Excessive secretion of the intestinal hormone cholecystokinin (CCK) was postulated to cause diet-related taurine depletion in cats. To test this hypothesis, plasma CCK-like immunoreactivity (CCK-LI) was measured in cats given four diets, two purified and two canned, that contained similar concentrations of protein, fat, moisture and taurine but produced variable rates of taurine depletion. Plasma CCK-LI was measured by RIA with a tyrosine-sulfate specific, C-terminal anti-serum, validated for use in cat plasma. As indicated by measurements of taurine in whole blood and urine, a purified diet containing casein maintained body taurine, whereas the same diet containing soybean protein and a commercial canned diet preserved either by freezing or cooking depleted body taurine. Preprandial and peak postprandial plasma CCK-LI in cats given the casein-containing diet were 10.6 +/- 1.4 and 27.6 +/- 4.8 pmol/L, respectively, approximately two- to tenfold greater than those reported in humans. Integrated postprandial plasma CCK-LI was less for cats given the casein diet than cats given both forms of the canned diet; it tended to be lower in cats given the casein diet than in cats given the soy protein diet. A negative linear correlation was observed between apparent nitrogen digestibilities of the diets and integrated plasma CCK-LI. The results indicated that diets that cause taurine depletion have lower protein digestibilities and cause greater endocrine secretion of CCK than diets that maintain body taurine status.
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http://dx.doi.org/10.1093/jn/125.10.2650 | DOI Listing |
Amino Acids
January 2025
Laboratory of Molecular Biology and Immunology, Department of Pharmacy, University of Patras, 26500, Rio-Patras, Greece.
Taurine, although not a coding amino acid, is the most common free amino acid in the body. Taurine has multiple and complex functions in protecting mitochondria against oxidative-nitrosative stress. In this comprehensive review paper, we introduce a novel potential role for taurine in protecting from deuterium (heavy hydrogen) toxicity.
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November 2024
Norwegian College of Fishery Science, UiT The Arctic University of Norway, Tromsø, Norway.
This study investigated how farmed blue mussels () can optimize human nutrient intake. A particular focus was on assessing nutrient preservation during steaming and freeze-drying, processes that could deplete nutrients. The study compared the content of essential amino acids and fatty acids in steamed and freeze-dried blue mussels to the nutritional needs of humans and farmed Atlantic salmon ().
View Article and Find Full Text PDFJ Hazard Mater
December 2024
Division of Toxicology, Wageningen University and Research, Stippeneng 4, 6708 WE Wageningen, the Netherlands.
Since the gut microbiota plays a crucial role in host metabolism and homeostasis, its alterations induced by xenobiotics such as pesticides, could pose a risk to host health. The pyrethroid insecticides were frequently detected in surface water (up to 13 mg/L worldwide), sediments, and agricultural products; additionally, some previous studies indicated that pyrethroid insecticides could cause disruption of gut homeostasis. Hence herein, the normally used pyrethroid lambda-cyhalothrin (LCT) was selected and studied for its effects on the intestinal microbial community and its related bile acid metabolism using mice as the model species.
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November 2024
Department of Dermatology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China.
Vitiligo is characterized by the depletion of melanocytes due to the activation of CD8 T cells. Taurine-upregulated gene 1 (TUG1), a long noncoding RNA, is involved in melanogenesis. This study aimed to explore the role and mechanism of TUG1 in vitiligo.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
August 2024
Department of Neurology, The Second Affiliated Hospital of Nanchang University, 330008 Nanchang, Jiangxi, China.
Background: Alzheimer's disease (AD) is a neurodegenerative disease that remains a serious global health issue. Ferroptosis has been recognized as a vital driver of pathological progression of AD. However, the detailed regulatory mechanisms of ferroptosis during AD progression remain unclear.
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