Abstract
Cellular and subcellular metabolic activities are crucial processes involved in the regulation of intracellular homeostasis, including cellular and subcellular signaling pathways. Dysregulation of intracellular regulation mechanisms is catastrophic and cumulates into cell death. To overcome the issue of dysregulation of intracellular regulation mechanisms, the preservation of subcellular and extracellular components is essential to maintain healthy cells with increased longevity. Several physiopathological changes occur during cell ageing, one of which is the dysregulation of intracellular physiology of the oxidative phosphorylation process. Nicotinamide mononucleotide (NMN) remains in the debut of anti-aging therapeutic effect. Aged myocardiocyte characterized by disrupted NMN and or its precursors or signaling pathways. Simultaneously, several other pathophysiological occur that collectively impair intracellular homeostasis. The NMN role in the antiaging effect remains unclear and several hypotheses have been introduced into describing the mechanism and the potential outcomes from NMN exogenous supply. Correction of the impaired intracellular homeostasis includes correction to the NMN metabolism. Additionally, autophagy correction, which is the key element in the regulation of intracellular intoxication, including oxidative stress, unfolding protein response, and other degradation of intracellular metabolites. Several signaling pathways are involved in the regulation mechanism of NMN effects on myocardiocyte health and further longevity. NMN protects myocardiocytes from ischemic injury by reducing anabolism and, increasing catabolism and further passing the myocardiocytes into dormant status. NMN applications include ischemic heart, disease, and failed heart, as well as dilated cardiomyopathies. Cytosolic and mitochondrial NADPH are independently functioning and regulating. Each of these plays a role in the determination of the longevity of the myocardiocytes. NMN has a cornerstone in the functionality of Sirtuins, which are an essential anti-senescent intrinsic molecule. The study aims to assess the role of NMN in the longevity and antisenescent of myocardiocytes.
Graphical Abstract
[1]
Tsao CW, Aday AW, Almarzooq ZI, et al. Heart disease and stroke statistics—2023 update: A report from the american heart association. Circulation 2023; 147(8): e93-e621.
[http://dx.doi.org/10.1161/CIR.0000000000001123]
[http://dx.doi.org/10.1161/CIR.0000000000001123]
[2]
Marzoog BA. Recent advances in molecular biology of metabolic syndrome pathophysiology: endothelial dysfunction as a potential therapeutic target. J Diabetes Metab Disord 2022; 21(2): 1903-11.
[http://dx.doi.org/10.1007/s40200-022-01088-y]
[http://dx.doi.org/10.1007/s40200-022-01088-y]
[3]
Marzoog BA. The metabolic syndrome puzzles; Possible pathogenesis and management. Curr Diabetes Rev 2023; 19(4): e290422204258.
[http://dx.doi.org/10.2174/1573399818666220429100411]
[http://dx.doi.org/10.2174/1573399818666220429100411]
[4]
Marzoog BA. Endothelial cell autophagy in the context of disease development. Anat Cell Biol 2023; 56(1): 16-24.
[http://dx.doi.org/10.5115/acb.22.098]
[http://dx.doi.org/10.5115/acb.22.098]
[5]
Abdullah Marzoog B. Adaptive and compensatory mechanisms of the cardiovascular system and disease risk factors in young males and females. New Emirates Med J 2022; 4(1): 1-7.
[http://dx.doi.org/10.2174/04666221128110145]
[http://dx.doi.org/10.2174/04666221128110145]
[6]
Yuan Y, Liang B, Liu XL, Liu WJ, Huang BH, Yang SB. Targeting NAD+: Is it a common strategy to delay heart aging? Cell Death Discov 2022; 8: 1-14.
[http://dx.doi.org/10.1038/s41420-022-01031-3]
[http://dx.doi.org/10.1038/s41420-022-01031-3]
[7]
Hosseini L, Vafaee MS, Badalzadeh R. Melatonin and nicotinamide mononucleotide attenuate myocardial ischemia/reperfusion injury via modulation of mitochondrial function and hemodynamic parameters in aged rats. J Cardiovasc Pharmacol Ther 2020; 25(3): 240-50.
[http://dx.doi.org/10.1177/1074248419882002]
[http://dx.doi.org/10.1177/1074248419882002]
[8]
Zhang R, Shen Y, Zhou L, et al. Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure. J Mol Cell Cardiol 2017; 112: 64-73.
[http://dx.doi.org/10.1016/j.yjmcc.2017.09.001]
[http://dx.doi.org/10.1016/j.yjmcc.2017.09.001]
[9]
Wang H, Sun Y, Pi C, et al. Nicotinamide mononucleotide supplementation improves mitochondrial dysfunction and rescues cellular senescence by NAD+/Sirt3 pathway in mesenchymal stem cells. Int J Mol Sci 2022; 23(23): 14739.
[http://dx.doi.org/10.3390/ijms232314739]
[http://dx.doi.org/10.3390/ijms232314739]
[10]
Marzoog BA, Vlasova TI. Myocardiocyte autophagy in the context of myocardiocytes regeneration: A potential novel therapeutic strategy. Egypt J Med Hum Genet 2022; 23(1): 41.
[http://dx.doi.org/10.1186/s43042-022-00250-8]
[http://dx.doi.org/10.1186/s43042-022-00250-8]
[11]
Abdullah MB. Autophagy as an anti-senescent in aging neurocytes. Curr Mol Med 2023; 24(2): 182-90.
[http://dx.doi.org/10.2174/1566524023666230120102718]
[http://dx.doi.org/10.2174/1566524023666230120102718]
[12]
Marzoog BA, Vlasova TI. Beta-cell autophagy under the scope of hypoglycemic drugs; possible mechanism as a novel therapeutic target. Obes Metab 2022; 18(4): 465-70.
[http://dx.doi.org/10.14341/omet12778]
[http://dx.doi.org/10.14341/omet12778]
[13]
Marzoog BA. Autophagy in cancer cell transformation: A potential novel therapeutic strategy. Curr Cancer Drug Targets 2022; 22(9): 749-56.
[http://dx.doi.org/10.2174/1568009622666220428102741]
[http://dx.doi.org/10.2174/1568009622666220428102741]
[14]
Tarantini S, Valcarcel-Ares MN, Toth P, et al. Nicotinamide mononucleotide (NMN) supplementation rescues cerebromicrovascular endothelial function and neurovascular coupling responses and improves cognitive function in aged mice. Redox Biol 2019; 24: 101192.
[http://dx.doi.org/10.1016/j.redox.2019.101192]
[http://dx.doi.org/10.1016/j.redox.2019.101192]
[15]
Marzoog BA. Transcription factors – the essence of heart regeneration: A potential novel therapeutic strategy. Curr Mol Med 2023; 23(3): 232-8.
[http://dx.doi.org/10.2174/1566524022666220216123650]
[http://dx.doi.org/10.2174/1566524022666220216123650]
[16]
Abdullah MB. Caveolae’s behavior in norm and pathology. Emir Med J 2023; 4(2): e080523216639.
[http://dx.doi.org/10.2174/0250688204666230508112229]
[http://dx.doi.org/10.2174/0250688204666230508112229]
[17]
Luo S, Zhao J, Zheng Y, Chen T, Wang Z. Biosynthesis of nicotinamide mononucleotide: Current metabolic engineering strategies, challenges, and prospects. Fermentation 2023; 9(7): 594.
[http://dx.doi.org/10.3390/fermentation9070594]
[http://dx.doi.org/10.3390/fermentation9070594]
[18]
Kropotov A, Kulikova V, Nerinovski K, et al. Equilibrative nucleoside transporters mediate the import of nicotinamide riboside and nicotinic acid riboside into human cells. Int J Mol Sci 2021; 22(3): 1391.
[http://dx.doi.org/10.3390/ijms22031391]
[http://dx.doi.org/10.3390/ijms22031391]
[19]
Picard M, Wallace DC, Burelle Y. The rise of mitochondria in medicine. Mitochondrion 2016; 30: 105-16.
[http://dx.doi.org/10.1016/j.mito.2016.07.003]
[http://dx.doi.org/10.1016/j.mito.2016.07.003]
[20]
Niu X, Stancliffe E, Gelman SJ, et al. Cytosolic and mitochondrial NADPH fluxes are independently regulated. Nat Chem Biol 2023; 19(7): 837-45.
[http://dx.doi.org/10.1038/s41589-023-01283-9]
[http://dx.doi.org/10.1038/s41589-023-01283-9]
[21]
Chen L, Zhang Z, Hoshino A, et al. NADPH production by the oxidative pentose-phosphate pathway supports folate metabolism. Nat Metab 2019; 1(3): 404-15.
[http://dx.doi.org/10.1038/s42255-019-0043-x]
[http://dx.doi.org/10.1038/s42255-019-0043-x]
[22]
Marzoog BA. Autophagy behavior in post-myocardial infarction injury. Cardiovasc Hematol Disord Drug Targets 2023; 23(1): 2-10.
[http://dx.doi.org/10.2174/1871529X23666230503123612]
[http://dx.doi.org/10.2174/1871529X23666230503123612]
[23]
Marzoog BA, Vlasova TI. Membrane lipids under norm and pathology. Eur J Clin Exp Med 2021; 19(1): 59-75.
[http://dx.doi.org/10.15584/ejcem.2021.1.9]
[http://dx.doi.org/10.15584/ejcem.2021.1.9]
[24]
Marzoog B. Lipid behavior in metabolic syndrome pathophysiology. Curr Diabetes Rev 2022; 18(6): e150921196497.
[http://dx.doi.org/10.2174/1573399817666210915101321]
[http://dx.doi.org/10.2174/1573399817666210915101321]
[25]
Marzoog BA. Tree of life: endothelial cell in norm and disease, the good guy is a partner in crime! Anat Cell Biol 2023; 56(2): 166-78.
[http://dx.doi.org/10.5115/acb.22.190]
[http://dx.doi.org/10.5115/acb.22.190]
[26]
Abdullah MB. Pathophysiology of cardiac cell injury in post-COVID-19 syndrome. Emir Med J 2023; 4(2): e280423216351.
[http://dx.doi.org/10.2174/0250688204666230428120808]
[http://dx.doi.org/10.2174/0250688204666230428120808]
[27]
Tang X, Li PH, Chen HZ. Cardiomyocyte senescence and cellular communications within myocardial microenvironments. Front Endocrinol 2020; 11: 280.
[http://dx.doi.org/10.3389/fendo.2020.00280]
[http://dx.doi.org/10.3389/fendo.2020.00280]
[28]
Tarragó MG, Chini CCS, Kanamori KS, et al. A potent and specific CD38 inhibitor ameliorates age-related metabolic dysfunction by reversing tissue NAD+ decline. Cell Metab 2018; 27(5): 1081-1095.e10.
[http://dx.doi.org/10.1016/j.cmet.2018.03.016]
[http://dx.doi.org/10.1016/j.cmet.2018.03.016]
[29]
Camacho-Pereira J, Tarragó MG, Chini CCS, et al. CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metab 2016; 23(6): 1127-39.
[http://dx.doi.org/10.1016/j.cmet.2016.05.006]
[http://dx.doi.org/10.1016/j.cmet.2016.05.006]
[30]
Tang X, Chen XF, Wang NY, et al. SIRT2 acts as a cardioprotective deacetylase in pathological cardiac hypertrophy. Circulation 2017; 136(21): 2051-67.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.117.028728]
[http://dx.doi.org/10.1161/CIRCULATIONAHA.117.028728]
[31]
Long AN, Owens K, Schlappal AE, Kristian T, Fishman PS, Schuh RA. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model. BMC Neurol 2015; 15(1): 19.
[http://dx.doi.org/10.1186/s12883-015-0272-x]
[http://dx.doi.org/10.1186/s12883-015-0272-x]
[32]
Yoshino J, Mills KF, Yoon MJ, Imai S. Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab 2011; 14(4): 528-36.
[http://dx.doi.org/10.1016/j.cmet.2011.08.014]
[http://dx.doi.org/10.1016/j.cmet.2011.08.014]
[33]
Yamamoto T, Byun J, Zhai P, Ikeda Y, Oka S, Sadoshima J. Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects the heart from ischemia and reperfusion. PLoS One 2014; 9(6): e98972.
[http://dx.doi.org/10.1371/journal.pone.0098972]
[http://dx.doi.org/10.1371/journal.pone.0098972]
[34]
Mills KF, Yoshida S, Stein LR, et al. Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice. Cell Metab 2016; 24(6): 795-806.
[http://dx.doi.org/10.1016/j.cmet.2016.09.013]
[http://dx.doi.org/10.1016/j.cmet.2016.09.013]
[35]
Lin Q, Zuo W, Liu Y, Wu K, Liu Q. NAD+ and cardiovascular diseases. Clin Chim Acta 2021; 515: 104-10.
[http://dx.doi.org/10.1016/j.cca.2021.01.012]
[http://dx.doi.org/10.1016/j.cca.2021.01.012]
[36]
Kondo H, Akoumianakis I, Badi I, et al. Effects of canagliflozin on human myocardial redox signalling: Clinical implications. Eur Heart J 2021; 42(48): 4947-60.
[http://dx.doi.org/10.1093/eurheartj/ehab420]
[http://dx.doi.org/10.1093/eurheartj/ehab420]
[37]
La Grotta R, Frigé C, Matacchione G, et al. Repurposing SGLT-2 inhibitors to target aging: Available evidence and molecular mechanisms. Int J Mol Sci 2022; 23(20): 12325.
[http://dx.doi.org/10.3390/ijms232012325]
[http://dx.doi.org/10.3390/ijms232012325]
[38]
Bereiter-Hahn J, Vöth M. Dynamics of mitochondria in living cells: Shape changes, dislocations, fusion, and fission of mitochondria. Microsc Res Tech 1994; 27(3): 198-219.
[http://dx.doi.org/10.1002/jemt.1070270303]
[http://dx.doi.org/10.1002/jemt.1070270303]
[39]
Zemirli N, Morel E, Molino D. Mitochondrial dynamics in basal and stressful conditions. Int J Mol Sci 2018; 19(2): 564.
[http://dx.doi.org/10.3390/ijms19020564]
[http://dx.doi.org/10.3390/ijms19020564]
[40]
Xu F, Liu C, Zhou D, Zhang L. TGF-β/SMAD pathway and its regulation in hepatic fibrosis. J Histochem Cytochem 2016; 64(3): 157-67.
[http://dx.doi.org/10.1369/0022155415627681]
[http://dx.doi.org/10.1369/0022155415627681]
[41]
Ma TT, Meng XM. TGF-β/smad and renal fibrosis. Adv Exp Med Biol 2019; 1165: 347-64.
[http://dx.doi.org/10.1007/978-981-13-8871-2_16]
[http://dx.doi.org/10.1007/978-981-13-8871-2_16]
[42]
Katsyuba E, Romani M, Hofer D, Auwerx J. NAD+ homeostasis in health and disease. Nat Metab 2020; 2(1): 9-31.
[http://dx.doi.org/10.1038/s42255-019-0161-5]
[http://dx.doi.org/10.1038/s42255-019-0161-5]
[43]
Nadeeshani H, Li J, Ying T, Zhang B, Lu J. Nicotinamide mononucleotide (NMN) as an anti-aging health product – Promises and safety concerns. J Adv Res 2022; 37: 267-78.
[http://dx.doi.org/10.1016/j.jare.2021.08.003]
[http://dx.doi.org/10.1016/j.jare.2021.08.003]
[44]
Nadtochiy SM, Wang YT, Nehrke K, Munger J, Brookes PS. Cardioprotection by nicotinamide mononucleotide (NMN): Involvement of glycolysis and acidic pH. J Mol Cell Cardiol 2018; 121: 155-62.
[http://dx.doi.org/10.1016/j.yjmcc.2018.06.007]
[http://dx.doi.org/10.1016/j.yjmcc.2018.06.007]
[45]
Marzoog BA. Systemic and local hypothermia in the context of cell regeneration. Cryo Lett 2022; 43(2): 66-73.
[http://dx.doi.org/10.54680/fr22210110112]
[http://dx.doi.org/10.54680/fr22210110112]
[46]
Marzoog BA. Autophagy behaviour in post-myocardial infarction injury. Cardiovasc Hematol Disord Targets 2023; 23(1): 2-10.
[47]
Marzoog BA, Vlasova TI. Transcription factors in deriving β cell regeneration: A potential novel therapeutic target. Curr Mol Med 2022; 22(5): 421-30.
[http://dx.doi.org/10.2174/1566524021666210712144638]
[http://dx.doi.org/10.2174/1566524021666210712144638]
[48]
Marzoog BA. Ageing increases the incidence rate of post coronary artery shunt complications. MedRxiv 2022; 2022.12.26.22283945.
[http://dx.doi.org/10.1101/2022.12.26.22283945]
[http://dx.doi.org/10.1101/2022.12.26.22283945]
[49]
Marzoog B. Anticoagulant status under COVID-19: The potential pathophysiological mechanism. J Appl Hematol 2022; 13(4): 167.
[http://dx.doi.org/10.4103/joah.joah_154_21]
[http://dx.doi.org/10.4103/joah.joah_154_21]
[50]
Segovia-Roldan M, Diez ER, Pueyo E. Melatonin to rescue the aged heart: Antiarrhythmic and antioxidant benefits. Oxid Med Cell Longev 2021; 2021: 1-18.
[http://dx.doi.org/10.1155/2021/8876792]
[http://dx.doi.org/10.1155/2021/8876792]
[51]
Lee J sook, Park AH, Lee SH, Lee SH, Kim JH, Yang SJ. Betalapachone, a modulator of NAD metabolism, prevents health declines in aged mice. PLoS One 2012; 7(10): e47122.
[http://dx.doi.org/10.1371/journal.pone.0047122]
[http://dx.doi.org/10.1371/journal.pone.0047122]
[52]
Diguet N, Trammell SAJ, Tannous C, et al. Nicotinamide riboside preserves cardiac function in a mouse model of dilated cardiomyopathy. Circulation 2018; 137(21): 2256-73.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.116.026099]
[http://dx.doi.org/10.1161/CIRCULATIONAHA.116.026099]
[53]
Yaku K, Okabe K, Nakagawa T. NAD metabolism: Implications in aging and longevity. Ageing Res Rev 2018; 47: 1-17.
[http://dx.doi.org/10.1016/j.arr.2018.05.006]
[http://dx.doi.org/10.1016/j.arr.2018.05.006]
[54]
Sagiv A, Biran A, Yon M, Simon J, Lowe SW, Krizhanovsky V. Granule exocytosis mediates immune surveillance of senescent cells. Oncogene 2013; 32(15): 1971-7.
[http://dx.doi.org/10.1038/onc.2012.206]
[http://dx.doi.org/10.1038/onc.2012.206]
[55]
Liu C, Zhang X, Hu M, et al. Metabolic targets in cardiac aging and rejuvenation. JCA 2022; 2(4): 46.
[http://dx.doi.org/10.20517/jca.2022.31]
[http://dx.doi.org/10.20517/jca.2022.31]
[56]
Abdellatif M, Sedej S, Kroemer G. NAD + metabolism in cardiac health, aging, and disease. Circulation 2021; 144(22): 1795-817.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.121.056589]
[http://dx.doi.org/10.1161/CIRCULATIONAHA.121.056589]
[57]
Soma M, Lalam SK. The role of nicotinamide mononucleotide (NMN) in anti-aging, longevity, and its potential for treating chronic conditions. Mol Biol Rep 2022; 49(10): 9737-48.
[http://dx.doi.org/10.1007/s11033-022-07459-1]
[http://dx.doi.org/10.1007/s11033-022-07459-1]
[58]
López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell 2013; 153(6): 1194-217.
[http://dx.doi.org/10.1016/j.cell.2013.05.039]
[http://dx.doi.org/10.1016/j.cell.2013.05.039]
[59]
Okabe K, Yaku K, Tobe K, Nakagawa T. Implications of altered NAD metabolism in metabolic disorders. J Biomed Sci 2019; 26(1): 34.
[http://dx.doi.org/10.1186/s12929-019-0527-8]
[http://dx.doi.org/10.1186/s12929-019-0527-8]
[60]
Sorrentino V, Romani M, Mouchiroud L, et al. Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity. Nature 2017; 552(7684): 187-93.
[http://dx.doi.org/10.1038/nature25143]
[http://dx.doi.org/10.1038/nature25143]
[61]
Gariani K, Menzies KJ, Ryu D, et al. Eliciting the mitochondrial unfolded protein response by nicotinamide adenine dinucleotide repletion reverses fatty liver disease in mice. Hepatology 2016; 63(4): 1190-204.
[http://dx.doi.org/10.1002/hep.28245]
[http://dx.doi.org/10.1002/hep.28245]
[62]
Hernandez-Segura A, Nehme J, Demaria M. Hallmarks of cellular senescence. Trends Cell Biol 2018; 28(6): 436-53.
[http://dx.doi.org/10.1016/j.tcb.2018.02.001]
[http://dx.doi.org/10.1016/j.tcb.2018.02.001]
[63]
Hong W, Mo F, Zhang Z, Huang M, Wei X. Nicotinamide mononucleotide: A promising molecule for therapy of diverse diseases by targeting NAD+ metabolism. Front Cell Dev Biol 2020; 8: 246.
[http://dx.doi.org/10.3389/fcell.2020.00246]
[http://dx.doi.org/10.3389/fcell.2020.00246]
[64]
Brown KD, Maqsood S, Huang JY, et al. Activation of SIRT3 by the NAD+ precursor nicotinamide riboside protects from noiseinduced hearing loss. Cell Metab 2014; 20(6): 1059-68.
[http://dx.doi.org/10.1016/j.cmet.2014.11.003]
[http://dx.doi.org/10.1016/j.cmet.2014.11.003]
[65]
Covarrubias AJ, Perrone R, Grozio A, Verdin E. NAD+ metabolism and its roles in cellular processes during ageing. Nat Rev Mol Cell Biol 2021; 22(2): 119-41.
[http://dx.doi.org/10.1038/s41580-020-00313-x]
[http://dx.doi.org/10.1038/s41580-020-00313-x]
[66]
Okabe K, Yaku K, Uchida Y, et al. Oral administration of nicotinamide mononucleotide is safe and efficiently increases blood nicotinamide adenine dinucleotide levels in healthy subjects. Front Nutr 2022; 9: 868640.
[http://dx.doi.org/10.3389/fnut.2022.868640]
[http://dx.doi.org/10.3389/fnut.2022.868640]
[67]
Huang H. A multicentre, randomised, double blind, parallel design, placebo controlled study to evaluate the efficacy and safety of uthever (NMN Supplement), an orally administered supplementation in middle aged and older adults. Front Aging 2022; 3: 851698.
[http://dx.doi.org/10.3389/fragi.2022.851698]
[http://dx.doi.org/10.3389/fragi.2022.851698]
[68]
Trammell SAJ, Schmidt MS, Weidemann BJ, et al. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nat Commun 2016; 7(1): 12948.
[http://dx.doi.org/10.1038/ncomms12948]
[http://dx.doi.org/10.1038/ncomms12948]
[69]
Airhart SE, Shireman LM, Risler LJ, et al. An open-label, nonrandomized study of the pharmacokinetics of the nutritional supplement nicotinamide riboside (NR) and its effects on blood NAD+ levels in healthy volunteers. PLoS One 2017; 12(12): e0186459.
[http://dx.doi.org/10.1371/journal.pone.0186459]
[http://dx.doi.org/10.1371/journal.pone.0186459]
[70]
Remie CME, Roumans KHM, Moonen MPB, et al. Nicotinamide riboside supplementation alters body composition and skeletal muscle acetylcarnitine concentrations in healthy obese humans. Am J Clin Nutr 2020; 112(2): 413-26.
[http://dx.doi.org/10.1093/ajcn/nqaa072]
[http://dx.doi.org/10.1093/ajcn/nqaa072]
[71]
Dollerup OL, Christensen B, Svart M, et al. A randomized placebocontrolled clinical trial of nicotinamide riboside in obese men: safety, insulin-sensitivity, and lipid-mobilizing effects. Am J Clin Nutr 2018; 108(2): 343-53.
[http://dx.doi.org/10.1093/ajcn/nqy132]
[http://dx.doi.org/10.1093/ajcn/nqy132]
[72]
Dollerup OL, Chubanava S, Agerholm M, et al. Nicotinamide riboside does not alter mitochondrial respiration, content or morphology in skeletal muscle from obese and insulin‐resistant men. J Physiol 2020; 598(4): 731-54.
[http://dx.doi.org/10.1113/JP278752]
[http://dx.doi.org/10.1113/JP278752]
Related Books
Frontiers in Clinical Drug Research - CNS and Neurological Disorders
Frontiers in Clinical Drug Research - CNS and Neurological Disorders
Frontiers in Clinical Drug Research - CNS and Neurological Disorders
Frontiers in Clinical Drug Research-Dementia
Frontiers in Clinical Drug Research - CNS and Neurological Disorders
