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Background: Nondiabetic patients with advanced coronary artery disease (CAD) were assessed for lipid peroxidation, LDL modifications and insulin action. Twenty-four patients and 10 normal controls were studied., Methods: Insulin tolerance test (Kitt), glucose, insulin lipoproteins, electronegatively charged, modified, low density lipoproteins (LDL-) and the thiobarbituric acid reactivity (TBARS), as an index of lipid peroxidation, were determined., Results: No difference was observed in insulin action (determined by insulin tolerance test) between patients with CAD (3.31 +/- 0.28%/min; range 0.73-6.13) and normal controls (3.59 +/- 0.42; range 1.76-6.06). The percentage of modified, electronegative LDL (LDL -) was higher in patients with CAD (0.5 +/- 0.48%; range 1.3-9.2) than that of controls (2.80 +/- 0.33; range 1.00-4.00; p = 0.013). TBARS were significantly (P = 0.043) higher in CAD patients (3.49 +/- 0.17 nmol/ml; range 2.4-5.5) than normal controls (1.47 +/- 0.12; range 1.07-2.10). A significantly negative correlation was observed between Kitt and TBARS (r= - 0.48; p = 0.016), and a significant (r = 0.46; p = 0.022) positive correlation was observed between plasma glucose and TBARS. On the contrary no correlation has been observed between LDL- and TBARS., Conclusions: We conclude that in patients with advanced coronary artery disease: A) there are increased circulating levels of modified low density lipoprotein; B) there is evidence of increased lipid peroxidation. This latter process is significantly influenced by the degree of insulin action.

Liver cirrhosis is characterized by an increased incidence of glucose intolerance, diabetes and insulin resistance. We report a cirrhotic man (41 years old) who developed glucose intolerance and diabetes with insulin resistance over a period of six years. This patient suffered from severe portal hypertension with oesophageal varices and a enormously increased spleen volume. The subject underwent prophylactic endoscopic sclerotherapy of oesophageal varices. Splenectomy was performed because of severe piastrinopenia with recurrent nose bleeding. During laparotomy, multiple liver biopsies confirmed diagnosis of liver cirrhosis. Intra-operatory exploration revealed a splenic vein thrombosis. For this reason the planned spleno-renal shunting was not performed and the patient was only submitted to splenectomy. Liver function improved in the month following splenectomy and concomitant decrease of insulin resistance was observed (with a reduction in daily insulin dosage from 126 to 10 I.U.). We propose the following explanations of this event: 1) A decrease of portal and pancreatic vein pressure may have induced a proportional decrease (as already reported) of glucagon secretion. 2) The ameliorated liver function may have induced an improvement of liver glucose, insulin and glucagon metabolism. 3) A reduction of insulin circulating level (proved by a decrease of C Peptide value) may have lessened the insulin receptor down-regulation.