Background/aims: The mechanism by which lactate, absorbed from the intestinal lumen or generated within the epithelium, crosses the basolateral membrane of the enterocyte and enters the bloodstream has not previously been characterized in detail.
Methods: L-lactate uptake into and efflux from isolated jejunal basolateral membrane vesicles was investigated at room temperature using rapid filtration techniques.
Results: Furosemide sensitive uptake of L-lactate was unaffected by cis sodium or proton gradients but could be stimulated by a trans gradient of bicarbonate and chloride. Kinetic analysis showed uptake to consist of a saturable component with a Michaelis constant (Km) of 3.2 mmol/L and a maximum velocity (Vmax) of 67 pmol.mg protein-1 x s-1 and a nonsaturable alpha-4-hydroxy-cinnamic acid insensitive component. Pyruvate, butyrate, acetate, valerate, and propionate competitively inhibited lactate uptake into the vesicles. Efflux of lactate from preloaded vesicles was furosemide sensitive and accelerated by a trans bicarbonate gradient as well as by 10 mmol/L acetate, butyrate, and pyruvate.
Conclusions: It is concluded that there is a short chain-fatty acid carrier system in the intestinal basolateral membrane, which operates as an anion exchanger.
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http://dx.doi.org/10.1016/0016-5085(94)90686-6 | DOI Listing |
Neuron
January 2025
Department of Biochemistry, Weill Cornell Medicine, New York, NY 10065, USA; Department of Psychiatry, Weill Cornell Medicine, New York, NY 10065, USA. Electronic address:
Dissecting how membrane receptors regulate neural circuits is critical for deciphering principles of neuromodulation and mechanisms of drug action. Here, we use a battery of optical approaches to determine how presynaptic metabotropic glutamate receptor 2 (mGluR2) in the basolateral amygdala (BLA) controls anxiety-related behavior in mice. Using projection-specific photopharmacological activation, we find that mGluR2-mediated presynaptic inhibition of ventromedial prefrontal cortex (vmPFC)-BLA, but not posterior insular cortex (pIC)-BLA, connections produces a long-lasting decrease in spatial avoidance.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
January 2025
Laboratoire de Physiopathologie et Régulation des Transports Ioniques, Université de Poitiers, France.
Despite the importance of ocular surface in human physiology and diseases, little is known about ion channel expression, properties and regulation in ocular epithelial cells. Furthermore, human primary epithelial cells have rarely been studied in favor of rat, mouse and especially rabbit animal models. Here, we developed primary human Meibomian gland (hMGEC) and conjunctival (hConEC) epithelial cells.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
Department of Pediatric Nephrology, Istanbul University- Cerrahpasa, Cerrahpasa Faculty of Medicine, 34098, Istanbul, Turkey.
Autosomal recessive proximal renal tubular acidosis (AR-pRTA) with ocular abnormalities is a rare syndrome caused by variants in the SLC4A4 gene, which encodes Na/HCO3 cotransporter (NBCe1). The syndrome primarily affects the kidneys, but also causes extra-renal manifestations. Pancreatic type NBCe1 is located at the basolateral membrane of the pancreatic ductal cells and together with CFTR chloride channel, it is involved in bicarbonate secretion.
View Article and Find Full Text PDFDokl Biochem Biophys
January 2025
Ryazan State Medical University, Ryazan, Russian Federation.
Introduction: Breast cancer resistance protein (BCRP) is an efflux membrane transporter that controls the pharmacokinetics of a large number of drugs. Its activity may change when taking some endo- and exogenous substances, thus making it a link in drug interactions.
Aim: The aim of the study was to develop a methodology for testing drugs for belonging to BCRP substrates and inhibitors in vitro.
Nanotoxicology
January 2025
Department of Pharmaceutical Sciences & Administration, School of Pharmacy, Westbrook College of Health Professions, University of New England, Portland, Maine, USA.
Important cell-based models of intestinal inflammation have been advanced in hopes of predicting the impact of nanoparticles on disease. We sought to determine whether a high level and extended exposure of nanoplastic might result in the added intestinal inflammation caused by nanoplastic reported in a mouse model of irritable bowel disease. The cell models consist of a Transwell©-type insert with a filter membrane upon which lies a biculture monolayer of Caco-2 and HT29-MTX-E12 made up the barrier cells (apical compartment).
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