ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
CD36-dependent signaling mediates fatty acid-induced gut release of secretin and cholecystokinin.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 101 citations in OpenAlex.
- How lipid ingestion is sensed: the mechanisms underlying intestinal hormone secretion.Clinical science (London, England : 1979) · 2026Review
- Lipid sensing and brain hormone receptors in food intake and glucose regulation.Nature reviews. Endocrinology · 2026Review
- Postoral receptors and alimentary taste: implications for energy intake and appetite.Chemical senses · 2025Review
- Crosstalk Within the Intestinal Epithelium: Aspects of Intestinal Absorption, Homeostasis, and Immunity.Biomedicines · 2024Review
- Applications of Enteroendocrine Cells (EECs) Hormone: Applicability on Feed Intake and Nutrient Absorption in Chickens.Animals : an open access journal from MDPI · 2023Review
- Oligofructose improves small intestinal lipid-sensing mechanisms via alterations to the small intestinal microbiota.Microbiome · 2023Article
- Fatty Acid Transport and Signaling: Mechanisms and Physiological Implications.Annual review of physiology · 2023Review
- Vascular and lymphatic regulation of gastrointestinal function and disease risk.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022Review
- Maternal secretin ameliorates obesity by promoting white adipose tissue browning in offspring.EMBO reports · 2022Article
- CD36 maintains the gastric mucosa and associates with gastric disease.Communications biology · 2021Article
- Luminal Chemosensory Cells in the Small Intestine.Nutrients · 2021Review
- Macronutrient Sensing in the Oral Cavity and Gastrointestinal Tract: Alimentary Tastes.Nutrients · 2021Review
- The metabolic impact of small intestinal nutrient sensing.Nature communications · 2021Review
- Endothelial Cell Receptors in Tissue Lipid Uptake and Metabolism.Circulation research · 2021Review
- CD36 Senses Dietary Lipids and Regulates Lipids Homeostasis in the Intestine.Frontiers in physiology · 2021Review
- Advances in fatty acids nutrition in dairy cows: from gut to cells and effects on performance.Journal of animal science and biotechnology · 2020Review
- Enteroendocrine Hormone Secretion and Metabolic Control: Importance of the Region of the Gut Stimulation.Pharmaceutics · 2020Review
- Neuropod Cells: The Emerging Biology of Gut-Brain Sensory Transduction.Annual review of neuroscience · 2020Review
- Palmitic Acid Affects Intestinal Epithelial Barrier Integrity and Permeability In Vitro.Antioxidants (Basel, Switzerland) · 2020Article
- Leptin mediates postprandial increases in body temperature through hypothalamus-adrenal medulla-adipose tissue crosstalk.The Journal of clinical investigation · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Genetic variants in the fatty acid (FA) translocase FAT/CD36 associate with abnormal postprandial lipids and influence risk for the metabolic syndrome. CD36 is abundant on apical enterocyte membranes in the proximal small intestine, where it facilitates FA uptake and FA-initiated signaling. We explored whether CD36 signaling influences FA-mediated secretion of cholecystokinin (CCK) and secretin, peptides released by enteroendocrine cells (EECs) in the duodenum/jejunum, which regulate events important for fat digestion and homeostasis. CD36 was immunodetected on apical membranes of secretin- and CCK-positive EECs and colocalized with cytosolic granules. Intragastric lipid administration to CD36 mice released less secretin (-60%) and CCK (-50%) compared with wild-type mice. Likewise, diminished secretin and CCK responses to FA were observed with CD36 intestinal segments in vitro, arguing against influence of alterations in fat absorption. Signaling mechanisms underlying peptide release were examined in STC-1 cells stably expressing human CD36 or a signaling-impaired mutant (CD36K/A). FA stimulation of cells expressing CD36 (vs. vector or CD36K/A) released more secretin (3.5- to 4-fold) and CCK (2- to 3-fold), generated more cAMP (2- to 2.5-fold), and enhanced protein kinase A activation. Protein kinase A inhibition (H-89) blunted secretin (80%) but not CCK release, which was reduced (50%) by blocking of calmodulin kinase II (KN-62). Coculture of STC-1 cells with Caco-2 cells stably expressing CD36 did not alter secretin or CCK release, consistent with a minimal effect of adjacent enterocytes. In summary, CD36 is a major mediator of FA-induced release of CCK and secretin. These peptides contribute to the role of CD36 in fat absorption and to its pleiotropic metabolic effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.