Adipose tissue, metabolic syndrome and polycystic ovary syndrome: from pathophysiology to treatment.

In the last few years, polycystic ovary syndrome (PCOS) has deserved major attention because it is linked to the same cluster of events that promote the metabolic syndrome. This review will point out the relationships between fat excess, insulin resistance and the metabolic syndrome. Adipocytes are actually considered as endocrine cells that synthesize and release molecules (adipokines) that play an endocrine/paracrine role, such as adiponectin, atrial natriuretic peptide, leptin, resistin, tumour necrosis factor alpha (TNFalpha). Metabolic syndrome is a chronic low-grade inflammatory condition in which adipokines play a major role. Isolated adipocytes from women with PCOS express higher mRNA concentrations of some adipokines involved in cardiovascular risk and insulin resistance. However, environmental factors and lifestyle play a major role in determining the appearance of the phenotypes of PCOS. In morbid obese women with PCOS, bariatric surgery decreases bodyweight and fat excess and reverses hyperandrogenism and sterility. In lean or overweight women with PCOS, changes in lifestyle in combination with drugs reducing visceral fat and insulin resistance reverse the symptoms and signs of PCOS. Promising treatments for PCOS seem to be insulin sensitizers such as metformin and glitazones.

Effects of combined treatment with simvastatin and L-carnitine on triglyceride levels in diabetic patients with hyperlipidaemia.

OBJECTIVE: To investigate the effects of L-carnitine, coadministered with simvastatin, on hypercholesterolaemia and hypertriglyceridaemia in patients with diabetes. DESIGN: Randomised, open, parallel-group study. SETTING: One investigational centre (hospital). PATIENTS: Thirty-two patients with type 2 diabetes mellitus and hyperlipidaemia (total cholesterol levels > 200 mg/dl and triglyceride levels >150 mg/dl). INTERVENTIONS: PATIENTS were randomised to receive simvastatin alone (n = 16) or simvastatin plus L-carnitine (n = 16) for 60 days. Both treatments were given orally. Simvastatin was administered, in both groups, at a dosage of 20 mg/day, while L-carnitine was administered at a dosage of 2000 mg/day twice daily. MAIN OUTCOME MEASURES AND RESULTS: Plasma levels of triglycerides, total cholesterol and high-density lipoprotein (HDL) cholesterol were measured at baseline and at 30 and 60 days after starting treatment. In both groups, there was a progressive improvement in all measured parameters during the study period. However, triglyceride levels decreased to a significantly greater extent in patients co-treated with L-carnitine (from 266.8 mg/dl at baseline to 153.8 mg/dl at 60 days) compared with those receiving simvastatin alone (from 300.2 to 227.8 mg/dl, respectively; p = 0.012 vs combined treatment). HDL-cholesterol levels increased from 49.8 mg/dl at baseline to 51.8 mg/dl at 60 days in the combined treatment group, and decreased from 51.2 to 47.8 mg/dl, respectively in simvastatin recipients, with a trend in favour of the combined treatment (p = 0.076), while no significant differences between groups were observed for total cholesterol levels. CONCLUSIONS: Combined treatment with L-carnitine and simvastatin resulted in greater antihyperlipidaemic effects (i.e. a less atherogenic plasma lipid profile) than with simvastatin alone. The results of this preliminary study strongly suggest that L-carnitine may have a role among antihyperlipidaemic strategies.