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Loại bỏ c-Jun N-terminal Kinase 1 bảo vệ chống lại các suy giảm nhận thức do chuyển hóa gây ra ở vùng hồi hải mã
Tóm tắt
Sự phát triển của những thay đổi chuyển hóa như kháng insulin đã được liên kết với sự rối loạn trong khả năng oxy hóa của ty thể, sự kích thích các phản ứng viêm thần kinh, và sự xuất hiện của các suy giảm nhận thức trong não. c-Jun N-terminal Kinase 1 (JNK1) được coi là một yếu tố điều hòa chính của những cơ chế này. Nghiên cứu hiện tại xác định hiệu ứng bảo vệ của việc loại bỏ JNK1 toàn thân trong điều kiện chế độ ăn nhiều chất béo (HFD). Cụ thể, dữ liệu cho thấy những con chuột thiếu JNK1 cho thấy sự nhạy cảm insulin và hoạt động ty thể tăng lên, cũng như giảm trọng lượng cơ thể, cùng với sự phản ứng của tế bào sao và vi khối u. Cuối cùng, những động vật này cũng được bảo vệ chống lại những suy giảm nhận thức do HFD gây ra như được đánh giá thông qua bài kiểm tra nhận dạng đối tượng mới, quan sát các gai nhánh, và các mức độ của BDNF hoặc các protein khác như spinophilin và ARC. Do đó, việc điều chỉnh hoạt động của JNK1 dường như là một cách tiếp cận đầy hứa hẹn cho việc thiết kế các liệu pháp nhằm điều trị các suy giảm nhận thức do chuyển hóa gây ra.
Từ khóa
#JNK1 #kháng insulin #suy giảm nhận thức #ty thể #phản ứng viêm thần kinh #BDNF #chế độ ăn nhiều chất béoTài liệu tham khảo
Gauthier S, Reisberg B, Zaudig M, Petersen RC, Ritchie K, Broich K, Belleville S, Brodaty H, Bennett D, Chertkow H, Cummings JL, de Leon M, Feldman H, Ganguli M, Hampel H, Scheltens P, Tierney MC, Whitehouse P, Winblad B, International Psychogeriatric Association Expert Conference on mild cognitive impairment (2006) Mild cognitive impairment. Lancet 367(9518):1262–1270
Drzezga A, Lautenschlager N, Siebner H, Riemenschneider M, Willoch F, Minoshima S, Schwaiger M, Kurz A (2003) Cerebral metabolic changes accompanying conversion of mild cognitive impairment into Alzheimer’s disease: a PET follow-up study. Eur J Nucl Med Mol Imaging 30(8):1104–1113
Mergenthaler P, Lindauer U, Dienel GA, Meisel A (2013) Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci 36(10):587–597
Belgardt BF, Mauer J, Brüning JC (2010) Novel roles for JNK1 in metabolism. Aging (Albany NY) 2(9):621–626
De Felice FG, Lourenco MV (2015) Brain metabolic stress and neuroinflammation at the basis of cognitive impairment in Alzheimer’s disease. Front Aging Neurosci 7(May):1–8
Grillo CA, Piroli GG, Lawrence RC, Wrighten SA, Green AJ, Wilson SP, Sakai RR, Kelly SJ, Wilson MA, Mott DD, Reagan LP (2015) Hippocampal insulin resistance impairs spatial learning and synaptic plasticity. Diabetes 64(11):3927–3936
Henneberg N, Hoyer S (1995) Desensitization of the neuronal insulin receptor: a new approach in the etiopathogenesis of late-onset sporadic dementia of the Alzheimer type (SDAT)? Arch Gerontol Geriatr 21(1):63–74
Hoyer S, Henneberg N, Knapp S, Lannert H, Martin E (1996) Brain glucose metabolism is controlled by amplification and desensitization of the neuronal insulin receptor. Ann N Y Acad Sci 17(777):374–379
de la Monte SM, Wands JR (2008) Alzheimer’s disease is type 3 diabetes-evidence reviewed. J Diabetes Sci Technol 2(6):1101–1113
Steen E, Terry BM, Rivera EJ, Cannon JL, Neely TR, Tavares R et al (2005) Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease – is this type 3 diabetes? J Alzheimers Dis 7:63–80
Sabapathy K (2012) Role of the JNK Pathway in human diseases. 1st ed. Vol. 106, Progress in Molecular Biology and Translational Science. Elsevier Inc., pp 145–169
Araujo EP, De Souza CT, Bordin S, Zollner RL, Saad MJA, Velloso LA et al (2005) Consumption of a fat-rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus. Endocrinology 146(10):4192–4199
Prada PO, Zecchin HG, Gasparetti AL, Torsoni MA, Ueno M, Hirata AE et al (2005) Western diet modulates insulin signaling, c-jun N-terminal kinase activity, and insulin receptor substrate-1 ser307 phosphorylation in a tissue-specific fashion. Endocrinology 146(3):1576–1587
Sabio G, Davis RJ (2010) CJun NH2-terminal kinase 1 (JNK1): roles in metabolic regulation of insulin resistance. Trends Biochem Sci 35(9):490–496
Mohammad H, Marchisella F, Ortega-Martinez S, Hollos P, Eerola K, Komulainen E, Kulesskaya N, Freemantle E, Fagerholm V, Savontaus E, Rauvala H, Peterson BD, van Praag H, Coffey ET (2018) JNK1 controls adult hippocampal neurogenesis and imposes cell-autonomous control of anxiety behaviour from the neurogenic niche. Mol Psychiatry 23(2):362–374
Grivennikov S, Vilcu C, Naugler W, Wynshaw-Boris A, Solinas G, Luo J-L et al (2007) JNK1 in hematopoietically derived cells contributes to diet-induced inflammation and insulin resistance without affecting obesity. Cell Metab 6(5):386–397
Becattini B, Zani F, Breasson L, Sardi C, D’Agostino VG, Choo MK et al (2016) JNK1 ablation in mice confers long-term metabolic protection from diet-induced obesity at the cost of moderate skin oxidative damage. FASEB J 30(9):3124–3132
Solinas G, Karin M (2010) JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction. FASEB J 24(8):2596–2611
de Lemos L, Junyent F, Camins A, Castro-Torres RD, Folch J, Olloquequi J, Beas-Zarate C, Verdaguer EAC (2017) Neuroprotective effects of the absence of JNK1 or JNK3 isoforms on kainic acid-induced temporal lobe epilepsy-like symptoms. Mol Neurobiol
Sabio G, Cavanagh-Kyros J, Jin Ko H, Young Jung D, Gray S, Jun JY et al (2009) Prevention of steatosis by hepatic JNK1. Cell Metab 10(6):491–498
Sabio G, Kennedy NJ, Cavanagh-Kyros J, Jung DY, Ko HJ, Ong H, Barrett T, Kim JK, Davis RJ (2010) Role of muscle c-Jun NH2-terminal kinase 1 in obesity-induced insulin resistance. Mol Cell Biol 30(1):106–115
Sabio G, Das M, Mora A, Zhang Z, Jun JY, Hwi JK et al (2008) A stress signaling pathway in adipose tissue regulates hepatic insulin resistance. Science (80- ) 322(5907):1539–1543
Belgardt BF, Mauer J, Wunderlich FT, Ernst MB, Pal M, Spohn G et al (2010) Hypothalamic and pituitary c-Jun N-terminal kinase 1 signaling coordinately regulates glucose metabolism. Proc Natl Acad Sci 107(13):6028–6033
Sabio G, Cavanagh-Kyros J, Barrett T, Jung DY, Ko HJ, Ong H, Morel C, Mora A, Reilly J, Kim JK, Davis RJ (2010) Role of the hypothalamic-pituitary-thyroid axis in metabolic regulation by JNK1. Genes Dev 24(3):256–264
Dong C, Yang DD, Wysk M, Whitmarsh AJ, Davis RJ, Flavell RA (1998) Defective T cell differentiation in the absence of Jnk1. Science. 5396(282):2092–2095
Busquets O, Eritja À, López BM, Ettcheto M, Manzine PR, Castro-Torres RD et al (2019) Role of brain c-Jun N-terminal kinase 2 in the control of the insulin receptor and its relationship with cognitive performance in a high-fat diet preclinical model. J Neurochem 149(2):161–310
Bevins RA, Besheer J (2006) Object recognition in rats and mice: a one-trial non-matching-to-sample learning task to study “recognition memory”. Nat Protoc 1(3):1306–1311
González-Reyes RE, Aliev G, Avila-Rodrigues M, Barreto GE (2016) Alterations in glucose metabolism on cognition: a possible link between diabetes and dementia. Curr Pharm Des 22(7):812–818
Yang ZH, Miyahara H, Takeo J, Katayama M (2012) Diet high in fat and sucrose induces rapid onset of obesity-related metabolic syndrome partly through rapid response of genes involved in lipogenesis, insulin signalling and inflammation in mice. Diabetol Metab Syndr 4(1):1–10
Morrison CD, Huypens P, Stewart LK, Gettys TW (2009) Implications of crosstalk between leptin and insulin signaling during the development of diet-induced obesity. Biochim Biophys Acta - Mol Basis Dis 1792(5):409–416
Thon M, Hosoi T, Ozawa K (2016) Possible integrative actions of leptin and insulin signaling in the hypothalamus targeting energy homeostasis. Front Endocrinol (Lausanne) 7(OCT):1–7
Bastard J-P, Maachi M, Lagathu C, Kim MJ, Caron M, Vidal H et al (2006) Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur Cytokine Netw 17(1):4–12
De La Monte SM, Tong M, Nguyen V, Setshedi M, Longato L, Wands JR (2010) Ceramide-mediated insulin resistance and impairment of cognitive-motor functions. J Alzheimers Dis 21(3):967–984
García-Ruiz I, Solís-Muñoz P, Fernández-Moreira D, Grau M, Colina F, Muñoz-Yagüe T et al (2014) High-fat diet decreases activity of the oxidative phosphorylation complexes and causes nonalcoholic steatohepatitis in mice. Dis Model Mech 7(11):1287–1296
Jodeiri Farshbaf M, Ghaedi K, Megraw TL, Curtiss J, Shirani Faradonbeh M, Vaziri P, Nasr-Esfahani MH (2016) Does PGC1α/FNDC5/BDNF elicit the beneficial effects of exercise on neurodegenerative disorders? NeuroMolecular Med 18(1):1–15
Garcia-Fuentes E, Murri M, Garrido-Sanchez L, Garcia-Serrano S, García-Almeida JM, Moreno-Santos I et al (2010) PPARγ expression after a high-fat meal is associated with plasma superoxide dismutase activity in morbidly obese persons. Obesity 18(5):952–958
Hardwick JP, Eckman K, Lee YK, Abdelmegeed MA, Esterle A, Chilian WM et al (2013) Eicosanoids in metabolic syndrome. Adv Pharmacol 66:157–266
Wisse BE (2004) The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity. J Am Soc Nephrol 15(11):2792–2800
Norden DM, Trojanowski PJ, Villanueva E, Navarro E, Godbout JP (2016) Sequential activation of microglia and astrocyte cytokine expression precedes increased Iba-1 or GFAP immunoreactivity following systemic immune challenge. Glia. 64(2):300–316
Chen WW, Zhang X, Huang WJ (2016) Role of neuroinflammation in neurodegenerative diseases (review). Mol Med Rep 13(4):3391–3396
Amor S, Peferoen LAN, Vogel DYS, Breur M, van der Valk P, Baker D, van Noort J (2014) Inflammation in neurodegenerative diseases - an update. Immunology. 142(2):151–166
Busquets O, Ettcheto M, Pallàs M, Beas-Zarate C, Verdaguer E, Auladell C, Folch J, Camins A (2017) Long-term exposition to a high fat diet favors the appearance of β-amyloid depositions in the brain of C57BL/6J mice. A potential model of sporadic Alzheimer’s disease. Mech Ageing Dev 162:38–45
Solinas G, Becattini B (2017) JNK at the crossroad of obesity, insulin resistance, and cell stress response. Mol Metab 6(2):174–184
Freeman LR, Haley-Zitlin V, Rosenberger DS, Granholm A-C (2014) Damaging effects of a high-fat diet to the brain and cognition: a review of proposed mechanisms. Nutr Neurosci 17(6):241–251
Shaw AE, Bamburg JR (2017) Peptide regulation of cofilin activity in the CNS: a novel therapeutic approach for treatment of multiple neurological disorders. Pharmacol Ther 175:17–27
Busquets O, Ettcheto M, Verdaguer E, Castro-Torres RD, Auladell C, Beas-Zarate C et al (2018) JNK1 inhibition by licochalcone A leads to neuronal protection against excitotoxic insults derived of kainic acid. Neuropharmacology 131:440–452
Copps KD, Hancer NJ, Opare-Ado L, Qiu W, Walsch C, White MF (2010) Irs1 serine 307 promotes insulin sensitivity in mice Kyle. Cell Metab 11(1):84–92
Hotamisligil GS, Peraldi P, Budavari A, Ellis R, White MF, Spiegelman BM (1996) IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-α- and obesity-induced insulin resistance. Science (80- ) 271(5249):665–670
Cordner ZA, Tamashiro KLK (2015) Effects of high-fat diet exposure on learning & memory. Physiol Behav 152:363–371