The effects of treatment with pitavastatin on inflammatory and platelet activation markers and adiponectin in 117 patients with hyperlipidemia were investigated to determine whether pitavastatin may prevent the progression of atherosclerotic changes in hyperlipidemic patients. Adiponectin levels prior to pitavastatin treatment in hyperlipidemic patients with and without diabetes were lower than levels in normolipidemic controls. Both total cholesterol and the low-density lipoprotein cholesterol decreased significantly after pitavastatin administration. Additionally, hyperlipidemic patients with or without type 2 diabetes exhibited a significant increase in adiponectin levels 6 months after pitavastatin treatment (diabetes: 3.52 ± 0.80 vs. 4.52 ± 0.71 µg/ml, p < 0.001; no diabetes: 3.48 ± 0.71 vs. 4.23 ± 0.82 µg/ml, p < 0.05). However, high-sensitivity C-reactive protein, platelet-derived microparticle and soluble P-selectin did not exhibit any differences before or after pitavastatin administration. Levels of adiponectin significantly increased after pitavastatin administration in the group of lower soluble P-selectin (soluble P-selectin before pitavastatin treatment <200 ng/ml). These results suggest that pitavastatin possesses an adiponectin-increasing effect in patients with hyperlipidemia and this effect is influenced by intensive platelet activation.

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The effects of blueberry leaf (BBL) on lipid metabolism were studied in obese rats. Feeding of BBL lowered levels of serum lipids and C-reactive protein and alleviated hepatic triglyceride accumulation in the rats. The hypolipidemic effect might be attributable to a reduction of lipogenesis and enhancement of lipolysis in the liver. These results suggest the use of blueberry leaf as a dietary hypolipidemic component.Key words: Vaccinium ashei reade; blueberry leaf; lipid metabolism; Otsuka Long-Evans Tokushima Fatty ratLifestyle-related diseases, such as hyperlipidemia, arteriosclerosis, diabetes mellitus, and hypertension, are widespread and increasingly prevalent diseases in industrialized countries, and they contribute to increases in cardiovascular morbidity and mortality. 1,2) Accompanied by rapid increases in the numbers of elderly people, this is important not only medically but also socioeconomically. Although the pathogenesis of lifestyle-related diseases is complicated and the precise mechanisms have not yet been elucidated, obesity has emerged as a major cardiovascular risk factor according to epidemiologic studies. [3][4][5] Obesity is defined as an increased mass of adipose tissue, and its prevalence and severity are markedly increasing in westernized countries. Otsuka Long-Evans Tokushima Fatty (OLETF) rats develop a syndrome with multiple metabolic and hormonal disorders that shares many features with human obesity. 6-9) OLETF rats have hyperphagia because they lack receptors for cholecystokinin, and become obese, developing hyperlipidemia, fatty liver, and type-2 diabetes. In this study, we examined effects of blueberry leaf (BBL) on lipid metabolism in obese OLETF rats.Vaccinium ashei reade (blueberry) belongs to the Ericaceae plant group, and infusions of its leaf are used as a folk medicine treatment for lifestyle-related diseases in Europe. 10,11) Martineau et al. demonstrated anti-diabetic properties of the Canadian lowbush blueberry in vitro. 11) Recently, we reported that blueberry leaf revealed strong inhibitory effects on angiotensinconverting enzyme activity in vitro, and that feeding of blueberry leaf suppressed the development of essential hypertension in spontaneously hypertensive rats in vivo. 12) The effects of blueberry leaf on lipid metabolism, however, have not been fully evaluated.To determine the physiological function of BBL, we evaluated the effect of BBL feeding on hepatic enzyme activities in relation to lipid metabolism in obese OLETF rats.Four-week-old male OLETF rats were provided by the Tokusima Research Institute (Otsuka Pharmaceutical, Tokushima, Japan). The rats were housed individually in metal cages in a temperature-controlled room (24 C) under a 12-h light/dark cycle. After a 1-week adaptation period on a powder chow diet (CE-2, Clea Japan, Tokyo), they were assigned to three groups (six rats each), each fed one of three diets: (i) a semisynthetic diet containing (in weight %) casein, 20; corn oil, 7; cornstarch, 15; vitamin mixture (AIN-76Ô), 1; mineral mixture ...

Non-alcoholic fatty liver disease (NAFLD) is emerging as the most common liver disease in industrialised countries. Various mushrooms have been used in Eastern folk medicine for the treatment of lifestyle diseases. We previously found that the dietary intake of powdered whole Panellus serotinus (Mukitake) alleviates NAFLD in obese, diabetic db/db mice. In the present study, we investigated the influence of Mukitake fractional extracts on the development of NAFLD in db/db mice. A significant reduction in the hepatic TAG content, macrovesicular hepatocytes and activities of key enzymes for de novo synthesis of the fatty acid was observed in both the water-soluble Mukitake extract (WE) diet and the ethanol-soluble Mukitake extract (EE) diet groups compared with the control diet group of the db/db mice. The serum level of monocyte chemoattractant protein-1 (MCP-1), which is known to exacerbate insulin resistance, was significantly decreased in the WE group. On the other hand, the serum level of adiponectin, which plays a protective role against the metabolic syndrome, was significantly increased in the EE group. Additionally, differential analysis between Mukitake and Shiitake, mycelia from the same family, using liquid chromatography time-of-flight MS technology revealed that only seven and five compounds exist in WE and EE from Mukitake, respectively. In conclusion, the present study demonstrated that Mukitake displays at least two different physiological actions that alleviate NAFLD: one through the reduction in inflammatory damage by its suppression in MCP-1 production and the other through an increase in level of serum adiponectin and the prevention of visceral fat accumulation.