Changes in neuropeptide Y [NPY] - Nerves and in NPY binding in the seminal vesicles and prostate gland of the Streptozotocin-treated diabetic rat

This study focuses on the Neuropeptide Y [NPY] nerves in the diabetic prostate gland and seminal vesicle; the investigation concerns the changes in the NPY innervation, and in the density of NPY-binding sites in the post-synaptic tissues are also examined. The NPY nerves were visualised using immunocytochemistry, and NPY-binding sites were examined using quantitative autoradiography. Streptozotocin-induced diabetes caused an increased density of NPY containing nerves combined with a reduction in the density of NPY-binding sites. This suggests that there may be an increase in NPY release associated with a down-regulation of NPY-receptors. In conclusion there is an increase in the density of staining for NPY in the axons and sympaqthetic varicosities in the diabetic seminal vesicle and prostate gland. Associated with these changes in the nerve terminals, it appears that the release of NPY in the seminal vesicle may be concomitantly increased as there is a statistically significant decrease in the number of NPY-binding sites in the tissues

Update in diabetic nephropathy

Diabetic nephropathy has become the leading cause of end-stage kidney disease worldwide and is associated with an increased cardiovascular risk. The earliest clinical manifestation is microalbuminuria. Tight blood glucose and blood pressure control reduce the risk of microalbuminuria. Once microalbuminuria is present, the rate of progression to end stage kidney disease and cardiovascular disease can be delayed by aggressive management of blood pressure, glucose, and lipids. Inhibition of the renin-angiotensin system is important in reducing intraglomerular pressure but other classes of antihypertensive agents may also be needed to obtain adequate control of systemic blood pressure. Such measures can at least reduce by half the rate of progression of nephropathy and cardiovascular disease