Thrombotic tendency in diabetes mellitus. Revisiting and revising a study initiated 30 years ago.

Studies initiated 30 years ago emphasized that dilute blood clot lysis time was longer in obese diabetic patients than in normal weight diabetics. It was also later reported that when compared to obese women with gluteal and femoral adiposity, the age matched men with abdominal obesity displayed a more delayed clot lysis, higher triglyceride levels and higher cholinesterase activity, as well as more increased concentration of plasminogen activator inhibitor-1 (PAL-1). According to authors' investigations and data in the literature, impaired fibrinolysis in overweight hypertriglyceridemic subjects are mainly due to increased plasma levels of coagulation factor XIII and PAI-1.

Controversy on high density lipoprotein raising therapy.

Decreased high density lipoproteins (HDL) plasma levels are a recognized independent risk factor for atherosclerotic cardiovascular disease. Attempts were therefore initiated to pharmacologically raise plasma HDL cholesterol, and the most impressive increase was obtained by inhibiting cholesteryl ester transfer protein (CETP) by means of the synthetic compound torcetrapib. Clinical trials were however disappointing, as torcetrapib increased mortality and did not reduce the progression of atherosclerosis.

The discovery by Gh. Benga of the first water channel protein in 1985 in Cluj-Napoca, Romania, A few years before P. Agre (2003 Nobel Prize in Chemistry).

The first water channel protein, now called aquaporin 1, was identified or "seen" in situ in the human red blood cell membrane by Benga's group in 1985. It was again "seen" when it was by chance purified by Agre'group in 1988 and was again identified when its main feature, the water transport property, was found by Agre's group in 1992. Consequently, the omission of Gh.

Pathogenic role of abnormal fatty acids and adipokines in the portal flow. Relevance for metabolic syndrome, hepatic steatosis and steatohepatitis.

Evidence has been provided that increased levels of non esterified fatty acids (NEFA) in the portal flow would produce insulin resistance and would also stimulate the hepatic protein synthesis, thereby explaining the increased plasma levels not only of apolipoprotein B, but also of other liver-derived enzymes and proteins occurring in overweight and hypertriglyceridemic patients. The high plasma concentration of triglyceride-rich lipoprotein would facilitate the transfer of cholesteryl esters from HDL and LDL to VLDL in exchange for triglycerides, a process mediated by liver-derived cholesteryl ester transfer protein (CETP). The triglyceride thereby acquired in HDL and LDL would then be hydrolyzed by hepatic lipase.

Lipolytic enzymes, metablic syndrome and atherosclerosis (revisiting and revising a 40 years old study).

More than 40 years ago, our laboratory reported that post-heparin lipolytic activity was decreased in patients with severe atherosclerotic disease, while values recorded in obese and hyperlipidemic subjects without clinically detectable atherosclerotic lesions did not significantly differ from normal weight normolipidemic controls. Because in 1967 data on pathophysiology of lipolytic enzymes were rather scarce, and mainly because our information facilities were limited in those years, we had difficulties in interpreting these results, and the study was to some extent awkwardly approached, as the investigated subjects were not considered according to their gender, body fat patterning and type of hyperlipoproteinemia, and the lipolytic activities of lipoprotein lipase and hepatic lipase had not been selectively assessed. Reviewing recent data in the literature it was noted that pre-heparin lipoprotein lipase mass assessed by ELISA was indeed significantly lower in insulin resistant coronary patients than in patients with no lesions, and correlated negatively with the severity of atherosclerotic lesions.