Although diabetic hepatopathy is potentially less common, it may be appropriate for addition to the list of target organ conditions related to diabetes. This study was designed to evaluate the hepatoprotective properties of green tea extract (GTE) in STZ-induced diabetes in rats. Wistar rats were made diabetic through single injection of STZ (75 mg/kg i.p.). The rats were randomly divided into four groups of 10 animals each: Group 1, healthy control; Group 2, nondiabetics treated with GTE administered orally (1.5%, w/v); Group 3, diabetics; Group 4, diabetics treated with GTE (1.5%, w/v) for 8 weeks. Serum biomarkers were assessed to determine hepatic injury. Malondialdehyde (MDA) and reduced glutathione (GSH) contents were measured to assess free radical activity in the liver tissue. Hepatic antioxidant activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) were also determined. The biochemical findings were matched with histopathological verifications. Liver MDA content and serum levels of ALT, AST, ALP, and bilirubin in Group 3 significantly increased compared to Group 1 (P < 0.05) and significantly decreased in Group 4 compared to Group 3 (P < 0.05). Serum albumin level and GSH, SOD, CAT, and GSH-Px contents of the liver in Group 3 were significantly decreased compared to Group 1 (P < 0.05) and were significantly increased in Group 4 compared to Group 3 (P < 0.05). Histopathologically, the changes were in the same direction with biochemical findings. This study proved the hepatoprotective activity of GTE in experimentally induced diabetic rats.

A 33-year-old woman with a 2 month history of vague ill health was admitted to hospital in hypoglycaemic coma. Preoperative investigation suggested malignant insulinoma as the probable cause of illness, but immunohistological examination of the tumour showed it to consist mainly of somatostatin-containing cells but sparse insulin-secreting cells were also present. Plasma immunoreactive somatostatin levels were from fifty to 200 times the upper limit of normal and rose in response to arginine and fell during diazoxide infusion. The hypoglycaemia was unusually sensitive to the hyperglycaemic effects of diazoxide and chlorothiazide and, with 5-fluorouracil as the only specific anti-tumour agent, there has been clinical, biochemical and radiological evidence of tumour regression.

The aim of the present study was to investigate whether the cholesteryl ester transfer protein (CETP) I405V polymorphism modifies the response to changes in the dietary ratio of polyunsaturated to saturated fat (P:S). The population included 85 healthy subjects with the different I405V genotypes (35 II, 36 IV, and 14 VV) assigned to two consecutive 28-day experimental period. All subjects consumed a high-P:S with P:S of 1.2 for the first period and a low-P:S with a P:S of 0.3 for the next 28-day period. At the first and end of each dietary period, serum lipid, lipoprotein, and CETP concentrations were measured. At screening, lipid or lipoprotein concentrations were not significantly different among CETP I405V genotype groups. After the low-P:S diet, subjects carrying V allele had greater reduction in apoA-I and HDL cholesterol (HDL-C) than subjects with II genotype. A genotype-by-diet interaction effect was observed on apoA-I (p=0.016) concentrations. In conclusion, the CETP I405V polymorphism contributes to the unfavorable changes of apoA-I and HDL-C when a high-P:S diet was replaced with a low-P:S diet.