Intestinal Inflammation and Regeneration-Interdigitating Processes Controlled by Dietary Lipids in Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a disease of chronic inflammatory conditions of the intestinal tract due to disturbance of the inflammation and immune system. Symptoms of IBD include abdominal pain, diarrhea, bleeding, reduced weight, and fatigue. In IBD, the immune system attacks the intestinal tract's inner wall, causing chronic inflammation and tissue damage. In particular, interlukin-6 and interlukin-17 act on immune cells, including T cells and macrophages, to amplify the immune responses so that tissue damage and morphological changes occur. Of note, excessive calorie intake and obesity also affect the immune system due to inflammation caused by lipotoxicity and changes in lipids supply. Similarly, individuals with IBD have alterations in liver function after sustained high-fat diet feeding. In addition, excess dietary fat intake, along with alterations in primary and secondary bile acids in the colon, can affect the onset and progression of IBD because inflammatory cytokines contribute to insulin resistance; the factors include the release of inflammatory cytokines, oxidative stress, and changes in intestinal microflora, which may also contribute to disease progression. However, interfering with de novo fatty acid synthase by deleting the enzyme acetyl-CoA-carboxylase 1 in intestinal epithelial cells (IEC) leads to the deficiency of epithelial crypt structures and tissue regeneration, which seems to be due to Lgr5+ intestinal stem cell function. Thus, conflicting reports exist regarding high-fat diet effects on IBD animal models. This review will focus on the pathological basis of the link between dietary lipids intake and IBD and will cover the currently available pharmacological approaches.

Research progress on chitin/chitosan-based emulsion delivery systems and their application in lipid digestion regulation.

Excessive lipid intake is linked to an elevated risk of health problems. However, reducing lipid contents may influence food structure and flavor. Some alternatives are needed to control the lipid absorption. Emulsions are common carriers for lipids, which can control the hydrolysis and absorption of lipids. Chitin (Ch) and chitosan (CS) are natural polysaccharides with good biodegradability, biocompatibility, and unique cationic properties. They have been reported to be able to delay lipolysis, which can be regarded as one of the most promising agents that regulates lipid digestion (LiD). The application of Ch/CS and their derivatives in emulsions are summarized in this review with a focus on their performances and mechanisms for LiD regulation, aiming to provide theoretical guidance for the development of novel Ch/CS emulsions, and the regulation of LiD. A reasonable design of emulsion interface can provide its resistance to the external environment and then control LiD. The properties of emulsion interface are the key factors affecting LiD. Therefore, systematic study on the relationship between Ch/CS-based emulsion structure and LiD can not only instruct the reasonable design of emulsion interface to accurately regulate LiD, but also provide scientific guidelines for applying Ch/CS in functional food, medicine and other fields.

Application of chitin/chitosan and their derivatives in emulsionsStrategies to improve emulsifying properties of chitin/chitosanDigestion behaviors of chitin/chitosan emulsions during gastrointestinal digestionRational design and potential mechanism of chitin/chitosan to regulate lipolysis.

Fat intake pattern in women with polycystic ovary syndrome.

RESEARCH QUESTION: Do women with polycystic ovary syndrome (PCOS) have a different fat intake pattern to women without PCOS? DESIGN: Case-control study of 276 women between 20 and 35 years old from the Murcia region of Spain. Cases (n = 121) attended the Department of Gynaecology and Obstetrics of the University Clinical Hospital and were diagnosed with PCOS using Rotterdam criteria. Controls (n = 155) were women without PCOS attending the gynaecological outpatient clinic for routine gynaecological examinations. Data from clinical, gynaecological and analytical examinations were collected, including a food frequency questionnaire. Associations between fat intake and presence of PCOS and its phenotypes were examined using multiple logistic regression, adjusting for potential confounding factors. RESULTS: Although no association was found between fatty acid intake and PCOS, significant associations were observed for some PCOS phenotypes. The PCOS phenotype characterized by hyperandrogenism + oligo/amenorrhoea + polycystic ovarian morphology ('H+O+POM') was significantly associated with a higher intake of polyunsaturated fat (odds ratio [OR] 4.0; 95% confidence interval [CI] 1.1-14.2; fourth quartile of highest intake [Q4] versus lowest intake quartile as reference [Q1]) and omega-6 fatty acids (OR 3.5; 95% CI 1.01-12.4; Q3 versus Q1). The 'H+O' phenotype was positively associated with saturated fat intake (OR 6.9; 95% CI 1.1-41.6; Q4 versus Q1). CONCLUSION: This exploratory study suggests that higher intakes of specific fatty acids are related to some PCOS phenotypes although no association was found for PCOS on a global basis. It is recommended that studies with larger sample size be performed to further explore these associations, thus contributing to establishing recommendations about fat intake adapted to different PCOS phenotypes.