Consuming food is essential for survival, maintaining health, and triggering positive emotions like pleasure. One of the factors that drive us toward such behavior is the presence of various compounds in foods. There are many methods to analyze these molecules in foods; however, it is difficult to analyze the spatial distribution of these compounds using conventional techniques, such as mass spectrometry combined with high-performance liquid chromatography or gas chromatography. Mass spectrometry imaging (MSI) is a two-dimensional ionization technology that enables detection of compounds in tissue sections without extraction, purification, separation, or labeling. There are many methods for ionization of analytes, including secondary ion mass spectrometry, matrix-assisted laser desorption/ionization, and desorption electrospray ionization. Such MSI technologies can provide spatial information on the location of a specific analyte in food. The number of studies utilizing MSI technologies in food science has been increasing in the past decade. This review provides an overview of some of the recent applications of MSI in food science and related fields. In the future, MSI will become one of the most promising technologies for visualizing the distribution of food components and for identifying food-related factors by their molecular weights to improve quality, quality assurance, food safety, nutritional analysis, and to locate administered food factors.

Allergic dermatitis is a skin disease with growing prevalence worldwide that has been associated with diets high in fats and sugars. Regular consumption of sucrose-containing beverages may increase the risk for several health problems, including allergic diseases and particularly asthma, but the association between sucrose consumption and allergic dermatitis is understudied. We investigated the effects of sucrose solution intake on allergic contact dermatitis in rats and found early exacerbation of 2,4-dinitrofluorobenzene (DNFB)-induced disease symptoms and altered composition of the gut microbiota after 14 d of intake. The levels of short-chain fatty acids—produced by fermentation by the intestinal microbiota—were not affected in the cecal contents and feces but decreased in the blood; this effect was especially notable for acetate. To restore blood acetate concentrations, triacetin was mixed with a 10% sucrose solution and fed to the rat model. This strategy prevented the early exacerbation of DNFB-induced symptoms. The decreased absorption of short-chain fatty acids from the intestinal lumen was not linked to the decreased expression of short-chain fatty acid transporters in the small intestine; instead, the mechanism involves a reduction in the sodium concentration in the intestinal lumen due to increased expression of sodium–glucose transporter 1 (SGLT1).

Background/Objectives: Allergic contact dermatitis (ACD), an inflammatory skin condition, is commonly treated with topical corticosteroids; however, long-term use of these drugs is associated with various risks, such as skin atrophy and steroid resistance. Triacetin (TA), a triglyceride metabolized to acetate, exerts anti-inflammatory affects by activating AMP-activated protein kinase (AMPK) and suppressing mast cell degranulation. Here, we aimed to assess the immediate and long-term effects of TA on ACD suppression, focusing on AMPK activation, using a 2,4-dinitrofluorobenzene-induced rodent model. Methods: Various concentrations of TA were topically applied to rats with 2,4-dinitrofluorobenzene-induced dermatitis. Ear thickness was measured, and histological analysis was performed to assess the inflammation, mast cell infiltration, and degranulation in the established models. AMPK activation was analyzed via Western blotting, and TA degradation was assessed via gas chromatography-mass spectrometry. Dorsomorphin (an AMPK inhibitor) was used to evaluate the effects of AMPK on ACD. Results: TA significantly inhibited inflammation and mast cell degranulation in a dose-dependent manner, with 0.25 mmol/L showing the most potent effects. It also activated AMPK activation. Notably, AMPK inhibition reversed the effects of TA. Conclusions: Overall, TA exerted immediate and long-term anti-inflammatory effects via AMPK activation and inhibition of mast cell degranulation, showing potential as a non-steroidal therapeutic for ACD.

Background/Objectives: Fasting-induced elevation of blood ketone body levels suppresses allergic reactions; however, the underlying mechanism remains unclear. This study investigated whether elevated ketone body levels affect allergic contact dermatitis (ACD) and explored nutritional interventions that effectively increase β-hydroxybutyrate (BHB) levels. Additionally, we examined the role of GPR109A, a receptor for β-hydroxybutyrate (BHB), in ketone body-induced allergy suppression through ingestion of a ketogenic substrate. Methods: To evaluate the effects of ketone body precursors, medium-chain triglyceride (MCT) oil or 1,3-butanediol (BD) was administered as a single oral dose (2 g/kg body weight) under fed conditions. Blood BHB concentrations were measured at the time of euthanasia. ACD was induced using 2,4-dinitrofluorobenzene (DNFB), and its severity was assessed by measuring ear swelling and mast cell (MC) degranulation. To determine whether GPR109A mediates ketone body-induced allergy suppression, mepenzolate bromide (MPN), a GPR109A antagonist, was subcutaneously administered before BD treatment. Results: Both MCT oil and BD significantly increased the blood BHB levels. Elevated BHB concentrations were accompanied by reduced ear swelling and MC degranulation in DNFB-treated mice. The anti-allergic effects of BD were abolished by MPN administration, indicating that these effects were mediated by GPR109A activation. Conclusions: Nutritional supplementation with ketogenic substrates, such as MCT oil and BD, may serve as a dietary intervention for ACD by elevating blood BHB levels. GPR109A activation appears to be involved in ketone body-induced allergy suppression, suggesting a mechanistic link between ketone metabolism and immunomodulation.