Abstract
Increasing apoA-I synthesis may improve HDL functionality and lower CVD risk. As theobromine and fat increase fasting apoA-I concentrations, and the intestine is involved in apoA-I production, the acute effects of both were studied on duodenal gene transcription to better understand underlying mechanisms. In this crossover study, 8 healthy men received once a low fat (LF) meal, a LF meal plus theobromine (850 mg), or a high fat (HF) meal. Five hours after meal intake duodenal biopsies were taken for microarray analysis. Theobromine and HF consumption did not change duodenal apoA-I expression. Theobromine did not change gene expression related to lipid and cholesterol metabolism, whereas those related to glycogen/glucose breakdown were downregulated. HF consumption increased gene expression related to lipid and cholesterol uptake and transport, and to glucose storage, while it decreased those related to glucose uptake. Furthermore, genes related to inflammation were upregulated, but inflammation markers in plasma were not changed. In healthy men, acute theobromine and fat consumption did not change duodenal apoA-I mRNA, but inhibited expression of genes related to glucose metabolism. Furthermore, HF intake activated in the duodenum expression of genes related to lipid and cholesterol metabolism and to inflammation.
Highlights
Over the past decade, interventions aiming to increase serum high-density lipoprotein (HDL) cholesterol (HDL-C) concentrations to reduce the risk of cardiovascular disease (CVD) have not been successful
Since apolipoprotein A-I (apoA-I) is produced in enterocytes and hepatocytes[7], and theobromine is absorbed in the small intestine[8,9], we were interested in exploring the effects of acute theobromine consumption on gene expression in postprandial human duodenal biopsies, following theobromine intake
In comparison to the LF shake, 113 and 286 genes were differentially expressed after adding theobromine to the LF diet (LF-TB) and comparing it with the HF shake, respectively (Supplementary data Fig. 1)
Summary
Interventions aiming to increase serum high-density lipoprotein (HDL) cholesterol (HDL-C) concentrations to reduce the risk of cardiovascular disease (CVD) have not been successful. Suggest that improving HDL functionality will more likely lower CVD risk than elevating circulating serum HDL-C concentrations[1]. In this respect, increasing serum apolipoprotein A-I (apoA-I) synthesis may be a promising approach, as serum apoA-I concentrations correlate with in vitro cholesterol efflux, a measure of HDL functionality[2,3,4]. The intestine is strongly involved in dietary lipid handling, the effects of fat intake on duodenal gene expression profiles have not been studied. A nutrigenomic approach to analyze differences in gene expression in human duodenal biopsies after adding 850 mg of theobromine to a LF meal, and after comparing HF with LF meal consumption to better understand effects of dietary theobromine and fat on duodenal apoA-I transcription and related pathways
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
