The hypoglycemic activity of olive leaf was studied. Maximum hypoglycemic activity was obtained from samples collected in the winter months, especially in February. One of the compounds responsible for this activity was oleuropeoside, which showed activity at a dose of 16 mg/kg. This compound also demonstrated antidiabetic activity in animals with alloxan-induced diabetes. The hypoglycemic activity of this compound may result from two mechanisms: (a) potentiation of glucose-induced insulin release, and (b) increased peripheral uptake of glucose.

The aim of the present study was to analyze whether consumption of a fiber-supplemented diet containing 3.5% Plantago ovata husks prevented many of the abnormalities clustered in the metabolic syndrome, including obesity, dyslipidemia, hypertension and endothelial dysfunction. For this purpose, obese Zucker rats, a model of type 2 diabetes, and their lean littermates were studied. Rats consumed a standard control diet or that diet supplemented with 3.5% P. ovata husks for 25 wk. Body weights were measured weekly. Systolic blood pressure (SBP) was measured monthly. At the end of the treatment, plasma concentrations of triglycerides, total cholesterol, FFAs, glucose, insulin, adiponectin, and tumor necrosis factor alpha (TNF-alpha) were determined, and studies on vascular function were performed using aortic rings. Rats fed the P. ovata husk-supplemented diet had a significantly reduced body weight gain compared with those fed the standard diet. Decreased endothelium-dependent relaxation in response to acetylcholine (ACh) by aortic rings from obese Zucker rats was improved in those fed the fiber-supplemented diet. The greater SBP, higher plasma concentrations of triglycerides, total cholesterol, FFA, glucose, insulin, and TNF-alpha, and the hypoadinectinemia that occurred in obese Zucker rats that consumed the control diet were significantly improved in those fed the fiber-supplemented diet. We conclude that intake of a P. ovata husk-supplemented diet prevents endothelial dysfunction, hypertension, and obesity development, and ameliorates dyslipidemia and abnormal plasma concentrations of adiponectin and TNF-alpha in obese Zucker rats.

In¯ammatory bowel disease is a chronic disease of the digestive tract, and usually refers to two related conditions, namely ulcerative colitis and Crohn's disease. The aetiology of in¯ammatory bowel disease remains unknown, although it is believed that an alteration in the intestinal immune system contributes to the in¯ammation that occurs. As in other in¯am-matory processes, in¯ammatory bowel disease is characterized by an up-regulation in the synthesis and release of different pro-in¯ammatory mediators, including reactive oxygen and nitrogen metabolites, eicosanoids, platelet-activating factor and cytokines. 1 All of these mediators contribute to the pathogenic cascade that initiates and perpetuates the in¯ammatory response of the gut. As a consequence, and until its aetiology has been completely elucidated, the best strategy to effectively down-regulate intestinal in¯ammation is to interfere with multiple stages of the in¯ammatory cascade, preferably with a single drug treatment. In fact, the SUMMARY Background: Morin, a bio¯avonoid with antioxidant properties, shows intestinal anti-in¯ammatory activity in the acute phase of the trinitrobenzenesulphonic acid model of rat colitis. Aim: To assess the anti-in¯ammatory activity of morin in the chronic stages of trinitrobenzenesulphonic acidinduced rat colitis. Methods: Rats were rendered colitic by a single colonic instillation of 30 mg of the hapten trinitrobenzenesulphonic acid dissolved in 0.25 mL of 50% ethanol. A group of colitic animals was given morin orally at doses of 25 mg/kg daily. Animals were sacri®ced every week for 4 weeks. Colonic damage was evaluated macroscopically and microscopically. Different biochemical markers of colonic in¯ammation were also assayed, including myeloperoxidase activity, leukotriene B 4 and

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Background and purpose: Bovine glycomacropeptide (BGMP) is an inexpensive, non-toxic milk peptide with antiinflammatory effects in rat experimental colitis but its mechanism of action is unclear. It is also unknown whether BGMP can ameliorate inflammation in proximal regions of the intestine. Our aim was therefore two-fold: first, to determine the antiinflammatory activity of BGMP in the ileum; second, to characterise its mechanism of action. Experimental approach: We used a model of ileitis induced by trinitrobenzenesulphonic acid in rats. Rats were treated orally with BGMP and its efficacy compared with that of oral 5-aminosalicylic acid or vehicle, starting 2 days before ileitis induction. Key results: BGMP pretreatment (500 mg kg À1 day À1 ) resulted in marked reduction of inflammatory injury, as assessed by lower extension of necrosis and damage score, myeloperoxidase, alkaline phosphatase, inducible nitric oxide synthase, interleukin 1b, tumour necrosis factor and interleukin 17. These effects were generally comparable to those of 5-aminosalicylic acid (200 mg kg À1 day À1 ). Neither compound affected the production of interferon g, tumour necrosis factor and interleukin 2 by mesenteric lymph node cells isolated from animals with ileitis. The expression of Foxp3 was increased in ileitis and not reduced significantly by BGMP or aminosalicylate treatment. Conclusions and implications:These results demonstrate that BGMP has anti-inflammatory activity in the ileum with similar efficacy to 5-aminosalicylic acid. The mechanism of action may involve Th17 and regulatory T cells and perhaps macrophages but probably not Th1 lymphocytes. Patients with Crohn's ileitis may benefit from treatment with BGMP.