Caffeine, generally known as a stimulant of gastric acid secretion (GAS), is a bitter-tasting compound that activates several taste type 2 bitter receptors (TAS2Rs). TAS2Rs are expressed in the mouth and in several extraoral sites, e.g., in the gastrointestinal tract, in which their functional role still needs to be clarified. We hypothesized that caffeine evokes effects on GAS by activation of oral and gastric TAS2Rs and demonstrate that caffeine, when administered encapsulated, stimulates GAS, whereas oral administration of a caffeine solution delays GAS in healthy human subjects. Correlation analysis of data obtained from ingestion of the caffeine solution revealed an association between the magnitude of the GAS response and the perceived bitterness, suggesting a functional role of oral TAS2Rs in GAS. Expression of TAS2Rs, including cognate TAS2Rs for caffeine, was shown in human gastric epithelial cells of the corpus/fundus and in HGT-1 cells, a model for the study of GAS. In HGT-1 cells, various bitter compounds as well as caffeine stimulated proton secretion, whereby the caffeineevoked effect was (i) shown to depend on one of its cognate receptor, TAS2R43, and adenylyl cyclase; and (ii) reduced by homoeriodictyol (HED), a known inhibitor of caffeine's bitter taste. This inhibitory effect of HED on caffeine-induced GAS was verified in healthy human subjects. These findings (i) demonstrate that bitter taste receptors in the stomach and the oral cavity are involved in the regulation of GAS and (ii) suggest that bitter tastants and bittermasking compounds could be potentially useful therapeutics to regulate gastric pH.gastric acid secretion | caffeine | homoeriodictyol | bitter taste receptors | TAS2Rs

Light as an external trigger is a valuable and easily controllable tool for directing chemical reactions with high spatial and temporal accuracy. Two o-nitrobenzyl derivatives, benzoyl- and thiophenyl-NPPOC, undergo photo-deprotection with significantly improved efficiency over that of the commonly used NPPOC group. The two- and twelvefold increase in photo-deprotection efficiency was proven using photolithograph synthesis of microarrays.

The biological consequences of chronic consumption of Maillard reaction products (MRPs) on renal function in health and renal disease are still incompletely understood. We investigated the metabolic and renal effects of a diet with varying MRP content in healthy and subtotally nephrectomized rats. Male Wistar rats were subjected to sham operation (control, C, n = 12), or to 5/6 nephrectomy (5/6NX, n = 12). Both groups were randomized into subgroups and pair-fed with either a MRP-poor or -rich diet for six weeks. The diet was prepared by replacing 5% or 25% of wheat starch by bread crust (BC). In spite of pair-feeding, the rats on the 25% BC diet gained more body weight (C: 183 +/- 6 g; C + 5% BC: 197 +/- 7 g; C + 25% BC: 229 +/- 6 g [P < 0.05]; 5/6NX: 165 +/- 10 g; 5/6NX + 5% BC: 202 +/- 3 g; 5/6NX + 25% BC: 209 +/- 8 g [P < 0.05]) and had a higher organ weight (heart, liver, lung, kidney/remnant kidney). Bread crust-enriched diet induced proteinuria (C: 15 +/- 5 mg/24 h; C + 5% BC: 19 +/- 4; C + 25% BC: 26 +/- 3 [P < 0.05]; 5/6NX: 30 +/- 7 mg/24 h; 5/6NX + 5% BC: 47 +/- 9; 5/6NX + 25% BC: 87 +/- 19 [P < 0.01]) and a rise in urinary transforming growth factor beta(1) excretion (C: 0.4 +/- 0.1 ng/24 h; C + 5% BC: 0.6 +/- 0.1; C + 25% BC: 1.2 +/- 0.3; 5/6NX: 0.5 +/- 0.1 ng/24 h; 5/6NX + 5% BC: 0.9 +/- 0.1; 5/6NX + 25% BC: 1.6 +/- 0.2 [P < 0.01]). Plasma creatinine or creatinine clearance were not affected significantly. In conclusion, our data suggests that long-term consumption of a diet rich in MRPs may lead to damage of the kidneys.

Red pepper and its major pungent principle, capsaicin (CAP), have been shown to be effective anti‐obesity agents by reducing energy intake, enhancing energy metabolism, decreasing serum triacylglycerol content, and inhibiting adipogenesis via activation of the transient receptor potential cation channel subfamily V member 1 (TRPV1). However, the binding of CAP to the TRPV1 receptor is also responsible for its pungent sensation, strongly limiting its dietary intake. Here, the effects of a less pungent structural CAP‐analog, nonivamide, on adipogenesis and underlying mechanisms in 3T3‐L1 cells were studied. Nonivamide was found to reduce mean lipid accumulation, a marker of adipogenesis, to a similar extent as CAP, up to 10.4% (P < 0.001). Blockage of the TRPV1 receptor with the specific inhibitor trans‐tert‐butylcyclohexanol revealed that the anti‐adipogenic activity of nonivamide depends, as with CAP, on TRPV1 receptor activation. In addition, in cells treated with nonivamide during adipogenesis, protein levels of the pro‐adipogenic transcription factor peroxisome‐proliferator activated receptor γ (PPARγ) decreased. Results from miRNA microarrays and digital droplet PCR analysis demonstrated an increase in the expression of the miRNA mmu‐let‐7d‐5p, which has been associated with decreased PPARγ levels. J. Cell. Biochem. 116: 1153–1163, 2015. © 2015 The Authors. Journal of Cellular Biochemistry published by Wiley Periodicals, Inc.