{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,31]],"date-time":"2023-10-31T11:12:08Z","timestamp":1698750728356},"reference-count":64,"publisher":"Akademiai Kiado Zrt.","issue":"33","content-domain":{"domain":["akjournals.com"],"crossmark-restriction":true},"short-container-title":["OH"],"published-print":{"date-parts":[[2021,8,15]]},"abstract":"<jats:p><jats:bold>\u00d6sszefoglal\u00f3.<\/jats:bold> Az emberek a lehet\u0151 leghosszabb ideig akarnak \u00e9lni, j\u00f3\n                    eg\u00e9szs\u00e9gben. Ha kik\u00fcsz\u00f6b\u00f6ln\u00e9nk a kedvez\u0151tlen k\u00fcls\u0151 k\u00f6r\u00fclm\u00e9nyeket, a v\u00e1rhat\u00f3\n                    \u00e9lettartam meghaladhatn\u00e1 a 100 \u00e9vet. A 20. \u00e9s 21. sz\u00e1zadban a j\u00f3l\u00e9ti\n                    t\u00e1rsadalmakban a v\u00e1rhat\u00f3 \u00e9lettartam jelent\u0151sen megn\u0151tt, \u00edgy Magyarorsz\u00e1gon is.\n                    Az \u00e1ttekintett irodalom alapj\u00e1n megvizsg\u00e1ltuk, hogy a genetika \u00e9s az \u00f6r\u00f6kl\u0151d\u00e9s\n                    mellett milyen endokrinol\u00f3giai \u00e9s metabolikus t\u00e9nyez\u0151k j\u00e1tszanak szerepet az\n                    \u00e9let meghosszabb\u00edt\u00e1s\u00e1ban. Megvizsg\u00e1ltunk minden endog\u00e9n t\u00e9nyez\u0151t, amely\n                    pozit\u00edvan vagy negat\u00edvan befoly\u00e1solhatja az \u00e9letkorral \u00f6sszef\u00fcgg\u0151 betegs\u00e9geket\n                    (Alzheimer-k\u00f3r, sz\u00edv- \u00e9s \u00e9rrendszeri betegs\u00e9gek, r\u00e1k) \u00e9s az \u00e9lettartamot.\n                    Kiemelt\u00fck a hyperinsulinaemia, az inzulinrezisztencia, a metabolikus szindr\u00f3ma\n                    \u00f6reged\u00e9st gyors\u00edt\u00f3 hat\u00e1s\u00e1t, az inzulinszer\u0171 n\u00f6veked\u00e9si hormon-1 ellentmond\u00e1sos\n                    szerep\u00e9t, valamint az \u00e9let meghosszabb\u00edt\u00e1s\u00e1ban r\u00e9szt vev\u0151, \u00fajabban felfedezett\n                    peptideket, mint a klotho \u00e9s a humanin. Ismertett\u00fck a mitochondriumok szerep\u00e9t\n                    az \u00e9lettartam meghat\u00e1roz\u00e1s\u00e1ban, bemutattuk a mitohormesis folyamat\u00e1t \u00e9s annak\n                    stresszv\u00e9d\u0151 funkci\u00f3j\u00e1t. Bemutattuk a rapamicin c\u00e9lszerv\u00e9t, az mTOR-t, amelynek\n                    g\u00e1tl\u00e1sa meghosszabb\u00edtja az \u00e9lettartamot, valamint a szirtuinokat. Kit\u00e9rt\u00fcnk az\n                    autophagia folyamat\u00e1ra, \u00e9s ismertett\u00fck a szenolitikumok szerep\u00e9t az \u00f6reged\u00e9sben.\n                    Az id\u0151skori autoimmunit\u00e1s cs\u00f6kken\u00e9se hozz\u00e1j\u00e1rul az \u00e9lettartam r\u00f6vid\u00fcl\u00e9s\u00e9hez,\n                    utaltunk a thymus koordin\u00e1l\u00f3 szerep\u00e9re. Kiemelt\u00fck a b\u00e9lmikrobiom fontos szerep\u00e9t\n                    az \u00e9lettartam szab\u00e1lyoz\u00e1s\u00e1ban. Hivatkoztunk a \u201ecenten\u00e1riusok\u201d megfigyel\u00e9s\u00e9b\u0151l\n                    nyert hum\u00e1nadatokra. Megvizsg\u00e1ltuk, milyen beavatkoz\u00e1si lehet\u0151s\u00e9gek \u00e1llnak\n                    rendelkez\u00e9sre az eg\u00e9szs\u00e9gben t\u00f6lthet\u0151 \u00e9lettartam meghosszabb\u00edt\u00e1s\u00e1hoz. Az\n                    \u00e9letm\u00f3dbeli lehet\u0151s\u00e9gek k\u00f6z\u00fcl kiemelt\u00fck a kal\u00f3riabevitel-cs\u00f6kkent\u00e9s \u00e9s a\n                    testmozg\u00e1s j\u00f3t\u00e9kony szerep\u00e9t. Megvizsg\u00e1ltuk egyes gy\u00f3gyszerek felt\u00e9telezett\n                    hat\u00e1sait. Ezek k\u00f6z\u00e9 tartozik a metformin, az akarb\u00f3z, a rezveratrol. E\n                    gy\u00f3gyszerek mindegyik\u00e9nek hat\u00e1sa hasonl\u00f3 a kal\u00f3riamegszor\u00edt\u00e1s\u00e9hoz. Nincs olyan\n                    \u201ecsodaszer\u201d, amely igazoltan meghosszabb\u00edtja az \u00e9lettartamot emberben. Egyes\n                    g\u00e9neknek \u00e9s g\u00e9nmut\u00e1ci\u00f3knak j\u00f3t\u00e9kony hat\u00e1suk van, de ezt k\u00f6rnyezeti t\u00e9nyez\u0151k,\n                    betegs\u00e9gek, balesetek \u00e9s m\u00e1s k\u00fcls\u0151 \u00e1rtalmak m\u00f3dos\u00edthatj\u00e1k. Kiemelj\u00fck az elh\u00edz\u00e1s,\n                    az alacsony fokozat\u00fa gyullad\u00e1s \u00e9s az inzulinrezisztencia \u00f6reged\u00e9sre gyakorolt\n                    gyors\u00edt\u00f3 hat\u00e1s\u00e1t. A metabolikus szindr\u00f3ma elterjedts\u00e9ge miatt ez jelent\u0151s\n                    n\u00e9peg\u00e9szs\u00e9g\u00fcgyi kock\u00e1zatot jelent. Az inzulin, a n\u00f6veked\u00e9si hormon \u00e9s az\n                    inzulinszer\u0171 n\u00f6veked\u00e9si faktorok hat\u00e1sainak \u00e9rt\u00e9kel\u00e9se tov\u00e1bbra is\n                    ellentmond\u00e1sos. Az eg\u00e9szs\u00e9ges, szellemileg \u00e9s fizikailag akt\u00edv \u00e9letm\u00f3d, a\n                    kal\u00f3riacs\u00f6kkent\u00e9s mindenk\u00e9ppen el\u0151ny\u00f6s. Az \u00e9letet meghosszabb\u00edt\u00f3 szerek\n                    \u00e9rt\u00e9kel\u00e9se m\u00e9g vitatott. Orv Hetil. 2021; 162(33): 1318\u20131327.<\/jats:p>\n                <jats:p><jats:bold>Summary.<\/jats:bold> People want to live as long as possible in good health. If\n                    we eliminate the unfavorable external conditions, the life expectancy could\n                    exceed 100 years. In the 20th and 21th centuries, life expectancy in welfare\n                    societies increased significantly, including in Hungary. Based on the reviewed\n                    literature, we examined what endocrinological and metabolic factors play a role\n                    in prolonging life in addition to genetics and inheritance. We examined all\n                    endogenous factors that can positively or negatively affect age-related diseases\n                    (Alzheimer\u2019s disease, cardiovascular disease, cancer) and longevity. We\n                    highlighted the aging effects of hyperinsulinemia, insulin resistance, metabolic\n                    syndrome, the controversial role of insulin-like growth factor-1, and more\n                    recently discovered peptides involved in prolonging lifespan, such as klotho and\n                    humanin. We described the role of mitochondria in determining longevity, we\n                    demonstrated the process of mitohormesis and its stress-protective function. We\n                    presented the target organ of rapamycin, mTOR, the inhibition of which prolongs\n                    lifespan, as well as sirtuins. We covered the process of autophagy and described\n                    the role of senolytics in aging. The decrease in autoimmunity in old age\n                    contributes to the shortening of life expectancy, we referred to the\n                    coordinating role of the thymus. We highlighted the important role of intestinal\n                    microbiome in the regulation of longevity. We referred to human data obtained\n                    from observations on \u201ccentenarians\u201d. We examined what intervention options are\n                    available to prolong healthy life expectancy. Among the lifestyle options, we\n                    highlighted the beneficial role of calorie reduction and exercise. We examined\n                    the putative beneficial effects of some drugs. These include metformin,\n                    acarbose, resveratrol. The effect of each of these drugs is similar to calorie\n                    restriction. There is no \u201cmiracle cure\u201d that has been shown to prolong life-span\n                    in humans. Some genes and gene mutations have beneficial effects, but this can\n                    be modified by environmental factors, diseases, accidents, and other external\n                    harms. We highlight the accelerating effects of obesity, low-grade inflammation,\n                    and insulin resistance on aging. Due to the prevalence of metabolic syndrome,\n                    this poses a significant risk to public health. The assessment of the effects of\n                    insulin, growth hormone, and insulin-like growth factors remains controversial.\n                    A healthy, mentally and physically active lifestyle, calorie reduction is\n                    definitely beneficial. The evaluation of life-prolonging agents is still\n                    controversial. Orv Hetil. 2021; 162(33): 1318\u20131327.<\/jats:p>","DOI":"10.1556\/650.2021.32200","type":"journal-article","created":{"date-parts":[[2021,8,31]],"date-time":"2021-08-31T10:06:01Z","timestamp":1630404361000},"page":"1318-1327","update-policy":"http:\/\/dx.doi.org\/10.1556\/policypage.crossmark.crossref.1","source":"Crossref","is-referenced-by-count":1,"title":["Endokrinol\u00f3giai t\u00e9nyez\u0151k \u00e9s metabolikus folyamatok szerepe az \u00e9lettartam szab\u00e1lyoz\u00e1s\u00e1ban"],"prefix":"10.1556","volume":"162","author":[{"given":"Tam\u00e1s","family":"Halmos","sequence":"first","affiliation":[{"name":"1 MAZSIHISZ Szeretetk\u00f3rh\u00e1z, Metabolikus Ambulancia, Budapest"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ilona","family":"Suba","sequence":"additional","affiliation":[{"name":"2 Bajcsy-Zsilinszky K\u00f3rh\u00e1z \u00e9s Rendel\u0151int\u00e9zet, T\u00fcd\u0151gondoz\u00f3 Int\u00e9zet, Budapest"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"425","reference":[{"key":"ref0","doi-asserted-by":"publisher","first-page":"1246","DOI":"10.1038\/s41591-018-0092-9","article-title":"Senolytics improve physical function and increase lifespan in old age","volume":"24","author":"1 Xu","year":"2018","unstructured":"1 Xu M, Pirtskhalava T, Farr JN, et al. 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J Transl Med. 2016; 14: 3.","journal-title":"J Transl Med"},{"key":"ref21","doi-asserted-by":"publisher","first-page":"109","DOI":"10.14336\/AD.2014.0305","article-title":"Metabolic syndrome, aging and involvement of oxidative stress","volume":"6","author":"22 Bonomini","year":"2015","unstructured":"22 Bonomini F, Rodella LF, Rezzani R. Metabolic syndrome, aging and involvement of oxidative stress. Aging Dis. 2015; 6: 109-120.","journal-title":"Aging Dis"},{"key":"ref22","doi-asserted-by":"publisher","first-page":"1031","DOI":"10.1093\/gerona\/glz061","article-title":"An elephant in ageing research","volume":"74","author":"23 Cheikhi","year":"2019","unstructured":"23 Cheikhi A, Barchowsky A, Sahu A, et al. An elephant in ageing research. J Gerontol A Biol Sci Med Sci. 2019; 74: 1031-1042.","journal-title":"J Gerontol A Biol Sci Med Sci"},{"key":"ref23","doi-asserted-by":"publisher","unstructured":"24 Olejnik A, Franczak A, Krzywonos-Zavadska A, et al. Corrigendum to \"The biological role of klotho protein in the development of cardiovascular diseases\". Biomed Res Int. 2020; 2020: 1463925. [Erratum: Biomed Res Int. 2018; 2018: 5171945.]","DOI":"10.1155\/2020\/1463925"},{"key":"ref24","doi-asserted-by":"publisher","first-page":"37","DOI":"10.1186\/s13045-017-0391-5","article-title":"Klotho, an anti-aging gene, acts as a tumor suppressor and inhibitor of IGF-1R signaling in diffuse large B cell lymphoma","volume":"10","author":"25 Zhou","year":"2017","unstructured":"25 Zhou X, Fang X, Jiang Y, et al. Klotho, an anti-aging gene, acts as a tumor suppressor and inhibitor of IGF-1R signaling in diffuse large B cell lymphoma. J Hematol Oncol. 2017; 10: 37.","journal-title":"J Hematol Oncol"},{"key":"ref25","doi-asserted-by":"publisher","first-page":"21","DOI":"10.1016\/j.ghir.2016.03.005","article-title":"Humanin: functional interface with IGF-I","volume":"29","author":"26 Xiao","year":"2016","unstructured":"26 Xiao J, Kim SJ, Cohen P, et al. Humanin: functional interface with IGF-I. Growth Horm IGF Res. 2016; 29: 21-27.","journal-title":"Growth Horm IGF Res"},{"key":"ref26","doi-asserted-by":"publisher","first-page":"14212","DOI":"10.1038\/s41598-018-32616-7","article-title":"Humanin prevents age-related cognitive decline in mice and is associated with improved cognitive age in humans","volume":"8","author":"27 Yen","year":"2018","unstructured":"27 Yen K, Wan J, Mehta HH, et al. Humanin prevents age-related cognitive decline in mice and is associated with improved cognitive age in humans. Sci Rep. 2018; 8: 14212.","journal-title":"Sci Rep"},{"key":"ref27","doi-asserted-by":"publisher","first-page":"123","DOI":"10.3389\/fnagi.2019.00123","article-title":"Humanin, a mitochondrial-derived peptide, released by astrocytes, prevents synapse loss in hippocampal neurons","volume":"11","author":"28 Z\u00e1rate","year":"2019","unstructured":"28 Z\u00e1rate SC, Traetta ME, Codagnone MC, et al. Humanin, a mitochondrial-derived peptide, released by astrocytes, prevents synapse loss in hippocampal neurons. Front Aging Neurosci. 2019; 11: 123.","journal-title":"Front Aging Neurosci"},{"key":"ref28","doi-asserted-by":"publisher","first-page":"11185","DOI":"10.18632\/aging.103534","article-title":"The mitochondrial derived peptide humanin is a regulator of lifespan and healthspan","volume":"12","author":"29 Yen","year":"2020","unstructured":"29 Yen K, Mehta HH, Kim SJ. The mitochondrial derived peptide humanin is a regulator of lifespan and healthspan. 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