Obesity and Hyperandrogenemia in Polycystic Ovary Syndrome: Clinical Implications.

Polycystic ovary syndrome (PCOS) is often accompanied with metabolic disturbances attributed to androgen excess and obesity, but the contribution of each has not been defined, and the occurrence of metabolic disturbances is usually not investigated. Ninety-nine women with PCOS and forty-one without PCOS were evaluated. The clinical biomarkers of alterations related to glucose (glucose, insulin, and clamp-derived glucose disposal - M), liver (aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transferase), and endothelium (arginine, asymmetric dymethylarginine, carotid intima-media thickness, and flow-mediated dilation) metabolism were measured; participants were categorized into four groups according to their obesity (OB) and hyperandrogenemia (HA) status as follows: Healthy (no-HA, lean), HA (HA, lean), OB (no-HA, OB), and HAOB (HA, OB). Metabolic disturbances were very frequent in women with PCOS (≈70%). BMI correlated with all biomarkers, whereas free testosterone (FT) correlated with only glucose- and liver-related indicators. Although insulin sensitivity and liver enzymes were associated with FT, women with obesity showed lower M (coef = 8.56 - 0.080(FT) - 3.71(Ob); p < 0.001) and higher aspartate aminotransferase (coef = 26.27 + 0.532 (FT) + 8.08 (Ob); p = 0.015) than lean women with the same level of FT. Women with obesity showed a higher risk of metabolic disorders than lean women, independent of hyperandrogenemia. Clinicians are compelled to look for metabolic alterations in women with PCOS. Obesity should be treated in all cases, but hyperandrogenemia should also be monitored in those with glucose-or liver-related disturbances.

Citrulline supplementation improves spatial memory in a murine model for Alzheimer's disease.

OBJECTIVES: Alzheimer's disease (AD) correlates with the dysfunction of metabolic pathways that translates into neurological symptoms. An arginine deficiency, a precursor of nitric oxide (NO), has been reported for patients with AD. We aimed to evaluate the effect of citrulline oral supplementation on cognitive decline in an AD murine model. METHODS: Three-month citrulline or water supplementation was blindly given to male and female wild-type and 3 × Tg mice with AD trained and tested in the Morris water maze. Cerebrospinal fluid and brain tissue were collected. Ultra-performance liquid chromatography was used for arginine determinations and the Griess method for NO. RESULTS: Eight-month-old male 3 × Tg mice with AD supplemented with citrulline performed significantly better in the Morris water maze task. Arginine levels increased in the cerebrospinal fluid although no changes were seen in brain tissue and only a tendency of increase of NO was observed. CONCLUSIONS: Citrulline oral administration is a viable treatment for memory improvement in the early stages of AD, pointing to NO as a viable, efficient target for memory dysfunction in AD.