The role of taurine in the treatment of congestive heart failure (CHF) in dogs without systemic deficiency is unexplored. Taurine might have beneficial cardiac effects aside from deficit replacement. We hypothesized that oral taurine supplementation administered to dogs with naturally-occurring CHF would suppress the renin-angiotensin aldosterone system (RAAS). Oral taurine was administered to 14 dogs with stable CHF. Serum biochemical variables, blood taurine concentrations, and comprehensive analysis of RAAS variables were compared before and 2 weeks after taurine supplementation added to background furosemide and pimobendan therapy for CHF. Whole blood taurine concentrations increased after supplementation (median 408 nMol/mL, range 248-608 before and median 493 nMol/mL, range 396-690 after; P = .006). Aldosterone to angiotensin II ratio (AA2) was significantly decreased after taurine supplementation (median 1.00, range 0.03-7.05 before and median 0.65, range 0.01-3.63 after; P = .009), but no other RAAS components significantly differed between timepoints. A subset of dogs showed marked decreases in RAAS metabolites after supplementation and these dogs were more likely to have been recently hospitalized for CHF treatment than dogs that did not show marked decreases in classical RAAS metabolites. Overall, taurine only lowered AA2 in this group of dogs, however, response heterogeneity was noted, with some dogs showing RAAS suppression.
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http://dx.doi.org/10.1038/s41598-023-37978-1 | DOI Listing |
Nutrients
December 2024
School of Exercise and Health, Shanghai University of Sport, Shanghai 200438, China.
Background: Taurine has been demonstrated to regulate and improve metabolic health. However, physiological and pathological differences among individuals with overweight or obesity may result in varied responses to taurine supplementation. This study aims to estimate the effects of long-term taurine supplementation on blood lipids, glycemia, and insulin sensitivity in adults with overweight or obesity through a systematic review and meta-analysis.
View Article and Find Full Text PDFJ Adv Res
January 2025
Department of Rehabilitation Medicine, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361003, China. Electronic address:
Objective: The aim of this study was to investigate the potential molecular mechanisms by which taurine protects against cartilage degeneration.
Methods: The anterior cruciate ligament transection (ACLT) surgery was used to construct an animal model of osteoarthritis (OA). Metabolomics was used to identify characteristic metabolites in osteoarthritic chondrocytes.
Life (Basel)
November 2024
Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Amino acids are basic building blocks of structural proteins and enzymes. They also act as signaling molecules and as fuel. They are characterized as essential if sufficient quantities must be supplied exogenously or as non-essential if they can be endogenously synthesized.
View Article and Find Full Text PDFBiomedicines
November 2024
Department of Nephrology, The First Affiliated Hospital of Xi'an Medical University, Xi'an 710077, China.
Objects: Taurine exhibits protective effects in the context of cardiovascular pathophysiology. A range of evidence suggests that hypertension activates inflammatory responses and oxidative stress in the paraventricular nucleus (PVN), elevating the arterial tone and sympathetic activity, while it induces gut-brain axis dysfunction in the context of hypertension. However, the mechanism underlying taurine's anti-hypertensive effects via the gut-brain axis remains unclear.
View Article and Find Full Text PDFBiomolecules
November 2024
Departments of Pediatrics, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 06229, Republic of Korea.
Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a complex mitochondrial disorder characterized by a wide range of systemic manifestations. Key clinical features include recurrent stroke-like episodes, seizures, lactic acidosis, muscle weakness, exercise intolerance, sensorineural hearing loss, diabetes, and progressive neurological decline. MELAS is most commonly associated with mutations in mitochondrial DNA, particularly the m.
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