (GH) leads to increased bone turnover, new bone formations and increased bone mineral density (BMD). This response is paralleled by an increased demand for bone substrate. We present a case in which the increased turnover induced by GH treatment revealed previously occult metabolic bone disease.The patient a 56-year-old male with panhypopituitarism following treatment for acromegaly, co...

ea0010ds2 | Beta cell growth: implications for Type 1and Type 2 diabetes | SFE2005

Islet mitogens – role in the maintenance of β-cell mass

Stoffel M

Beta-cell hyperplasia is an important adaptive mechanisms to maintain normoglycemia during physiological growth and in obesity. Increasing evidence suggests that the β-cell mass is dynamic and that increase demands on insulin secretion in insulin resistance and pregnancy can lead to rapid and marked changes in the β-cell mass. The mass of β-cells is governed by the balance of ß cell growth (replication) and by β-cell death (apoptosis). The molecular ba...

ea0010ds3 | Beta cell growth: implications for Type 1and Type 2 diabetes | SFE2005

β-cell death in type 2 diabetes: a link to type 1 diabetes

Donath M

A decrease in the number of functional insulin producing beta-cells contributes to the pathophysiology of type 2 diabetes. The putative factors responsible for the maladaptation of beta-cells include hyperglycaemia, cytokines, dyslipidemia and leptin. Islet inflammation, autoimmunity and some drugs may be secondary modulators. Predetermined amount of beta-cell mass, sensitivity to pro-apoptotic signals and regeneration potential of beta-cells are predisposing factors. The mech...

ea0009s8 | Symposium 1: Endocrine complications of systemic disorders | BES2005

The endocrinology of critical care

Cooper M

Critical illness due to sepsis, trauma, surgery, organ failure or burns is associated with dramatic effects on most hormonal axes. Complex changes occur at the hypothalamic, pituitary, circulatory and tissue levels of hormone action. In the early stages of critical illness these changes appear to be adaptive but this may not be the case in prolonged illness. Common problems faced by endocrinologists are the recognition of pre-existing endocrine disorders in critically ill pati...

ea0009s18 | Symposium 4: Intracellular transport for steroids | BES2005

The molecular mechanism of nuclear trafficking

Stewart M

Nuclear pore complexes (NPCs) facilitate the transport of macromolecular cargoes across the nuclear envelope by carrier molecules. The energy for this active transport mechanism is provided by the Ras-family GTPase, Ran, that orchestrates most nuclear trafficking cycles. The RanGEF (RCC1) is located in the nucleus while its GAP is located in the cytoplasm. The nuclear import of steroids, bound to their receptor, is mediated by importins alpha and beta. In the cytoplasm, import...