Journal articles on the topic 'Carnosinol'
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1
O’Toole, Timothy E., Xiaohong Li, Daniel W. Riggs, David J. Hoetker, Shahid P. Baba, and Aruni Bhatnagar. "Urinary Levels of the Acrolein Conjugates of Carnosine Are Associated with Cardiovascular Disease Risk." International Journal of Molecular Sciences 22, no. 3 (January 30, 2021): 1383. http://dx.doi.org/10.3390/ijms22031383.
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Carnosine is a naturally occurring dipeptide (β-alanine-L-histidine) which supports physiological homeostasis by buffering intracellular pH, chelating metals, and conjugating with and neutralizing toxic aldehydes such as acrolein. However, it is not clear if carnosine can support cardiovascular function or modify cardiovascular disease (CVD) risk. To examine this, we measured urinary levels of nonconjugated carnosine and its acrolein conjugates (carnosine-propanal and carnosine-propanol) in participants of the Louisville Healthy Heart Study and examined associations with indices of CVD risk. We found that nonconjugated carnosine was significantly associated with hypertension (p = 0.011), heart failure (p = 0.015), those categorized with high CVD risk (p < 0.001), body mass index (BMI; p = 0.007), high sensitivity C-reactive protein (hsCRP; p = 0.026), high-density lipoprotein (HDL; p = 0.007) and certain medication uses. Levels of carnosine-propanal and carnosine-propanol demonstrated significant associations with BMI, blood glucose, HDL and diagnosis of diabetes. Carnosine-propanal was also associated with heart failure (p = 0.045) and hyperlipidemia (p = 0.002), but no associations with myocardial infarction or stroke were identified. We found that the positive associations of carnosine conjugates with diabetes and HDL remain statistically significant (p < 0.05) in an adjusted, linear regression model. These findings suggest that urinary levels of nonconjugated carnosine, carnosine-propanal and carnosine-propanol may be informative biomarkers for the assessment of CVD risk—and particularly reflective of skeletal muscle injury and carnosine depletion in diabetes.
2
Jukić, Ivana, Nikolina Kolobarić, Ana Stupin, Anita Matić, Nataša Kozina, Zrinka Mihaljević, Martina Mihalj, et al. "Carnosine, Small but Mighty—Prospect of Use as Functional Ingredient for Functional Food Formulation." Antioxidants 10, no. 7 (June 28, 2021): 1037. http://dx.doi.org/10.3390/antiox10071037.
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Carnosine is a dipeptide synthesized in the body from β-alanine and L-histidine. It is found in high concentrations in the brain, muscle, and gastrointestinal tissues of humans and is present in all vertebrates. Carnosine has a number of beneficial antioxidant properties. For example, carnosine scavenges reactive oxygen species (ROS) as well as alpha-beta unsaturated aldehydes created by peroxidation of fatty acid cell membranes during oxidative stress. Carnosine can oppose glycation, and it can chelate divalent metal ions. Carnosine alleviates diabetic nephropathy by protecting podocyte and mesangial cells, and can slow down aging. Its component, the amino acid beta-alanine, is particularly interesting as a dietary supplement for athletes because it increases muscle carnosine, and improves effectiveness of exercise and stimulation and contraction in muscles. Carnosine is widely used among athletes in the form of supplements, but rarely in the population of cardiovascular or diabetic patients. Much less is known, if any, about its potential use in enriched food. In the present review, we aimed to provide recent knowledge on carnosine properties and distribution, its metabolism (synthesis and degradation), and analytical methods for carnosine determination, since one of the difficulties is the measurement of carnosine concentration in human samples. Furthermore, the potential mechanisms of carnosine’s biological effects in musculature, metabolism and on immunomodulation are discussed. Finally, this review provides a section on carnosine supplementation in the form of functional food and potential health benefits and up to the present, neglected clinical use of carnosine.
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Tanida, Mamoru, Akira Niijima, Yutaka Fukuda, Hajime Sawai, Nobuo Tsuruoka, Jiao Shen, Shigeru Yamada, Yoshinobu Kiso, and Katsuya Nagai. "Dose-dependent effects of l-carnosine on the renal sympathetic nerve and blood pressure in urethane-anesthetized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 2 (February 2005): R447—R455. http://dx.doi.org/10.1152/ajpregu.00275.2004.
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The physiological function of l-carnosine (β-alanyl-l-histidine) synthesized in mammalian muscles has been unclear. Previously, we observed that intravenous (IV) injection of l-carnosine suppressed renal sympathetic nerve activity (RSNA) in urethane-anesthetized rats, and l-carnosine administered via the diet inhibited the elevation of blood pressure (BP) in deoxycorticosterone acetate salt hypertensive rats. To identify the mechanism, we examined effects of IV or intralateral cerebral ventricular (LCV) injection of various doses of l-carnosine on RSNA and BP in urethane-anesthetized rats. Lower doses (1 μg IV; 0.01 μg LCV) of l-carnosine significantly suppressed RSNA and BP, whereas higher doses (100 μg IV; 10 μg LCV) elevated RSNA and BP. Furthermore, we examined effects of antagonists of histaminergic (H1 and H3) receptors on l-carnosine-induced effects. When peripherally and centrally given, thioperamide, an H3 receptor antagonist, blocked RSNA and BP decreases induced by the lower doses of peripheral l-carnosine, whereas diphenhydramine, an H1 receptor antagonist, inhibited increases induced by the higher doses of peripheral l-carnosine. Moreover, bilateral lesions of the hypothalamic suprachiasmatic nucleus eliminated both effects on RSNA and BP induced by the lower (1 μg) and higher (100 μg) doses of peripheral l-carnosine. These findings suggest that low-dose l-carnosine suppresses and high-dose l-carnosine stimulates RSNA and BP, that the suprachiasmatic nucleus and histaminergic nerve are involved in the activities, and that l-carnosine acts in the brain and possibly other organs.
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Weigand, Tim, Benjamin Singler, Thomas Fleming, Peter Nawroth, Karel D. Klika, Christian Thiel, Hans Baelde, et al. "Carnosine Catalyzes the Formation of the Oligo/Polymeric Products of Methylglyoxal." Cellular Physiology and Biochemistry 46, no. 2 (2018): 713–26. http://dx.doi.org/10.1159/000488727.
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Background/Aims: Reactive dicarbonyl compounds, such as methylglyoxal (MG), contribute to diabetic complications. MG-scavenging capacities of carnosine and anserine, which have been shown to mitigate diabetic nephropathy, were evaluated in vitro and in vivo. Methods: MG-induced cell toxicity was characterized by MTT and MG-H1-formation, scavenging abilities by Western Blot and NMR spectroscopies, cellular carnosine transport by qPCR and microplate luminescence and carnosine concentration by HPLC. Results: In vitro, carnosine and anserine dose-dependently reduced N-carboxyethyl lysine (CEL) and advanced glycation end products (AGEs) formation. NMR studies revealed the formation of oligo/polymeric products of MG catalyzed by carnosine or anserine. MG toxicity (0.3-1 mM) was dose-dependent for podocytes, tubular and mesangial cells whereas low MG levels (0.2 mM) resulted in increased cell viability in podocytes (143±13%, p<0.001) and tubular cells (129±3%, p<0.001). Incubation with carnosine/anserine did not reduce MG-induced toxicity, independent of incubation times and across large ranges of MG to carnosine/anserine ratios. Cellular carnosine uptake was low (<0.1% in 20 hours) and cellular carnosine concentrations remained unaffected. The putative carnosine transporter PHT1 along with the taurine transporter (TauT) was expressed in all cell types while PEPT1, PEPT2 and PHT2, also belonging to the proton-coupled oligopeptide transporter (POT) family, were only expressed in tubular cells. Conclusion: While carnosine and anserine catalyze the formation of MG oligo/polymers, the molar ratios required for protection from MG-induced cellular toxicity are not achievable in renal cells. The effect of carnosine in vivo, to mitigate diabetic nephropathy may therefore be independent upon its ability to scavenge MG and/or carnosine is mainly acting extracellularly.
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Hwang, Byungdoo, Jun-Hui Song, Sung Lyea Park, Jee Taek Kim, Wun-Jae Kim, and Sung-Kwon Moon. "Carnosine Impedes PDGF-Stimulated Proliferation and Migration of Vascular Smooth Muscle Cells In Vitro and Sprout Outgrowth Ex Vivo." Nutrients 12, no. 9 (September 3, 2020): 2697. http://dx.doi.org/10.3390/nu12092697.
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Carnosine, a naturally producing dipeptide, exhibits various beneficial effects. However, the possible role of carnosine in vascular disorders associated with pathological conditions, including proliferation and migration of vascular smooth muscle cells (VSMCs), largely remains unrevealed. Here, we investigated the regulatory role and mechanism of carnosine in platelet-derived growth factor (PDGF)-induced VSMCs. Carnosine inhibited the proliferation of PDGF-induced VSMCs without any cytotoxic effects. Carnosine treatment also induced G1-phase cell cycle arrest by causing a p21WAF1-mediated reduction in the expression of both cyclin-dependent kinases (CDKs) and cyclins in PDGF-treated VSMCs. Carnosine treatment suppressed c-Jun N-terminal kinase (JNK) phosphorylation in PDGF-stimulated signaling. Additionally, carnosine significantly prevented the migration of VSMCs exposed to PDGF. Carnosine abolished matrix metalloproteinase (MMP)-9 activity via reduced transcriptional binding activity of NF-κB, Sp-1, and AP-1 motifs in PDGF-treated VSMCs. Moreover, using aortic assay ex vivo, it was observed that carnosine addition attenuated PDGF-stimulated sprout outgrowth of VSMCs. Taken together, these results demonstrated that carnosine impeded the proliferation and migration of PDGF-stimulated VSMCs by regulating cell cycle machinery, JNK signaling, and transcription factor-mediated MMP-9 activity as well as prevented ex vivo sprout outgrowth of blood vessels. Thus, carnosine may be a potential candidate for preventing vascular proliferative disease.
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Everaert, Inge, Youri Taes, Emile De Heer, Hans Baelde, Ana Zutinic, Benito Yard, Sibylle Sauerhöfer, et al. "Low plasma carnosinase activity promotes carnosinemia after carnosine ingestion in humans." American Journal of Physiology-Renal Physiology 302, no. 12 (June 15, 2012): F1537—F1544. http://dx.doi.org/10.1152/ajprenal.00084.2012.
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A polymorphism in the carnosine dipeptidase-1 gene ( CNDP1), resulting in decreased plasma carnosinase activity, is associated with a reduced risk for diabetic nephropathy. Because carnosine, a natural scavenger/suppressor of ROS, advanced glycation end products, and reactive aldehydes, is readily degraded in blood by the highly active carnosinase enzyme, it has been postulated that low serum carnosinase activity might be advantageous to reduce diabetic complications. The aim of this study was to examine whether low carnosinase activity promotes circulating carnosine levels after carnosine supplementation in humans. Blood and urine were sampled in 25 healthy subjects after acute supplementation with 60 mg/kg body wt carnosine. Precooled EDTA-containing tubes were used for blood withdrawal, and plasma samples were immediately deproteinized and analyzed for carnosine and β-alanine by HPLC. CNDP1 genotype, baseline plasma carnosinase activity, and protein content were assessed. Upon carnosine ingestion, 8 of the 25 subjects (responders) displayed a measurable increase in plasma carnosine up to 1 h after supplementation. Subjects with no measurable increment in plasma carnosine (nonresponders) had ∼2-fold higher plasma carnosinase protein content and ∼1.5-fold higher activity compared with responders. Urinary carnosine recovery was 2.6-fold higher in responders versus nonresponders and was negatively dependent on both the activity and protein content of the plasma carnosinase enzyme. In conclusion, low plasma carnosinase activity promotes the presence of circulating carnosine upon an oral challenge. These data may further clarify the link among CNDP1 genotype, carnosinase, and diabetic nephropathy.
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Tanaka, Ken-Ichiro, and Masahiro Kawahara. "Carnosine and Lung Disease." Current Medicinal Chemistry 27, no. 11 (April 23, 2020): 1714–25. http://dx.doi.org/10.2174/0929867326666190712140545.
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Carnosine (β-alanyl-L-histidine) is a small dipeptide with numerous activities, including antioxidant effects, metal ion chelation, proton buffering capacity, and inhibitory effects on protein carbonylation and glycation. Carnosine has been mostly studied in organs where it is abundant, including skeletal muscle, cerebral cortex, kidney, spleen, and plasma. Recently, the effect of supplementation with carnosine has been studied in organs with low levels of carnosine, such as the lung, in animal models of influenza virus or lipopolysaccharide-induced acute lung injury and pulmonary fibrosis. Among the known protective effects of carnosine, its antioxidant effect has attracted increasing attention for potential use in treating lung disease. In this review, we describe the in vitro and in vivo biological and physiological actions of carnosine. We also report our recent study and discuss the roles of carnosine or its related compounds in organs where carnosine is present in only small amounts (especially the lung) and its protective mechanisms.
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Liu, Yali, Dan Su, Ling Zhang, Shaofeng Wei, Kuangyi Liu, Mi Peng, Hanyun Li, and Yonggui Song. "Endogenous L-Carnosine Level in Diabetes Rat Cardiac Muscle." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/6230825.
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A novel method for quantitation of cardiac muscle carnosine levels using HPLC-UV is described. In this simple and reliable method, carnosine from the rat cardiac muscle and the internal standard, thymopentin, were extracted by protein precipitation with acetonitrile. The method was linear up to 60.96 μg·mL−1for L-carnosine. The calibration curve was linear in concentration ranges from 0.5 to 60.96 μg·mL−1. The relative standard deviations obtained for intra- and interday precision were lower than 12% and the recoveries were higher than 90% for both carnosine and internal standard. We successfully applied this method to the analysis of endogenous carnosine in cardiac muscle of the diabetes rats and healthy control rats. The concentration of carnosine was significantly lower in the diabetes rats group, compared to that in the healthy control rats. These results support the usefulness of this method as a means of quantitating carnosine and illustrate the important role of L-carnosine in cardiac muscle.
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Perim, Pedro Henrique, André Barroso Heibel, Guilherme Giannini Artioli, Bruno Gualano, and Bryan Saunders. "Low efficiency of β-alanine supplementation to increase muscle carnosine." Revista Brasileira de Educação Física e Esporte 34, no. 3 (November 20, 2020): 357–64. http://dx.doi.org/10.11606/1807-5509202000030357.
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Supplementation with β-alanine (BA) increases muscle carnosine content, although the amount of BA used for muscle carnosine loading has been suggested to be low. However, methodological issues may have underestimated the amount of BA used. The aim of this study was to determine the estimated amount of BA converted to muscle carnosine, using a retrospective analysis from a 4-week randomized controlled trial investigating the effects of BA supplementation on muscle carnosine content of the m. vastus lateralis. Twenty-five males (age 27±5 years, height 1.74±0.09 m, body mass 77.4±11.5 kg) were supplemented with 6.4 g·day-1 of BA (N=17) or placebo (PL; N=8) for 28 days. Pre- and postsupplementation participants provided a muscle biopsy subsequently analysed for carnosine content using HPLC. Data were analysed using mixed-models and Pearson’s correlations. Muscle carnosine content increased by +11.0±6.7 mmol·kg-1dm (P<0.0001) in BA, with no change in PL (P=0.99). The estimated amount of BA converted to muscle carnosine was 2.1±1.2% (Range: 0.5 to 4.5%) of the total dose ingested. Pearson’s correlations showed that pre-supplementation carnosine was correlated to post-supplementation carnosine in the BA group (r=0.65, r2=0.38, P=0.009), but not the absolute change in carnosine (r=-0.28, r2=0.08, P=0.28) or the amount of BA used (r=-0.31, r2=0.10, P=0.22). The estimated amount of ingested BA used for carnosine synthesis was extremely low following 4 weeks of BA supplementation at 6.4 g·day-1. Data suggest that very little of the BA ingested is used for muscle carnosine synthesis and highlights the potential for further work to optimise BA supplementation in humans.
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Perim, Pedro Henrique, André Barroso Heibel, Guilherme Giannini Artioli, Bruno Gualano, and Bryan Saunders. "Low efficiency of β-alanine supplementation to increase muscle carnosine." Revista Brasileira de Educação Física e Esporte 34, no. 3 (September 30, 2020): 357–64. http://dx.doi.org/10.11606/issn.1981-4690.v34i3p357-364.
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Supplementation with β-alanine (BA) increases muscle carnosine content, although the amount of BA used for muscle carnosine loading has been suggested to be low. However, methodological issues may have underestimated the amount of BA used. The aim of this study was to determine the estimated amount of BA converted to muscle carnosine, using a retrospective analysis from a 4-week randomized controlled trial investigating the effects of BA supplementation on muscle carnosine content of the m. vastus lateralis. Twenty-five males (age 27±5 years, height 1.74±0.09 m, body mass 77.4±11.5 kg) were supplemented with 6.4 g·day-1 of BA (N=17) or placebo (PL; N=8) for 28 days. Pre- and postsupplementation participants provided a muscle biopsy subsequently analysed for carnosine content using HPLC. Data were analysed using mixed-models and Pearson’s correlations. Muscle carnosine content increased by +11.0±6.7 mmol·kg-1dm (P<0.0001) in BA, with no change in PL (P=0.99). The estimated amount of BA converted to muscle carnosine was 2.1±1.2% (Range: 0.5 to 4.5%) of the total dose ingested. Pearson’s correlations showed that pre-supplementation carnosine was correlated to post-supplementation carnosine in the BA group (r=0.65, r2=0.38, P=0.009), but not the absolute change in carnosine (r=-0.28, r2=0.08, P=0.28) or the amount of BA used (r=-0.31, r2=0.10, P=0.22). The estimated amount of ingested BA used for carnosine synthesis was extremely low following 4 weeks of BA supplementation at 6.4 g·day-1. Data suggest that very little of the BA ingested is used for muscle carnosine synthesis and highlights the potential for further work to optimise BA supplementation in humans.
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Moustafa, Eslam M., Ida Ritacco, Emilia Sicilia, Nino Russo, and Tamer Shoeib. "Collision-induced dissociation products of the protonated dipeptide carnosine: structural elucidation, fragmentation pathways and potential energy surface analysis." Physical Chemistry Chemical Physics 17, no. 19 (2015): 12673–82. http://dx.doi.org/10.1039/c5cp00958h.
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CID experiments on protonated carnosine, [carnosine + H]+, employing several collision energies were shown to yield eleven different fragment ions, with the production of [carnosine–H2O + H]+ and [carnosine–NH3 + H]+ being the lowest energy processes.
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Hasanein, Parisa, and Zhila Felegari. "Chelating effects of carnosine in ameliorating nickel-induced nephrotoxicity in rats." Canadian Journal of Physiology and Pharmacology 95, no. 12 (December 2017): 1426–32. http://dx.doi.org/10.1139/cjpp-2016-0647.
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The kidney is one of the main organs affected by nickel toxicity. We investigated the protective effects of carnosine on nickel-induced oxidative stress in kidney of rats. Animals received NiSO4 (20 mg·kg−1·day−1 intragastrically) and (or) carnosine (10 mg·kg−1·day−1 intragastrically) for 21 days and then were evaluated for biochemical, molecular, and histopathological alterations. Nickel caused an increase in renal levels of malondialdehyde and a decrease in reduced glutathione, catalase, and superoxide dismutase levels and total antioxidant capacity. Carnosine prevented the prooxidant and antioxidant imbalance induced by nickel. Nickel-treated rats showed an increase in serum creatinine, urea, and uric acid with a concomitant decrease in albumin. Nickel markedly accumulated in kidney of exposed rats, but its concentration was effectively reduced by carnosine treatment. Carnosine corrected the biochemical abnormalities and the elevated renal TNF-α and IL-6 levels in the nickel-treated group. It also attenuated nickel-induced abnormalities in renal architecture. Although carnosine showed antioxidant and anti-inflammatory effects in renal tissue of nickel-exposed rats, we cannot clearly attribute the protective effect of carnosine to these effects. Instead, the beneficial effect of carnosine observed in the current study may be due to chelation between nickel and carnosine. Thus, carnosine may represent a therapeutic option to protect against nickel-induced nephrotoxicity that deserves further consideration and examination.
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Morsy, Mohamed A., Mahmoud Kandeel, Ahmed R. N. Ibrahim, Seham A. Abdel-Gaber, Shery Jacob, Katharigatta N. Venugopala, Pottathil Shinu, and Mahmoud El-Daly. "Carnosine Potentiates Doxorubicin-Induced Cytotoxicity in Resistant NCI/ADR-RES Cells by Inhibiting P-Glycoprotein—In Silico and In Vitro Evidence." Molecules 27, no. 21 (October 30, 2022): 7383. http://dx.doi.org/10.3390/molecules27217383.
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The activity of the P-glycoprotein (P-gp) transporter encoded by the ABCB1 gene confers resistance to anticancer drugs and contributes to cancer-related mortality and morbidity. Recent studies revealed the cytotoxic effects of the endogenous dipeptide carnosine. The current study aimed to investigate the role of carnosine as a potential inhibitor of P-gp activity. We used molecular docking and molecular dynamic simulations to study the possible binding and stability of carnosine-P-gp interactions compared with verapamil. In vitro assays using doxorubicin-resistant NCI/ADR-RES cells were established to test the effects of carnosine (10–300 µM) on P-gp activity by the rhodamine-123 efflux assay and its effect on cell viability and doxorubicin-induced cytotoxicity. Verapamil (10 µM) was used as a positive control. The results showed that carnosine binding depends mainly on hydrogen bonding with GLU875, GLN946, and ALA871, with a higher average Hbond than verapamil. Carnosine showed significant but weaker than verapamil-induced rhodamine-123 accumulation. Carnosine and verapamil similarly inhibited cell viability. However, verapamil showed a more significant potentiating effect on doxorubicin-induced cytotoxicity than a weaker effect of carnosine at 300 µM. These results suggest that carnosine inhibits P-gp activity and potentiates doxorubicin-induced cytotoxicity at higher concentrations. Carnosine might be a helpful lead compound in the fight against multidrug-resistant cancers.
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Baye, Estifanos, Jozef Ukropec, Maximilian de Courten, Aya Mousa, Timea Kurdiova, Josphin Johnson, Kirsty Wilson, et al. "Carnosine Supplementation Improves Serum Resistin Concentrations in Overweight or Obese Otherwise Healthy Adults: A Pilot Randomized Trial." Nutrients 10, no. 9 (September 7, 2018): 1258. http://dx.doi.org/10.3390/nu10091258.
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Adipokines play an important role in the regulation of glucose metabolism. We have previously shown that carnosine supplementation in overweight or obese non-diabetic individuals improves glucose metabolism but does not change adiponectin concentrations. However, its effect on other adipokines has not been investigated. Herein we further determined the effect of carnosine supplementation on serum adipsin, resistin and leptin. Twenty-two overweight or obese otherwise healthy adults were randomly assigned to receive either 2 g of carnosine (n = 13) or identically looking placebo (n = 9) for 12 weeks. Serum adipsin, leptin and resistin were analyzed using a bead-based multiplex assay. Carnosine supplementation decreased serum resistin concentrations compared to placebo (mean change from baseline: −35 ± 83 carnosine vs. 35 ± 55 ng/mL placebo, p = 0.04). There was a trend for a reduction in serum leptin concentrations after carnosine supplementation (−76 ± 165 ng/mL carnosine vs. 20 ± 28 ng/mL placebo, p = 0.06). The changes in leptin and resistin concentrations were inversely related to the change in concentration for urinary carnosine (r = −0.72, p = 0.0002; r = −0.67, p = 0.0009, respectively), carnosine-propanal (r = −0.56, p = 0.005; r = −0.63, p = 0.001, respectively) and carnosine-propanol (r = −0.61, p = 0.002; r = −0.60, p = 0.002, respectively). There were no differences between groups in change in adipsin concentrations. Our findings show carnosine supplementation may normalize some, but not all, of the serum adipokine concentrations involved in glucose metabolism, in overweight and obese individuals. Further clinical trials with larger samples are needed to confirm these results.
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Bex, T., W. Chung, A. Baguet, S. Stegen, J. Stautemas, E. Achten, and W. Derave. "Muscle carnosine loading by beta-alanine supplementation is more pronounced in trained vs. untrained muscles." Journal of Applied Physiology 116, no. 2 (January 15, 2014): 204–9. http://dx.doi.org/10.1152/japplphysiol.01033.2013.
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Carnosine occurs in high concentrations in human skeletal muscle and assists working capacity during high-intensity exercise. Chronic beta-alanine (BA) supplementation has consistently been shown to augment muscle carnosine concentration, but the effect of training on the carnosine loading efficiency is poorly understood. The aim of the present study was to compare muscle carnosine loading between trained and untrained arm and leg muscles. In a first study ( n = 17), reliability of carnosine quantification by proton magnetic resonance spectroscopy (1H-MRS) was evaluated in deltoid and triceps brachii muscles. In a second study, participants ( n = 35; 10 nonathletes, 10 cyclists, 10 swimmers, and 5 kayakers) were supplemented with 6.4 g/day of slow-release BA for 23 days. Carnosine content was evaluated in soleus, gastrocnemius medialis, and deltoid muscles by 1H-MRS. All the results are reported as arbitrary units. In the nonathletes, BA supplementation increased carnosine content by 47% in the arm and 33% in the leg muscles (not significant). In kayakers, the increase was more pronounced in arm (deltoid) vs. leg (soleus + gastrocnemius) muscles (0.089 vs. 0.049), whereas the reverse pattern was observed in cyclists (0.065 vs. 0.084). Swimmers had significantly higher increase in carnosine in both deltoid (0.107 vs. 0.065) and gastrocnemius muscle (0.082 vs. 0.051) compared with nonathletes. We showed that 1) carnosine content can be reliably measured by 1H-MRS in deltoid muscle, 2) carnosine loading is equally effective in arm vs. leg muscles of nonathletes, and 3) carnosine loading is more pronounced in trained vs. untrained muscles.
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Baguet, Audrey, Jan Bourgois, Lander Vanhee, Eric Achten, and Wim Derave. "Important role of muscle carnosine in rowing performance." Journal of Applied Physiology 109, no. 4 (October 2010): 1096–101. http://dx.doi.org/10.1152/japplphysiol.00141.2010.
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The role of the presence of carnosine (β-alanyl-l-histidine) in millimolar concentrations in human skeletal muscle is poorly understood. Chronic oral β-alanine supplementation is shown to elevate muscle carnosine content and improve anaerobic exercise performance during some laboratory tests, mainly in the untrained. It remains to be determined whether carnosine loading can improve single competition-like events in elite athletes. The aims of the present study were to investigate if performance is related to the muscle carnosine content and if β-alanine supplementation improves performance in highly trained rowers. Eighteen Belgian elite rowers were supplemented for 7 wk with either placebo or β-alanine (5 g/day). Before and following supplementation, muscle carnosine content in soleus and gastrocnemius medialis was measured by proton magnetic resonance spectroscopy (1H-MRS) and the performance was evaluated in a 2,000-m ergometer test. At baseline, there was a strong positive correlation between 100-, 500-, 2,000-, and 6,000-m speed and muscle carnosine content. After β-alanine supplementation, the carnosine content increased by 45.3% in soleus and 28.2% in gastrocnemius. Following supplementation, the β-alanine group was 4.3 s faster than the placebo group, whereas before supplementation they were 0.3 s slower ( P = 0.07). Muscle carnosine elevation was positively correlated to 2,000-m performance enhancement ( P = 0.042 and r = 0.498). It can be concluded that the positive correlation between baseline muscle carnosine levels and rowing performance and the positive correlation between changes in muscle carnosine and performance improvement suggest that muscle carnosine is a new determinant of rowing performance.
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Jain, Saurabh, Eun-Sun Kim, Donghyun Kim, David Burrows, Milena De Felice, Minyeong Kim, Seung-Hoon Baek, et al. "Comparative Cerebroprotective Potential of d- and l-Carnosine Following Ischemic Stroke in Mice." International Journal of Molecular Sciences 21, no. 9 (April 26, 2020): 3053. http://dx.doi.org/10.3390/ijms21093053.
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l-carnosine is an attractive therapeutic agent for acute ischemic stroke based on its robust preclinical cerebroprotective properties and wide therapeutic time window. However, large doses are needed for efficacy because carnosine is rapidly degraded in serum by carnosinases. The need for large doses could be particularly problematic when translating to human studies, as humans have much higher levels of serum carnosinases. We hypothesized that d-carnosine, which is not a substrate for carnosinases, may have a better pharmacological profile and may be more efficacious at lower doses than l-carnosine. To test our hypothesis, we explored the comparative pharmacokinetics and neuroprotective properties of d- and L-carnosine in acute ischaemic stroke in mice. We initially investigated the pharmacokinetics of d- and L-carnosine in serum and brain after intravenous (IV) injection in mice. We then investigated the comparative efficacy of d- and l-carnosine in a mouse model of transient focal cerebral ischemia followed by in vitro testing against excitotoxicity and free radical generation using primary neuronal cultures. The pharmacokinetics of d- and l-carnosine were similar in serum and brain after IV injection in mice. Both d- and l-carnosine exhibited similar efficacy against mouse focal cerebral ischemia. In vitro studies in neurons showed protection against excitotoxicity and the accumulation of free radicals. d- and l-carnosine exhibit similar pharmacokinetics and have similar efficacy against experimental stroke in mice. Since humans have far higher levels of carnosinases, d-carnosine may have more favorable pharmacokinetics in future human studies.
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Hoetker, David, Weiliang Chung, Deqing Zhang, Jingjing Zhao, Virginia K. Schmidtke, Daniel W. Riggs, Wim Derave, Aruni Bhatnagar, David Bishop, and Shahid P. Baba. "Exercise alters and β-alanine combined with exercise augments histidyl dipeptide levels and scavenges lipid peroxidation products in human skeletal muscle." Journal of Applied Physiology 125, no. 6 (December 1, 2018): 1767–78. http://dx.doi.org/10.1152/japplphysiol.00007.2018.
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Carnosine and anserine are dipeptides synthesized from histidine and β-alanine by carnosine synthase (ATPGD1). These dipeptides, present in high concentration in the skeletal muscle, form conjugates with lipid peroxidation products such as 4-hydroxy trans-2-nonenal (HNE). Although skeletal muscle levels of these dipeptides could be elevated by feeding β-alanine, it is unclear how these dipeptides and their conjugates are affected by exercise training with or without β-alanine supplementation. We recruited 20 physically active men, who were allocated to either β-alanine or placebo-feeding group matched for peak oxygen consumption, lactate threshold, and maximal power. Participants completed 2 wk of a conditioning phase followed by 1 wk of exercise training, a single session of high-intensity interval training (HIIT), followed by 6 wk of HIIT. Analysis of muscle biopsies showed that the levels of carnosine and ATPGD1 expression were increased after CPET and decreased following a single session and 6 wk of HIIT. Expression of ATPGD1 and levels of carnosine were increased upon β-alanine-feeding after CPET, whereas ATPGD1 expression decreased following a single session of HIIT. The expression of fiber type markers myosin heavy chain I and IIa remained unchanged after CPET. Levels of carnosine, anserine, carnosine-HNE, carnosine-propanal, and carnosine-propanol were further increased after 9 wk of β-alanine supplementation and exercise training but remained unchanged in the placebo-fed group. These results suggest that carnosine levels and ATPGD1 expression fluctuates with different phases of training. Enhancing carnosine levels by β-alanine feeding could facilitate the detoxification of lipid peroxidation products in the human skeletal muscle.NEW & NOTEWORTHY Carnosine synthase expression and carnosine levels are altered in the human skeletal muscle during different phases of training. During high-intensity interval training, β-alanine feeding promotes detoxification of lipid peroxidation products and increases anserine levels in the skeletal muscle.
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Cianciaruso, B., S. Fukuda, M. R. Jones, and J. D. Kopple. "Net release or uptake of histidine and carnosine in kidney of dogs." American Journal of Physiology-Endocrinology and Metabolism 248, no. 1 (January 1, 1985): E51—E57. http://dx.doi.org/10.1152/ajpendo.1985.248.1.e51.
Full textAbstract:
Previous studies are equivocal as to whether the dog kidney produces histidine. Because one possible source of renal histidine is carnosine (beta-alanyl-L-histidine), we investigated net renal production (release) or utilization (uptake) (Qmet) of histidine and carnosine in 19 female dogs after they were fed histidine-free (9 dogs) or histidine-containing diets (10 dogs). Diets were fed in short-(2-11 days) or long-term (52-57 days) studies. Dogs were infused with half-normal saline for 120 min followed by an infusion of half-normal saline containing carnosine, 50 mumol/min. Renal Qmet histidine, calculated from either plasma or whole blood values, was positive during infusion of half-normal saline. During carnosine infusion, Qmet histidine increased markedly, and there was net renal uptake of carnosine. The Qmet histidine and carnosine were not different in the dogs fed histidine-free vs. histidine-containing diets. Thus there is net renal release of histidine in female dogs that increases when carnosine is administered. Qmet histidine or carnosine do not change adaptively when dogs are fed histidine-free diets.
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Dieter, B. P., C. J. Macias, T. J. Sharpe, B. Roberts, M. Wille, A. Young, C. Reisenauer, B. Cantrell, and W. M. Bayly. "Transdermal delivery of carnosine into equine skeletal muscle." Comparative Exercise Physiology 17, no. 5 (September 14, 2021): 429–34. http://dx.doi.org/10.3920/cep200077.
Full textAbstract:
The dipeptide carnosine consists of β-alanine and L-histidine. It plays a major role in skeletal muscle metabolism, especially as an intracellular buffer and antioxidant. Increasing intramuscular carnosine has been shown to improve recovery from exercise and increase anaerobic threshold and time-to-exhaustion. Dietary supplementation with carnosine does not effectively increase intramuscular carnosine due to the presence of carnosinase in the blood. However, an effective transdermal delivery process could expediently increase intramuscular concentrations of carnosine. This study’s objective was to examine the efficacy of a transdermal system for delivering carnosine into the skeletal muscle of horses, using a randomised, placebo controlled, crossover study. Carnosine plus a proprietary transdermal delivery agent or the agent alone (placebo) were applied to the middle gluteal muscles of 10 Thoroughbred racehorses, and muscle biopsies were taken before and 30, 60, and 120 min after application. Muscle carnosine concentration was measured using an enzyme-linked immunosorbent assay. A two-way repeated measures analysis of variance was used to test for the main effects of time and treatment (placebo or carnosine) as well as an interaction between time and treatment. Independent F-tests examined the change in intramuscular carnosine levels from baseline to each time point (30, 60, and 120 min). There was a significant main effect of treatment (P=0.004), no significant main effect for time (P=0.18), and a non-significant interaction of treatment with time (P=0.08). Mean intramuscular carnosine concentrations increased from baseline to 120 min. Compared to concentrations following placebo application, carnosine was greater by ~35% at 30 min (P=0.002) and ~46% after 60 min (P=0.044), but not at 120 min (P=0.20). The results indicated that intramuscular carnosine can be increased using a transdermal delivery system within 60 min of application which could have important implications for the health of horses, and their capacity to perform and recover from physical activity.
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Tanaka, Rosana Aramaki, Flávia Maria de Moraes Ramos, Solange Maria de Almeida, Mário Roberto Vizioli, and Frab Norberto Bóscolo. "Evaluation of radioprotective effect of carnosine (beta- alanyl-1- histidine) on the wound healing in rats." Journal of Applied Oral Science 13, no. 3 (September 2005): 253–58. http://dx.doi.org/10.1590/s1678-77572005000300010.
Full textAbstract:
The purpose of this study was to evaluate the radioprotective effect of carnosine (beta- alanyl-1-histidine) on the wound healing in rats. Therefore, 48 male rats were submitted to a surgical procedure to perform a rectangular wound in the anterior-dorsal region. The animals were divided into 4 experimental groups randomly chosen: control; irradiated; carnosine irradiated and carnosine group. The irradiated and carnosine irradiated group were exposed to a dose (6Gy) of gamma irradiation, in the whole body, 72 hours after surgery. The carnosine and carnosine irradiated groups, in addition to the surgical procedure and the irradiation, received two doses of carnosine aqueous solution, the first one being injected 48 hours after surgery, and the second one 1 hour and 30 minutes before irradiation. The tissue repair of the 4 groups was evaluated at 4, 7, 14, and 21 days after inflicting the wound, by morphological, histochemical and histophysical methods. At all examined periods, it could be observed that the animals from the carnosine irradiated group presented a better developed granulation tissue than the irradiated group and closely similar to that of the control group. Thus, under the experimental conditions used, it was possible to conclude that carnosine is an effective radioprotective substance.
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Stegen, Sanne, Bram Stegen, Giancarlo Aldini, Alessandra Altomare, Luca Cannizzaro, Marica Orioli, Sarah Gerlo, et al. "Plasma carnosine, but not muscle carnosine, attenuates high-fat diet-induced metabolic stress." Applied Physiology, Nutrition, and Metabolism 40, no. 9 (September 2015): 868–76. http://dx.doi.org/10.1139/apnm-2015-0042.
Full textAbstract:
There is growing in vivo evidence that the dipeptide carnosine has protective effects in metabolic diseases. A critical unanswered question is whether its site of action is tissues or plasma. This was investigated using oral carnosine versus β-alanine supplementation in a high-fat diet rat model. Thirty-six male Sprague–Dawley rats received a control diet (CON), a high-fat diet (HF; 60% of energy from fat), the HF diet with 1.8% carnosine (HFcar), or the HF diet with 1% β-alanine (HFba), as β-alanine can increase muscle carnosine without increasing plasma carnosine. Insulin sensitivity, inflammatory signaling, and lipoxidative stress were determined in skeletal muscle and blood. In a pilot study, urine was collected. The 3 HF groups were significantly heavier than the CON group. Muscle carnosine concentrations increased equally in the HFcar and HFba groups, while elevated plasma carnosine levels and carnosine–4-hydroxy-2-nonenal adducts were detected only in the HFcar group. Elevated plasma and urine Nε-(carboxymethyl)lysine in HF rats was reduced by ∼50% in the HFcar group but not in the HFba group. Likewise, inducible nitric oxide synthase mRNA was decreased by 47% (p < 0.05) in the HFcar group, but not in the HFba group, compared with HF rats. We conclude that plasma carnosine, but not muscle carnosine, is involved in preventing early-stage lipoxidation in the circulation and inflammatory signaling in the muscle of rats.
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Peters, Verena, Benito Yard, and Claus Peter Schmitt. "Carnosine and Diabetic Nephropathy." Current Medicinal Chemistry 27, no. 11 (April 23, 2020): 1801–12. http://dx.doi.org/10.2174/0929867326666190326111851.
Full textAbstract:
Diabetic Nephropathy (DN) is a major complication in patients with type 1 or type 2 diabetes and represents the leading cause of end-stage renal disease. Novel therapeutic approaches are warranted. In view of a polymorphism in the carnosinase 1 gene CNDP1, resulting in reduced carnosine degradation activity and a significant DN risk reduction, carnosine (β-alanyl-L-histidine) has gained attention as a potential therapeutic target. Carnosine has anti-inflammatory, antioxidant, anti-glycation and reactive carbonyl quenching properties. In diabetic rodents, carnosine supplementation consistently improved renal histology and function and in most studies, also glucose metabolism. Even though plasma half-life of carnosine in humans is short, first intervention studies in (pre-) diabetic patients yielded promising results. The precise molecular mechanisms of carnosine mediated protective action, however, are still incompletely understood. This review highlights the recent knowledge on the role of the carnosine metabolism in DN.
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Ferraris, R. P., J. Diamond, and W. W. Kwan. "Dietary regulation of intestinal transport of the dipeptide carnosine." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 2 (August 1, 1988): G143—G150. http://dx.doi.org/10.1152/ajpgi.1988.255.2.g143.
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Uptake of the dipeptide L-carnosine was measured in everted intestinal sleeves of mice whose dietary protein level or else proportion of protein in the form of free amino acids was varied experimentally. Carnosine uptake was highest in the jejunum, regardless of ration. Compared with a low-protein (18%) ration, a high-protein (72%) ration stimulated carnosine uptake by 30-70% in duodenum and jejunum (but not in ileum). This stimulation was observed even in the presence of peptidase inhibitors that inhibit cell surface hydrolysis of dipeptides. Measured carnosine hydrolysis was low or negligible. Carnosine uptake was the same in mice fed 54% unhydrolyzed casein, 54% partly hydrolyzed casein, and 54% free amino acids formulated so as to stimulate a complete hydrolysate of casein. Thus carnosine uptake is regulated by dietary levels of amino acids, peptides, and proteins, all of which seem equally effective at inducing carnosine transporters.
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Derave, Wim, Mahir S. Özdemir, Roger C. Harris, Andries Pottier, Harmen Reyngoudt, Katrien Koppo, John A. Wise, and Eric Achten. "β-Alanine supplementation augments muscle carnosine content and attenuates fatigue during repeated isokinetic contraction bouts in trained sprinters." Journal of Applied Physiology 103, no. 5 (November 2007): 1736–43. http://dx.doi.org/10.1152/japplphysiol.00397.2007.
Full textAbstract:
Carnosine (β-alanyl-l-histidine) is present in high concentrations in human skeletal muscle. The ingestion of β-alanine, the rate-limiting precursor of carnosine, has been shown to elevate the muscle carnosine content. We aimed to investigate, using proton magnetic resonance spectroscopy (proton MRS), whether oral supplementation with β-alanine during 4 wk would elevate the calf muscle carnosine content and affect exercise performance in 400-m sprint-trained competitive athletes. Fifteen male athletes participated in a placebo-controlled, double-blind study and were supplemented orally for 4 wk with either 4.8 g/day β-alanine or placebo. Muscle carnosine concentration was quantified in soleus and gastrocnemius by proton MRS. Performance was evaluated by isokinetic testing during five bouts of 30 maximal voluntary knee extensions, by endurance during isometric contraction at 45% maximal voluntary contraction, and by the indoor 400-m running time. β-Alanine supplementation significantly increased the carnosine content in both the soleus (+47%) and gastrocnemius (+37%). In placebo, carnosine remained stable in soleus, while a small and significant increase of +16% occurred in gastrocnemius. Dynamic knee extension torque during the fourth and fifth bout was significantly improved with β-alanine but not with placebo. Isometric endurance and 400-m race time were not affected by treatment. In conclusion, 1) proton MRS can be used to noninvasively quantify human muscle carnosine content; 2) muscle carnosine is increased by oral β-alanine supplementation in sprint-trained athletes; 3) carnosine loading slightly but significantly attenuated fatigue in repeated bouts of exhaustive dynamic contractions; and 4) the increase in muscle carnosine did not improve isometric endurance or 400-m race time.
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Kamal, Mohamed A., Huidi Jiang, Yongjun Hu, Richard F. Keep, and David E. Smith. "Influence of genetic knockout of Pept2 on the in vivo disposition of endogenous and exogenous carnosine in wild-type and Pept2 null mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R986—R991. http://dx.doi.org/10.1152/ajpregu.90744.2008.
Full textAbstract:
Carnosine (β-alanyl-l-histidine), an endogenous dipeptide substrate of the proton-coupled oligopeptide transporter PEPT2, plays an important role in many physiological processes. This study examined the effect of PEPT2 on the disposition of endogenous and exogenous carnosine in wild-type and Pept2 null mice. After exogenous dosing of [3H]carnosine (1 nmol/g iv bolus), a marked increase was observed in its systemic clearance in Pept2 null mice (0.50 vs. 0.29 ml/min), resulting in a decreased systemic exposure of dipeptide (area under the curve = 43.7 vs. 73.0 min×μM). Carnosine uptake was substantially reduced in the kidney of Pept2 null mice, and renal clearance increased 18-fold in this genotype (206 vs. 11.5 μl/min). Fractional reabsorption of carnosine in Pept2 null mice was only one-fifth that in wild-type animals (0.20 vs. 0.94). PEPT2 also had a substantial impact in brain where the cerebrospinal fluid (CSF)-to-plasma concentration ratio of carnosine was eightfold greater in Pept2 null mice (0.70 vs. 0.08). With respect to endogenous carnosine levels, significant reductions were observed in Pept2 null compared with wild-type mice for choroid plexus (0.026 vs. 0.20 mmol/kg), olfactory bulb (1.12 vs. 1.79 mmol/kg), and spleen (0.019 vs. 0.029 mmol/kg). In contrast, carnosine levels in the skeletal muscle of Pept2 null mice were significantly increased (1.70 vs. 1.14 mmol/kg), and no differences were observed between genotypes for endogenous carnosine levels in plasma and CSF. These results demonstrate that PEPT2 significantly modulates the disposition of exogenous carnosine. However, endogenous carnosine levels may be under homeostatic control to maintain systemic and central concentrations under physiological in vivo conditions.
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Kilis-Pstrusinska, Katarzyna. "Carnosine and Kidney Diseases: What We Currently Know?" Current Medicinal Chemistry 27, no. 11 (April 23, 2020): 1764–81. http://dx.doi.org/10.2174/0929867326666190730130024.
Full textAbstract:
: Carnosine (beta-alanyl-L-histidine) is an endogenously synthesised dipeptide which is present in different human tissues e.g. in the kidney. Carnosine is degraded by enzyme serum carnosinase, encoding by CNDP1 gene. Carnosine is engaged in different metabolic pathways in the kidney. It reduces the level of proinflammatory and profibrotic cytokines, inhibits advanced glycation end products’ formation, moreover, it also decreases the mesangial cell proliferation. Carnosine may also serve as a scavenger of peroxyl and hydroxyl radicals and a natural angiotensin-converting enzyme inhibitor. : This review summarizes the results of experimental and human studies concerning the role of carnosine in kidney diseases, particularly in chronic kidney disease, ischemia/reperfusion-induced acute renal failure, diabetic nephropathy and also drug-induced nephrotoxicity. The interplay between serum carnosine concentration and serum carnosinase activity and polymorphism in the CNDP1 gene is discussed. : Carnosine has renoprotective properties. It has a promising potential for the treatment and prevention of different kidney diseases, particularly chronic kidney disease which is a global public health issue. Further studies of the role of carnosine in the kidney may offer innovative and effective strategies for the management of kidney diseases.
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Kim, Eun-Hye, Eun-Sun Kim, Donggeun Shin, Donghyun Kim, Sungbin Choi, Young-Jun Shin, Kyeong-A. Kim, et al. "Carnosine Protects against Cerebral Ischemic Injury by Inhibiting Matrix-Metalloproteinases." International Journal of Molecular Sciences 22, no. 14 (July 13, 2021): 7495. http://dx.doi.org/10.3390/ijms22147495.
Full textAbstract:
Stroke is one of the leading causes of death and disability worldwide. However, treatment options for ischemic stroke remain limited. Matrix-metalloproteinases (MMPs) contribute to brain damage during ischemic strokes by disrupting the blood-brain barrier (BBB) and causing brain edemas. Carnosine, an endogenous dipeptide, was found by us and others to be protective against ischemic brain injury. In this study, we investigated whether carnosine influences MMP activity. Brain MMP levels and activity were measured by gelatin zymography after permanent occlusion of the middle cerebral artery (pMCAO) in rats and in vitro enzyme assays. Carnosine significantly reduced infarct volume and edema. Gelatin zymography and in vitro enzyme assays showed that carnosine inhibited brain MMPs. We showed that carnosine inhibited both MMP-2 and MMP-9 activity by chelating zinc. Carnosine also reduced the ischemia-mediated degradation of the tight junction proteins that comprise the BBB. In summary, our findings show that carnosine inhibits MMP activity by chelating zinc, an essential MMP co-factor, resulting in the reduction of edema and brain injury. We believe that our findings shed new light on the neuroprotective mechanism of carnosine against ischemic brain damage.
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Tsuji, Takahiro, Kazumi Furuhara, Maria Gerasimenko, Anna Shabalova, Stanislav M. Cherepanov, Kana Minami, Haruhiro Higashida, and Chiharu Tsuji. "Oral Supplementation with L-Carnosine Attenuates Social Recognition Deficits in CD157KO Mice via Oxytocin Release." Nutrients 14, no. 4 (February 14, 2022): 803. http://dx.doi.org/10.3390/nu14040803.
Full textAbstract:
The outcomes of supplementation with L-carnosine have been investigated in clinical trials in children with autism spectrum disorder (ASD). However, reports on the effects of L-carnosine in humans have been inconsistent, and the efficacy of L-carnosine supplementation for improving ASD symptoms has yet to be investigated in animal studies. Here, we examined the effects of oral supplementation with L-carnosine on social deficits in CD157KO mice, a murine model of ASD. Social deficits in CD157KO mice were assessed using a three-chamber social approach test. Oral supplementation with L-carnosine attenuated social behavioral deficits. The number of c-Fos-positive oxytocin neurons in the supraoptic nucleus and paraventricular nucleus was increased with L-carnosine supplementation in CD157KO mice after the three-chamber social approach test. We observed an increase in the number of c-Fos-positive neurons in the basolateral amygdala, a brain region involved in social behavior. Although the expression of oxytocin and oxytocin receptors in the hypothalamus was not altered by L-carnosine supplementation, the concentration of oxytocin in cerebrospinal fluid was increased in CD157KO mice by L-carnosine supplementation. These results suggest that L-carnosine supplementation restores social recognition impairments by augmenting the level of released oxytocin. Thus, we could imply the possibility of a safe nutritional intervention for at least some types of ASD in the human population.
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DAĞLI, Fatma, Inayet GUNTURK, Gönül Şeyda SEYDEL, and Cevat YAZICI. "Deneysel hipertiroidide fiziksel ve vital bulguların ve karnozinin etkisinin değerlendirilmesi." Cukurova Medical Journal 47, no. 3 (September 30, 2022): 1059–66. http://dx.doi.org/10.17826/cumj.1099652.
Full textAbstract:
Purpose: This study aims to investigate the effects of experimental hyperthyroidism and carnosine which is known to have antioxidant properties on physical and vital findings in rats, and to determine the relationship between these parameters and free T3 (FT3) levels.
Materials and Methods: Rats were analyzed in 7 groups (each containing 12 animals); control (CONT), hyperthyroidism-1 (T:10-day L-thyroxine (L-T4) administration), hyperthyroidism-2 (T-T: 20-day L-T4 administration), Carnosine (10 day carnosine administration), Hyperthyroidism-1 + Carnosine (T-C), Hyperthyroidism-2 + Carnosine (T-TC), and Carnosine + Hyperthyroidism-1 (C-T). In order to create a hyperthyroidism model, L-thyroxine (L-T4) doses of 300 µg/kg rat weight/day and carnosine doses of 300 µg/kg rat weight/ day were intraperitoneally (ip) administered to the rats.
Results: After 10 and 20 days of thyroxine administration, FT3 levels (T:3.640.51pg/mL, T-T: 4.060.91pg/mL) and body temperature (T:37.10.3oC, T-T: 37.60.3oC), significantly increased while body weight decreased (T:240.722.0g, T-T:263.028.7g). Carnosine administration only prevented the increase of FT3 levels, but had no effect on other parameters.
Conclusion: The increased FT3 levels observed with L-T4 administration were consistent with the physical and vital findings, but carnosine administration did not reflect the expected effects on the physical findings observed in the hyperthyroid condition.
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Dolu, Nazan, Hale Acer, and Ali Yucel Kara. "Investigation of Dose-Related Effects of Carnosine on Anxiety with Sympathetic Skin Response and T-maze." Acta Medica (Hradec Kralove, Czech Republic) 57, no. 3 (2014): 112–18. http://dx.doi.org/10.14712/18059694.2014.49.
Full textAbstract:
Carnosine is a dipeptide formed of the amino acids β-alanine and histidine. Only a limited number of studies have examined the effects of carnosine on sympathetic nerve activation and anxiety. The present study was undertaken to determine the dose-related effects of carnosine on anxiety in the elevated T-maze test (ETM) with electrodermal activity (EDA). Carnosine was injected in three groups of rats with doses of 10 (low dose), 100 (medium dose) and 1000 (high dose) mg/kg i.p. Physiological saline was injected in the sham group. The anxiety scores of the rats were measured with ETM 20 minutes after injection. Then, SCL was measured. The decreased number of entries into the open arm (NEOA), the percentage of time spent in the open arm (% TSOA) and higher EDA [shown by skin conductance level (SCL)] indicate higher anxiety. The NEOA and % TSOA were lower in the high-dose group than in the other groups. SCL was lower in the medium-dose carnosine group than in the high-dose carnosine and sham groups. SCL was higher in the high-dose group than in the medium-dose and sham groups. Our results suggest that high-dose carnosine produced anxiety-like effects as assessed in the SCL and ETM. Medium-dose carnosine acted as an anxiolytic. The anxiety-related responses of carnosine depend on its dose-related effect.
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Antonova, N. A., G. M. Sorokoumova, T. N. Fedorova, S. L. Stvolynsky, D. A. Abaimov, V. I. Popenko, and V. I. Shvets. "CARNOSINE-CONTAINING LIPOSOMES: PREPARATION AND PROPERTIES." Fine Chemical Technologies 11, no. 6 (December 28, 2016): 55–62. http://dx.doi.org/10.32362/2410-6593-2018-13-2-55-62.
Full textAbstract:
Carnosine is a natural dipeptide antioxidant. It is proved that it protects human’s cells from oxidative stress. However, it has a short lifetime in a human organism due to the carnosinase activity. In order to solve this problem we used carnosine encapsulated in liposomes. Thus, the aim of this study was the creation of a new liposomal carnosine drug form. We used two encapsulation methods that show different carnosine behavior: a passive and an active one. We took into account that conditions of obtaining liposomes such as lipid composition, pH and temperature are important. In this study the lipid composition providing the maximum encapsulation efficiency was determined. Dipalmitoylphosphotidylcholine (DPPC) and its mixture with cholesterol (Chol) wereused as composition lipids. It was shown that the active encapsulation method using the creation of ammonium sulphate pH gradient provided the best results: 41.7% encapsulation efficiency (according to NMR spectroscopy) when using DPPC:Chol (7:3) mixture as lipids. Moreover, the properties of the liposomes were studied. Using the dynamic light scattering and electron microscopy methods carnosine liposomes (DPPC:Chol) were shown to be spherical nanoparticles with an average size of 133 nm. Carnosine release kinetics studied with the use of a France’s cell showed that carnosine was released in 24 hours (liposomal composition DPPC:Chol was 7:3). A study of carnosinase action on liposomal carnosine showed that the maximum amount of carnosine remained unchanged in DPPC:Chol liposomes (7:3). The results of the study make it possible to conclude that liposomal carnosine has a better activity in the human organism.
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Baguet, Audrey, Inge Everaert, Benito Yard, Verena Peters, Johannes Zschocke, Ana Zutinic, Emile De Heer, Tomasz Podgórski, Katarzyna Domaszewska, and Wim Derave. "Does low serum carnosinase activity favor high-intensity exercise capacity?" Journal of Applied Physiology 116, no. 5 (March 1, 2014): 553–59. http://dx.doi.org/10.1152/japplphysiol.01218.2013.
Full textAbstract:
Given the ergogenic properties of β-alanyl-L-histidine (carnosine) in skeletal muscle, it can be hypothesized that elevated levels of circulating carnosine could equally be advantageous for high-intensity exercises. Serum carnosinase (CN1), the enzyme hydrolyzing the dipeptide, is highly active in the human circulation. Consequently, dietary intake of carnosine usually results in rapid degradation upon absorption, yet this is less pronounced in subjects with low CN1 activity. Therefore, acute carnosine supplementation before high-intensity exercise could be ergogenic in these subjects. In a cross-sectional study, we determined plasma CN1 activity and content in 235 subjects, including 154 untrained controls and 45 explosive and 36 middle- to long-distance elite athletes. In a subsequent double-blind, placebo-controlled, crossover study, 12 men performed a cycling capacity test at 110% maximal power output (CCT 110%) following acute carnosine (20 mg/kg body wt) or placebo supplementation. Blood samples were collected to measure CN1 content, carnosine, and acid-base balance. Both male and female explosive athletes had significantly lower CN1 activity (14% and 21% lower, respectively) and content (30% and 33% lower, respectively) than controls. Acute carnosine supplementation resulted only in three subjects in carnosinemia. The CCT 110% performance was not improved after carnosine supplementation, even when accounting for low/high CN1 content. No differences were found in acid-base balance, except for elevated resting bicarbonate following carnosine supplementation and in low CN1 subjects. In conclusion, explosive athletes have lower serum CN1 activity and content compared with untrained controls, possibly resulting from genetic selection. Acute carnosine supplementation does not improve high-intensity performance.
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Palin, Marie-France, Jérôme Lapointe, Claude Gariépy, Danièle Beaudry, and Claudia Kalbe. "57 Carnosine prevents oxidative damage in myoblast cells derived from porcine skeletal muscle." Journal of Animal Science 97, Supplement_3 (December 2019): 59. http://dx.doi.org/10.1093/jas/skz258.122.
Full textAbstract:
Abstract Carnosine (β-alanyl-L-histidine) is a molecule naturally and exclusively present in muscle food with the highest concentrations found in skeletal muscles and brain of the animal. Among its numerous biochemical properties, carnosine has antioxidant activity which include metal ion chelation and free radical scavenging. We have recently reported that high muscle carnosine content in pig is associated with better meat quality. Moreover, supplementing pigs with β-alanine reduced oxidative damage to Longissimus muscle (LM) lipids and proteins. Among previously reported antioxidant activities, carnosine was found to limit the production of reactive oxygen species (ROS) and increase antioxidant enzyme activities. However, these studies were mainly conducted in rodents and cell lines and mechanisms in play remain to be characterized. To determine the effect of carnosine in preventing oxidative damage and characterize the mechanisms in play, we have undertaken experiments using the progeny (myoblasts) of satellite cells isolated from the LM of newborn piglets. Cells were treated with carnosine (0, 10, 25 and 50 mM) for 48 h and were then either collected immediately or treated with H2O2 (0.3 mM, 1 h) to induce an oxidative stress. Our results showed that carnosine prevents oxidative stress through the reduction of total intracellular ROS and by modulating the antioxidant system in myoblasts.Carnosine increased the mRNA abundance of NEF2L2, a transcription factor activated by oxidative stress, and several of its downstream regulated antioxidant genes. Western blot analyses further suggest that the protective effect of carnosine on H2O2-induced oxidative stress is mediated through the p38 MAPK intracellular pathway. Finally, the addition of carnosine to H2O2-treated myoblasts increased the basal cellular oxygen consumption rate (OCR), the ATP-linked OCR and proton leaks, thus suggesting an effect of carnosine on mitochondrial functions. Taken together, these findings demonstrate the important role of carnosine in preventing oxidative damage in porcine muscle cells.
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Kralik, Gordana, Zlata Kralik, and Kristina Gvozdanović. "CARNOSINE – POLYFUNCTIONAL BIOLOGICALLY ACTIVE INGREDIENT." Poljoprivreda 28, no. 2 (December 20, 2022): 81–88. http://dx.doi.org/10.18047/poljo.28.2.11.
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In this paper, authors summarise studies refferering to enrichment of breast and thigh muscles with carnosine that has an important function in physiological processes. Research has shown that carnosine improves quality of chicken meat. By adding amino acids β-alanine and L-histidine in chickens’ feed, carnosine synthesizes in skeletal muscles, brain, heart muscle and olfactory receptor cells. It has been determined that the content of carnosine depends on the type of muscle (white or dark meat), broiler genotype as well as sex. Chicken meat is sensitive to oxidation processes, but lipid oxidation can be efficiently prevented by enriching meat with carnosine.
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Caruso, Giuseppe, Claudia Fresta, Nicolò Musso, Mariaconcetta Giambirtone, Margherita Grasso, Simona Spampinato, Sara Merlo, et al. "Carnosine Prevents Aβ-Induced Oxidative Stress and Inflammation in Microglial Cells: A Key Role of TGF-β1." Cells 8, no. 1 (January 17, 2019): 64. http://dx.doi.org/10.3390/cells8010064.
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Carnosine (β-alanyl-L-histidine), a dipeptide, is an endogenous antioxidant widely distributed in excitable tissues like muscles and the brain. Carnosine is involved in cellular defense mechanisms against oxidative stress, including the inhibition of amyloid-beta (Aβ) aggregation and the scavenging of reactive species. Microglia play a central role in the pathogenesis of Alzheimer’s disease, promoting neuroinflammation through the secretion of inflammatory mediators and free radicals. However, the effects of carnosine on microglial cells and neuroinflammation are not well understood. In the present work, carnosine was tested for its ability to protect BV-2 microglial cells against oligomeric Aβ1-42-induced oxidative stress and inflammation. Carnosine prevented cell death in BV-2 cells challenged with Aβ oligomers through multiple mechanisms. Specifically, carnosine lowered the oxidative stress by decreasing NO and O2−• intracellular levels as well as the expression of iNOS and Nox enzymes. Carnosine also decreased the secretion of pro-inflammatory cytokines such as IL-1β, simultaneously rescuing IL-10 levels and increasing the expression and the release of TGF-β1. Carnosine also prevented Aβ-induced neurodegeneration in mixed neuronal cultures challenged with Aβ oligomers, and these neuroprotective effects were completely abolished by SB431542, a selective inhibitor of the type-1 TGF-β receptor. Our data suggest a multimodal mechanism of action of carnosine underlying its protective effects on microglial cells against Aβ toxicity with a key role of TGF-β1 in mediating these protective effects.
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Bao, Yun, Saidan Ding, Jiaoyan Cheng, Yuan Liu, Bingyu Wang, Huijuan Xu, Yao Shen, and Jianxin Lyu. "Carnosine Inhibits the Proliferation of Human Cervical Gland Carcinoma Cells Through Inhibiting Both Mitochondrial Bioenergetics and Glycolysis Pathways and Retarding Cell Cycle Progression." Integrative Cancer Therapies 17, no. 1 (December 23, 2016): 80–91. http://dx.doi.org/10.1177/1534735416684551.
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Carnosine has been demonstrated to play an antitumorigenic role in certain types of cancer. However, its underlying mechanism is unclear. In this study, the roles of carnosine in cell proliferation and its underlying mechanism were investigated in the cultured human cervical gland carcinoma cells HeLa and cervical squamous carcinoma cells SiHa. The results showed that carnosine exerted a significant inhibitory effect on the proliferation of HeLa cells, whereas its inhibitory action on the proliferation of SiHa cells was much weaker. Carnosine decreased the ATP content through inhibiting both mitochondrial respiration and glycolysis pathways in cultured HeLa cells but not SiHa cells. Carnosine reduced the activities of isocitrate dehydrogenase and malate dehydrogenase in TCA (tricarboxylic acid) cycle and the activities of mitochondrial electron transport chain complex I, II, III, and IV in HeLa cells but not SiHa cells. Carnosine also decreased the mRNA and protein expression levels of ClpP, which plays a key role in maintaining the mitochondrial function in HeLa cells. In addition, carnosine induced G1 arrest by inhibiting the G1-S phase transition in both HeLa and SiHa cells. Taken together, these findings suggest that carnosine has a strong inhibitory action on the proliferation of human cervical gland carcinoma cells rather than cervical squamous carcinoma cells. Mitochondrial bioenergetics and glycolysis pathways and cell cycle may be involved in the carnosine action on the cell proliferation in cultured human cervical gland carcinoma cells HeLa.
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Caruso, Giuseppe, Justyna Godos, Sabrina Castellano, Agnieszka Micek, Paolo Murabito, Fabio Galvano, Raffaele Ferri, Giuseppe Grosso, and Filippo Caraci. "The Therapeutic Potential of Carnosine/Anserine Supplementation against Cognitive Decline: A Systematic Review with Meta-Analysis." Biomedicines 9, no. 3 (March 4, 2021): 253. http://dx.doi.org/10.3390/biomedicines9030253.
Full textAbstract:
Carnosine is a natural occurring endogenous dipeptide that was proposed as an anti-aging agent more than 20 years ago. Carnosine can be found at low millimolar concentrations at brain level and different preclinical studies have demonstrated its antioxidant, anti-inflammatory, and anti-aggregation activity with neuroprotective effects in animal models of Alzheimer’s disease (AD). A selective deficit of carnosine has also been linked to cognitive decline in AD. Different clinical studies have been conducted to evaluate the impact of carnosine supplementation against cognitive decline in elderly and AD subjects. We conducted a systematic review with meta-analysis, in accordance with the PRISMA guidelines coupled to the PICOS approach, to investigate the therapeutic potential of carnosine against cognitive decline and depressive symptoms in elderly subjects. We found five studies matching the selection criteria. Carnosine/anserine was administered for 12 weeks at a dose of 1 g/day and improved global cognitive function, whereas no effects were detected on depressive symptoms. These data suggest a preliminary evidence of clinical efficacy of carnosine against cognitive decline both in elderly subjects and mild cognitive impairment (MCI) patients, although larger and long-term clinical studies are needed in MCI patients (with or without depression) to confirm the therapeutic potential of carnosine.
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Schwank-Xu, Cheng, Elisabete Forsberg, Magnus Bentinger, Allan Zhao, Ishrath Ansurudeen, Gustav Dallner, Sergiu-Bogdan Catrina, Kerstin Brismar, and Michael Tekle. "L-Carnosine Stimulation of Coenzyme Q10 Biosynthesis Promotes Improved Mitochondrial Function and Decreases Hepatic Steatosis in Diabetic Conditions." Antioxidants 10, no. 5 (May 17, 2021): 793. http://dx.doi.org/10.3390/antiox10050793.
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Mitochondrial dysfunction in type 2 diabetes leads to oxidative stress, which drives disease progression and diabetes complications. L-carnosine, an endogenous dipeptide, improves metabolic control, wound healing and kidney function in animal models of type 2 diabetes. Coenzyme Q (CoQ), a component of the mitochondrial electron transport chain, possesses similar protective effects on diabetes complications. We aimed to study the effect of carnosine on CoQ, and assess any synergistic effects of carnosine and CoQ on improved mitochondrial function in a mouse model of type 2 diabetes. Carnosine enhanced CoQ gene expression and increased hepatic CoQ biosynthesis in db/db mice, a type 2 diabetes model. Co-administration of Carnosine and CoQ improved mitochondrial function, lowered ROS formation and reduced signs of oxidative stress. Our work suggests that carnosine exerts beneficial effects on hepatic CoQ synthesis and when combined with CoQ, improves mitochondrial function and cellular redox balance in the liver of diabetic mice. (4) Conclusions: L-carnosine has beneficial effects on oxidative stress both alone and in combination with CoQ on hepatic mitochondrial function in an obese type 2 diabetes mouse model.
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Sun, Chenliang, Qinfeng Wu, Xuejie Zhang, Qianru He, and Hongsheng Zhao. "Mechanistic Evaluation of the Protective Effect of Carnosine on Acute Lung Injury in Sepsis Rats." Pharmacology 100, no. 5-6 (2017): 292–300. http://dx.doi.org/10.1159/000479879.
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This study analyzes the sepsis healing therapeutic potential of carnosine against experimentally sepsis-induced male albino rats. Carnosine in 2 different doses, 25 mg/kg and 50 mg/kg, were administered for 30 consecutive days. At the end of the treatment, lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase and myeloperoxidase activities were measured. Lungs weight and total protein content were determined in the bronchoalveolar fluid (BALF). Cytokines such as macrophage inhibitory factor (MIF), interleukin-8 (IL-8) and tumour necrosis factor-alpha (TNF-α) were determined in the BALF. In addition, the histopathological analysis was also carried out to understand the effect of carnosine in the cellular architecture. Carnosine treatment significantly renormalized the lipid peroxidation and other antioxidant enzymes. IL-β, TNF-α, and MIF were found to be reduced after carnosine treatment. After carnosine treatment, the intensity of sepsis was significantly reduced evidenced by histopathological analysis. In western blot analysis, carnosine treatment causes the upregulation of IκBα together with the downregulation of the expressions of p65 and p-IKKα/β (Ser 180/Ser 181).
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Rybakova, Yu S., A. L. Kalen, J. C. Eckers, T. N. Fedorova, P. C. Goswami, and E. H. Sarsour. "Increased manganese superoxide dismutase and cyclin B1 expression in carnosine-induced inhibition of glioblastoma cell proliferation." Biomeditsinskaya Khimiya 61, no. 4 (2015): 510–18. http://dx.doi.org/10.18097/pbmc20156104510.
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Carnosine is an endogenous dipeptide with antiproliferative properties. Here we show that carnosine selectively inhibits proliferation of human glioblastoma cells (U-118-MG) compared to breast (MB231) and oral (Cal27 and FaDu) cancer cells. Carnosine-induced inhibition of U-118-MG proliferation is associated with a significant: decrease in cellular reactive oxygen species levels, increase in manganese superoxide dismutase (MnSOD) and increase in cyclin B1 expression resulting in G2-block. We conclude that the antiproliferative property of carnosine is due to its ability to enhance MnSOD and cyclin B1 expression. These results will be of significance to the potential application of carnosine in brain cancer therapy
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Liu, Yaojun, Wenqiang Shen, Tao Liu, Rainer Mosenthin, Yinghui Bao, Peng Chen, Wenbo Hao, et al. "Improved Satellite Cell Proliferation Induced by L-Carnosine Benefits Muscle Growth of Pigs in Part through Activation of the Akt/mTOR/S6K Signaling Pathway." Agriculture 12, no. 7 (July 8, 2022): 988. http://dx.doi.org/10.3390/agriculture12070988.
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(1) Background: L-carnosine (β-alanyl-L-histidine), a natural dipeptide, exists at relatively high concentrations in skeletal muscles, and has been shown to protect cells from adverse conditions due to its antioxidant, anti-aging, anti-glycation, and buffering properties. Satellite cells (SCs), residing on the myofiber surface, are crucial for muscle post-growth and regeneration. However, the effects of L-carnosine on muscle development of pigs in vivo, on proliferation and growth of SCs in vitro, and the relationship between SCs and muscle development have not yet been investigated. (2) Methods: The objective of this study was to assess the effect of dietary L-carnosine on growth performance and longissimus dorsi muscle development of pigs in vivo, and to elaborate its molecular mechanisms in vitro using L-carnosine-treated SCs. (3) Results: It was shown that L-carnosine supplementation (0.2 and 2 mM) increased (p < 0.05) SC proliferation and cell percentage in the synthesis (S) phase and decreased cell percentage in the resting (G0)/first gap (G1)/phase. Moreover, average daily gain (ADG) of pigs fed diets containing 0.1% of L-carnosine was higher (p < 0.05) than that of pigs fed diets without L-carnosine, and the longissimus dorsi muscle weight of pigs assigned to the L-carnosine treatments was 7.95% higher compared to control pigs. Both in the longissimus dorsi muscle and cultured SCs of pigs, the Akt/mTOR/S6K signaling pathway was activated (p < 0.05), suggesting that L-carnosine improved muscle growth and SC proliferation of pigs. (4) Conclusions: Considering the important role of SCs in post-natal muscle growth, there is evidence that L-carnosine may improve muscle growth of pigs through promoting SC proliferation via activating the Akt/mTOR/S6K signaling pathway.
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Baguet, Audrey, Harmen Reyngoudt, Andries Pottier, Inge Everaert, Stefanie Callens, Eric Achten, and Wim Derave. "Carnosine loading and washout in human skeletal muscles." Journal of Applied Physiology 106, no. 3 (March 2009): 837–42. http://dx.doi.org/10.1152/japplphysiol.91357.2008.
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Carnosine (β-alanyl-l-histidine) is present in high concentrations in human skeletal muscles. The oral ingestion of β-alanine, the rate-limiting precursor in carnosine synthesis, has been shown to elevate the muscle carnosine content both in trained and untrained humans. Little human data exist about the dynamics of the muscle carnosine content, its metabolic regulation, and its dependence on muscle fiber type. The present study aimed to investigate in three skeletal muscle types the supplementation-induced amplitude of carnosine synthesis and its subsequent elimination on cessation of supplementation (washout). Fifteen untrained males participated in a placebo-controlled double-blind study. They were supplemented for 5–6 wk with either 4.8 g/day β-alanine or placebo. Muscle carnosine was quantified in soleus, tibialis anterior, and medial head of the gastrocnemius by proton magnetic resonance spectroscopy (MRS), before and after supplementation and 3 and 9 wk into washout. The β-alanine supplementation significantly increased the carnosine content in soleus by 39%, in tibialis by 27%, and in gastrocnemius by 23% and declined postsupplementation at a rate of 2–4%/wk. Average muscle carnosine remained increased compared with baseline at 3 wk of washout (only one-third of the supplementation-induced increase had disappeared) and returned to baseline values within 9 wk at group level. Following subdivision into high responders (+55%) and low responders (+15%), washout period was 15 and 6 wk, respectively. In the placebo group, carnosine remained relatively constant with variation coefficients of 9–15% over a 3-mo period. It can be concluded that carnosine is a stable compound in human skeletal muscle, confirming the absence of carnosinase in myocytes. The present study shows that washout periods for crossover designs in supplementation studies for muscle metabolites may sometimes require months rather than weeks.
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Nelson, TE, GP Zaloga, and PR Roberts. "CARNOSINE." Anesthesia & Analgesia 86, Supplement (April 1998): 75SCA. http://dx.doi.org/10.1097/00000539-199804001-00075.
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Arnould, J. M. "Mise en évidence in vitro de la biosynthèse d'histamine à partir de carnosine par le rein de souris gravide." Canadian Journal of Physiology and Pharmacology 65, no. 1 (January 1, 1987): 70–74. http://dx.doi.org/10.1139/y87-013.
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Kidneys of pregnant mice synthesize histamine when incubated in the presence of carnosine, manganese, and pyridoxal phosphate. Intensity of biosynthesis increases linearly with the amount of enzyme and the incubation time. The reaction can only be catalysed by two enzymes that are located in kidneys and act in succession: carnosinase, which hydrolyzes carnosine into its two moieties, and histidine decarboxylase, which transforms histidine, a product of carnosine degradation, into histamine. The biosynthesis of histamine from carnosine seems to increase with the progress of pregnancy. In nonpregnant mice, kidneys do not effect this biosynthesis. The above results directly demonstrate that carnosine may be used for histamine synthesis when the activity of histidine decarboxylase is high, as in pregnant mouse kidney. Vertebrate carnosine, its role still enigmatic, might thus be mainly a potential histidine reservoir that would be mobilized any time there is a significant requirement for histidine, such as for histamine biosynthesis.
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Xing, Lujuan, MacKenzie E. Chee, Hua Zhang, Wangang Zhang, and Yoshinori Mine. "Carnosine—a natural bioactive dipeptide: bioaccessibility, bioavailability and health benefits." Journal of Food Bioactives 5 (March 31, 2019): 8–17. http://dx.doi.org/10.31665/jfb.2019.5174.
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Carnosine is a natural dipeptide synthesized by both vertebrate and invertebrate organisms and has functional properties that are specific to muscle and excitable tissues. Recent in vivo and in vitro studies have shown that carnosine presents metal chelating and antioxidant activities and has the ability to inhibit protein carbonylation and glycoxidation. This review describes the health benefits of carnosine in relation to its bioaccessibility, bioavailability and biochemical properties as well as providing the current state-of-the-art knowledge on the potential use of carnosine as a nutraceutical. The therapeutic potential of carnosine has also been investigated by a number of preclinical and clinical studies for diseases such as diabetes and its associated complications, as well as fatigue, ageing, and some neurological disorders. Altogether the current literature provides supportive evidence on the use of carnosine as a natural dietary supplement with significant health boosting efficiency and without any side effects.
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Alhamdani, Mohamed-Saiel Saeed, Hasan Fayadh Al-Azzawie, and Fawzi K. H. Abbas. "Decreased Formation of Advanced Glycation End-Products in Peritoneal Fluid by Carnosine and Related Peptides." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 27, no. 1 (January 2007): 86–89. http://dx.doi.org/10.1177/089686080702700118.
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Background Formation of advanced glycation end-products (AGEs) is a major problem in uremic patients treated with peritoneal dialysis (PD). Application of additives with known anti-glycosylation properties to PD fluid may be beneficial in minimizing the formation of AGEs. This study aimed to evaluate the effect of carnosine and its related peptides homocarnosine and anserine against the formation of AGEs in PD fluid. Methods PD solutions (1.5% dextrose) were incubated with human serum albumin (HSA) or collagen (type IV) with or without 10 mmol/L of each of carnosine, anserine, homo-carnosine, histidine, and aminoguanidine. The formation of AGEs was followed by fluorescence spectrophotometry at weekly intervals for 7 weeks. For the determination of the acute effect of carnosine and related compounds, HSA and collagen were incubated with 4.25% dextrose PD solutions for 24 hours, followed by incubation with 20 mmol/L of carnosine and related compounds for another 24 hours. The rate of AGE formation was monitored by fluorescence spectrophotometry. Results Carnosine and related compounds showed effective regression in AGE formation in both types of proteins in both long- and short-term exposure to PD fluids at a rate of effectiveness of the order of carnosine > homocarnosine > anserine, aminoguanidine > histidine in long-term exposure, and homocarnosine > carnosine > aminoguanidine > anserine > histidine in short-term exposure. Conclusion Carnosine and related peptides could suppress the formation of AGEs initiated by PD fluid. This observation may provide a new therapeutic approach for the prevention and treatment of the AGE-related complications in PD patients.
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Lai, Po-Yu, Shu-Chen Hsieh, Chih-Chung Wu, and Shu-Ling Hsieh. "ID: 1029 Effects of carnosine on regulation of migration and invasion in human colorectal cancer cells." Biomedical Research and Therapy 4, S (September 5, 2017): 104. http://dx.doi.org/10.15419/bmrat.v4is.305.
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Colorectal cancer is the third most commonly diagnosed cancer in the word. Carnosine is an endogenous dipeptide found in vertebrate skeletal muscles. It is known to have anti-fatigue, antioxidative, antihypertensive, antidiabetic, and cancer inhibiting effects. However, little research has been done regarding its influence on the metastasis of colon cancer. This study cultivated HCT-116 human colon cancer cells as a test model in order to investigate the impact of carnosine on the migration and invasion of human colon cancer cells. The results showed that 48-hour treatments of HCT-116 cells with 0.5, 1, or 5 mM carnosine each significantly inhibited the migration ability of the cells (P < 0.05). The 48-hour treatments with 0.5, 1, or 5 mM carnosine were also found to significantly reduce MMP-9 activity (P < 0.05), but not MMP-2 expression. Furthermore, when HCT-116 cells treated with 1 or 5 mM carnosine, invasion ability are significantly decreased and significantly increased E-cadherin expression (P < 0.05). On the other hand, the protein of TIMP-1, an inhibitor of MMP-9, is signification increased after 1 or 5 mM carnosine treatment (P<0.05). In addition, the u-PA protein level are significantly decreased after carnosine treatment.
The results indicate that carnosine can regulate the migration and invasion by regulating MMPs and its regulator molecular expression in HCT-116 cells.
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Dissette, Valeria, Carlo Bignozzi, Giuseppe Valacchi, Alessandra Pecorelli, Stefano Manfredini, and Silvia Vertuani. "Evaluation of the Transepidermal Penetration of a Carnosine Complex in Gel Formulation by 3D Skin Models." Cosmetics 5, no. 4 (November 14, 2018): 67. http://dx.doi.org/10.3390/cosmetics5040067.
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Carnosine has several physiological roles, from intracellular pH buffering to antioxidant activities, which all depend on bioavailability. This study was conducted in a human skin 3D model and focuses on the effects of the topical delivery of carnosine, from a dermo-cosmetic gel, through the stratum corneum in the presence of a magnesium ion as a complexing agent. To evaluate possible enhancement for small peptide delivery to the skin from simple cosmetic formulations, we discovered that complexation was able to improve the delivery of carnosine into human skin 3D models by application in gel formulation. The concentrations of carnosine released in the underlying media and those that remained in the reconstructed human epidermis (RHE) tissues after 24 and 48 h exposure were measured. Moreover, the influence of magnesium ions was also evaluated comparing the same formulation with and without the salt. The results obtained in this study support hypothesis that magnesium can influence the delivery of small peptides and that the gel formulation based on the carnosine-magnesium complex allows for superior delivery of carnosine in the lower skin layer at a concentration up to 60% more than carnosine alone.
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Blancquaert, L., I. Everaert, A. Baguet, T. Bex, S. Barbaresi, S. de Jager, E. Lievens, et al. "Acute preexercise supplementation of combined carnosine and anserine enhances initial maximal power of Wingate tests in humans." Journal of Applied Physiology 130, no. 6 (June 1, 2021): 1868–78. http://dx.doi.org/10.1152/japplphysiol.00602.2020.
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Current results reveal that carnosine and anserine competitively bind to the highly active carnosinase enzyme in human plasma. Acute combined carnosine and anserine supplementation is therefore described as novel strategy to raise plasma anserine and carnosine. We report that indices of maximal exercise/muscle power during the initial stage of a Wingate test were significantly improved by preexercise 20–25mg/kg body wt anserine and carnosine supplementation, pointing toward a novel acute nutritional strategy to improve high-intensity exercise performance.