Metabolic effects of replacing sucrose by isomaltulose in subjects with type 2 diabetes: a randomized double-blind trial.

Objective: To test the hypothesis that replacement of sucrose with isomaltulose in sweet foods and beverages improves metabolic control in patients with type 2 diabetes.

Research Design And Methods: One hundred ten patients with type 2 diabetes were randomized to receive sweet foods containing either 50 g/day isomaltulose or sucrose for 12 weeks as part of their habitual diet under free-living conditions. HbA(1c) at 12 weeks was the primary outcome parameter.

Novel findings on the metabolic effects of the low glycaemic carbohydrate isomaltulose (Palatinose).

The slow digestible disaccharide isomaltulose (iso; Palatinose) is available as novel functional carbohydrate ingredient for manufacturing of low glycaemic foods and beverages. Although basically characterised, various information on physiological effects of iso are still lacking. Thus, the objective of the present study was to expand scientific knowledge of physiological characteristics of iso by a set of three human intervention trials.

Human rectal mucosal gene expression after consumption of digestible and non-digestible carbohydrates.

The effect of regular consumption of the low-digestible and prebiotic isomalt versus the digestible sucrose on gene expression in rectal mucosa was examined in a randomized double-blind crossover trial. Nineteen healthy volunteers received 30 g isomalt per day or 30 g sucrose as part of a controlled diet over two 4-week test periods with a 4-week washout period in between. At the end of each test phase rectal biopsies were obtained.

Histone-deacetylase inhibitors induce the cathelicidin LL-37 in gastrointestinal cells.

Unlabelled: Histone-deacetylase (HDAC) -inhibitors enhance acetylation of core proteins and this is linked to formation of transcriptionally active chromatin in various cells. In this study, the effect of HDAC inhibitors (butyrate, trichostatin A (TSA)) on the expression of the cathelicidin LL-37 in colon, gastric and hepatocellular cells was investigated.

Methods: LL-37 expression was assessed in colon, gastric and hepatocellular cancer cells after treatment with HDAC-inhibitors.

Butyrate inhibits leukocyte adhesion to endothelial cells via modulation of VCAM-1.

Background: Leukocyte recruitment to areas of inflammation depends on Integrin-VCAM/ICAM interaction. Blocking the vascular cell adhesion molecule (VCAM-1) and the intracellular adhesion molecule (ICAM-1) may have therapeutic benefit for the inflammatory component of bowel disease. Notably, the induction of ICAM and VCAM is mediated by a nuclear factor kappaB (NF-kappaB)-dependent mechanism.

Establishment of a colonic adenoma cell line (GEKI-2): spectral karyotype analysis and functional characterization.

Background And Aims: On the genetic level colonic carcinogenesis is best described by the adenoma-carcinoma sequence, but it may be modulated by exogenous factors, particularly by dietary factors and chemopreventive agents. The protective effects of exogenous factors are thought to be exerted rather in the early stages of the adenoma-carcinoma sequence. Thus, an in vitro model consisting of cells stemming from an colon adenoma would be desirable.

Effect of enzyme-resistant starch on formation of 1,N(2)-propanodeoxyguanosine adducts of trans-4-hydroxy-2-nonenal and cell proliferation in the colonic mucosa of healthy volunteers.

The effect of enzyme-resistant starch (RS) on the development of colon cancer was reported to include both chemopreventive activity in humans and tumorigenic activity in animals. A study was performed to detect the influence of enzyme-RS on lipid peroxidation-induced DNA damage and cell proliferation. During two 4-week periods, 12 volunteers consumed a controlled diet in which starchy foods were enriched with a highly resistant amylomaize starch (Hylon VII) in the high-RS period and with an available corn starch in the low-RS period (second period).

Butyrate-enhanced TNFalpha-induced apoptosis is associated with inhibition of NF-kappaB.

Background: Tumor necrosis factor (TNFalpha)-induced apoptosis is limited by concomitant activation of nuclear factor kappa B (NF-kappaB)-dependent anti-apoptotic genes. Butyrate inhibits NF-kappaB activation so that co-treatment with butyrate effectively enhances TNFalpha-induced apoptosis. In this context, the inhibition of NF-kappaB activation and subsequent modulation of (NF-kappaB)-dependent genes was assessed

Materials And Methods: Human colon adenocarcinoma cells (SW620) were incubated with TNFalpha and butyrate.