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▎ Wetin na Semaglutid?
semaglutid na lכng akt glukagon lεk pεptida-1 (GLP-1) rεsεpכta agonist we de εkstεnd di haf layf fכ nεchכral GLP-1 tru strכkchכral modifyushכn. i de miks di fysiolojikal ifekt dεm we GLP-1 de gi, i de protεkt insulin sekreshכn insay wan we we dipεnd pan glukכs, i de inhibit glukagon rilis, delay di gεstrik εmpti, εn i de εnhans satiety. I de kɔntrol di blɔd glukɔs lɛvɛl fayn fayn wan pan di wan dɛn we gɛt tayp 2 mɛtabolism, i de ridyus di bɔdi wet bad bad wan pan pipul dɛn we fat ɔ we gɛt bɔku bɔku bɔdi, ɛn i de ridyus di risk fɔ gɛt tin dɛn we kin apin to dɛn at ɛn blɔd. Na pεptida we gεt tu bεnεfit dεm fכ kכntrכl glukכs na di bכdi, fכ lכs wet, εn pכtεnshal protεkshכn fכ di kכdivaskyul.
▎ Di Strukchɔ we di Semaglutid gɛt
Sos: Pub Chem., ɛn ɔda pipul dɛn |
Sikεns: His-Aib-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Val-Sεr-Sεr-Tyr-Lyu-Glu-Gly-Gln-Ala-Ala-Lys (Aeea-Aeea-γ-glu-oktadekanedioik)-Glu-Phe-Ile-Ala-Trp-Lyu-Val-Arg-Gly-Arg-Gly-OH Mɔlikul Fɔmula: C 187H 291N 45O59 Molikul Weyt: 4114 g/mol CAS Nɔmba 910463-68-2 PubChem CID 56843331. Di wan dɛn we de wok Di tin dɛn we gɛt di sem minin: Rybelsus; Ozempic we dɛn kɔl ; Wegovy we de na di wɔl |
▎ Semaglutid Risach
Wetin na di risach bakgrɔn fɔ Semaglutid?
di divεlכpmεnt fכ Semaglutid kכmכt frכm di εksplכreshכn fכ GLP-1 in fysiolojikal ifekt dεm. Sayɛnsman dɛn bin inspɛkt exendin-4 insay lizad saliva fɔ divɛlɔp di fɔs jɛnɛreshɔn GLP-1 riseptɔ agonist. fכ pursyu wan lכng-akt tritmεnt opshכn, dεn divεlכp Semaglutid tru kεmikכl modifyushכn fכ di GLP-1 pεptida chen, wit di adishכn fכ fεt asid chen fכ εksεnd in haf-layf. As di risach bin de go bifo, i bin de sho bak se i ebul fɔ lɔs yu wet ɛn fɔ mek yu nɔ gɛt sik dɛn we de ambɔg yu at ɛn blɔd ɛn fɔ trit yu.
Wetin na di we aw Semaglutid de wok?
Rεgulεshכn fכ insulin εn glukagon sekreshכn:
as GLP-1 rεsεpכta agonist (GLP-1 RA), Semaglutid de stimulat pankrεas β-sεl dεm fכ sekret insulin we i de inhεbit α-sεl dεm fכ sekret glukagon. afta yu it, we di glukכs lεvεl na di bכdi go כp, di sεmaglutayd de biεn di GLP-1 rεsεpכta dεm, we de aktibכt di dכwnstrim signal path dεm fכ mek di β sεl dεm rilis insulin, we de mek di bכdi tek εn yutilize glukכs, εn i de lכs di blכd glukכs lεvεl. bay we i de inhibit glukagon sekreshכn εn ridyus di hεpatik glukכs autput, i de stεbyul di bכdi glukכs lεvεl mכr. כnda nכmal fysiolojikal kכndishכn dεm, di bכdi de mεnten stebul bכdi glukכs lεvεl bay we i de rεgεl di bεlε bitwin insulin εn glukagon. Semaglutid de miks di ifekt dεm we GLP-1 de gi, we de optimiz dis rεgεdyushכn prכsεs [1,2]..

Figure 1 Di mεtabolism- εn כbisiti-rεlatεd ifekt dεm fכ GLP-1 [3] ..
Inhibishכn fכ di hεpatik glukonεojεnεsis:
semaglutid de inhεbit di hεpatik glukonεojεnεsis prכsεs. Gluconeogenesis na di rod we di liva de mek glukoz we i de fast ɔ we i de angri, we de mek di blɔd glukɔs stebul we di blɔd glukɔs lɛvɛl smɔl. כltu, insay patכlayz kכndishכn dεm lεk mεtabolism, glukoneojεnεsis kin bi כva aktif, we kin mek di blכd glukכs lεvεl dεm go εlevεt. semaglutid de akt pan rilevεnt signal path dεm fכ ridyus di εksprεshכn כ aktvכti fכ di ki gluconeogenesis εnzym dεm, we de mek di hεpatik glukכs prodakshכn dכn εn i de εp fכ kכntrכl di glukכs na di bכdi [1]..
Efεkt dεm pan εnεji mεtabolism εn apɛtit:
Semaglutid gεt rεgεdyushכn ifekt pan εnεji mεtabolism εn apεtit. i de ridyus di enεji we yu de it, we kin bi bay we i de akt pan di sεntri nεv sεstem fכ infכlכ di apεtit rεguleshכn sεnta dεm, we de mek yu fil fכ ful εn ridyus di it we i de it. apat frכm dat, Semaglutid gεt sכm ifekt pan di εnεji we i de spεnd, fכs fכ rich di wet rεgulεshכn tru di rεdכks εnεji intayk, we de εp fכ lכs di wet fכ di wan dεm we fat. Insay trayal, di pasɛnt dɛn we de yuz Semaglutid kin ripɔt bɔku tɛm se dɛn nɔ kin want fɔ it ɛn dɛn kin lɔs dɛn wet afta dat [1,4]..
di pכtεnshal mεkanism dεm fכ akshכn pan di kכdivaskyul sistεm: Semaglutid kin εksyεrt bεnεfit ifekt pan di kכdivaskyul sistεm tru mכltipכl mεkanism dεm. Na wan say, i kin mek di glukɔs na di blɔd ɛn di bɔdi wet dɔŋ, ɛn dis kin mek di damej we di mɛtabolik disɔda kin kam wit di at ɛn di blɔd sistɛm nɔ bɔku. na di כda say, Semaglutid kin akt dayrekt pan di kכdivaskyul tisu dεm, lεk fכ impruv di vaskulεr εndoteyl fכnshכn, ridyus inflammatory rεspכns εn כksidεtiv strεs, stεbyul di atεrosklεrotik plek dεm, εn lכs di risk fכ kכdivaskyul sik dεm. di risach we Cigrovski du sho se Semaglutid kin impruv di wok we di vaskulכr εndoteyl sεl dεm de du fכ sekret naytrik כksid, εnhans vasodilayshכn, εn protεkt di kכdivaskyul sistεm [5]..
Dairekt ifekt pan di kadyak fכnshכn:
stכdi dεm we dεn jכs du dεn fכnshכn se akyu εkspכzכn to Semaglutid kin indyuz wan dכz-dipεndεnt strכng positifu inotropik ifekt pan hכman atrial trabekula dεm we nכ de inkrεs di tεndens fכ aritmia. dis ifekt kin kכmכt frכm inkrεs pan sarcoplasmic reticulum Ca2+ riuptek, impruv atrial fכnshכn, εn i de hכld pכsitiv implεkshכn fכ simptom rilif in hat fεil pasεnshכn dεm. insay riletid εkspεriεns, atrial trabekul dεm we dεn εkspכz to Semaglutid sho sכmtεm εnhans kכntraktil fכs witout inkrεs pan aritmia [6]..
Wetin na di aplikeshɔn dɛn fɔ Semaglutid?
Fɔ tayp 2 mɛtabolism:
Dɛn kin yuz semaglutid fɔ trit tayp 2 mɛtabolism. Ilɛksɛf dɛn gi am bay mɔt ɔ bay we dɛn gi am injɛkshɔn ɔnda di bɔdi, i kin rili mek di ɛmoglobin A1c (HbA1c) lɛvɛl go dɔŋ [1]..
Fɔ tritmɛnt fɔ di wan dɛn we fat:
Semaglutid de sho se i gɛt impɔtant ɛfifikɛshɔn fɔ trit pɔsin we fat pasmak. Klinik trayal dεm sho se di wan dεm we fat we dεn trit wit semaglutide kin gεt bכku weit lכs, we kin kam wit rεdכks di wεst sεkshכn, impruv di blכd prεshכn paramita, lכw HbA1c lεvεl, εn impruv lipid profayl (εgz., rεdכks tכtal kכlestכl, lכw-dεnsiti lipoprotein kכlestכl, εn triglisεrayd, εn inkrεs hεy-dεnsiti lipoprotein kכlestכl). di ifekt dεm we i de du fכ lכs wet bεtε pas di wan dεm we de fכ plasebo εn כda mεdikeshכn dεm fכ lכs wet, i de mit di standad dεm we di EMA εn FDA dεn put fכ mεdikeshכn dεm we de lכs wet, εn i de gi nyu tritmεnt opshכn fכ di wan dεm we fat [1,2]..
Ridyus risk fɔ gɛt sik dɛn we de ambɔg di at ɛn di blɔd:
Fɔ big pipul dɛm we gɛt tayp 2 mɛtabolism ɛn we dɛn no se gɛt at sik, Semaglutid kin ridyus di risk fɔ gɛt sik na dɛn at ɛn blɔd. Stɔdi dɛm lɛk di SUSTAIN 6 ɛn PIONEER 6 trayal dɛn sho se i nɔ infɛriɔriti ɛn sef fɔ Sabkyutan ɛn ɔral Semaglutid insay di at ɛn di blɔd wɛlbɔdi, ɛn di SELECT trayal kɔnfyus mɔ in pɔtɛnɛshɛl advantej fɔ impɔtant di kadiovaskular autkam, ɛp fɔ ridyus di risk fɔ di kadivaskular ivin dɛm [1]..
Di tin dɛn we kin mek pɔsin protɛkt di rεnal:
In wan maws mכdel fכ rεnal ischemia-rεpεrfyushכn injuri, Semaglutid dεn sho rεnal prכtektiv ifekt dεm. i de ridyus di lεvεl dεm fכ inflammatory mכlikul dεm lεk tumor nεkrכsis fכktכ-α (TNF-α) εn in rεsεpכta, intalyukin-6 (IL-6), i de dכn di F8 prostaglandin prodakshכn, i de inkrεs di PI3K εn AKT lεvεl dεm na di rεnal tisu, εn i de mek di rεnal injuri, we de sho se Semaglutid kin gεt tεrapi pכtεnshal fכ akyu kidni injuri [7].
Dɔn
as GLP-1 rεsεptכr agonist, Semaglutid de kכntro di bכdi glukכs lεvεl dεm fayn fayn wan pan pasεn dεm we gεt tayp 2 mεtabolism bay we i de rεgεl insulin εn glukagon sekreshכn, inhεbit hεpatik glukoneojεnεsis, εn infכlכw εnεji mεtabolism εn apɛtit, we i de ridyus bכdi wet bכku pan pipul dεm we fat. I gɛt di tin dɛn we de protɛkt di at ɛn di blɔd, i de ridyus di risk fɔ gɛt sik dɛn we de ambɔg di at ɛn di blɔd, ɛn i de protɛkt di kidni dɛn. I gɛt tritmɛnt ifɛkt pan akyu kidni injuri, dayabitik nɛfropati, ɛn ɔda kidni sik dɛn.
Bɔt di pɔsin we rayt di buk
Di tin dɛn we wi dɔn tɔk bɔt, na ɔl di tin dɛn we Cocer Peptides dɔn du risach, ɛdit ɛn kɔmpilayt.
Sayɛns Jɔnal Author
Hegner, P. de na di Yunivasiti ɔf Rigensbɔg na Jamani ɛn i gɛt bɔku tin dɛn we i de du fɔ du risach. Dɛn tin ya na di at ɛn di blɔd sistɛm ɛn di at, usay i de fɛn di we aw dɛn de du tin ɛn aw fɔ trit di sik dɛn we de ambɔg di at ɛn di blɔd; bayokεmistri εn mכlikul bayoloji, we de fכkus fכ כnkov mכlikul bayolojikal εn bayokεmik riakshכn mεkanism dεm εn rεgεdyushכn prכsεs dεm; famakɔlɔji ɛn famasi, we de ɛmpɛsh di divɛlɔpmɛnt fɔ drɔgs ɛn ɛvalueshɔn fɔ di ɛfifikɛshɔn; ɛn di respiratory system ɛn bak di jenɛral ɛn intanɛnt mɛrɛsin, we de kɔnsɛntret pan di diagnosis ɛn tritmɛnt fɔ di respiratory diseases ɛn di kɔmɔn intanɛnt mɛdikal kɔndishɔn dɛm. Na masta sabi bukman we dɔn du bɔku tin dɛn pan mɛrɛsin. Hegner P de list in di rεfrεns כf saytεshכn [6].
▎ Saytayshɔn dɛn we gɛt fɔ du wit dis
[1] Oleszczuk R, Kozińska I, Gras-Ozimek J, ɛn ɔda pipul dɛn. Semaglutid fכ di tritmεnt fכ fat[J]. J ɔ rnal ɔ f Ɛdyukeshɔn, Ɛlth ɛn Spɔt, 2022. https://api.semanticscholar.org/CorpusID:245423376.
[2] Christou G. A., Katsiki N., Blundell J., ɛn ɔda pipul dɛn. Semaglutid as prכmis antiobesity dכg[J]. Obesiti Rivyu, 2019,20 (6): 805-815.DOI: 10.1111/obr.12839.
[3] Kurtzhals P, Flindt Kreiner F, Singh Bindra R. Di rol we di wet kכntrכl de ple fכ di mεnejmεnt fכ tayp 2 mεtabolism mεlitus: Pεrspεktiv dεm pan semaglutide[J]. Mεtabolism Risach εn Klinik Prεktis, 2023,203.DOI:10.1016/j.diabres.2023.110881.
[4] Chao A. M., Tronieri J. S., Amaro A., ɛn ɔda pipul dɛn. Semaglutid fכ di tritmεnt fכ fat[J]. Trends in Kardiovaskyuɛl Mɛdisin, 2023,33(3):159-166.DOI:10.1016/j.tcm.2021.12.008.
[5] Cigrovski BM, Strollo F. Semaglutid-ay-katch risal[J]. Wol Jɔnal fɔ Mɛtabolism, 2023,14(4):424-434.DOI:10.4239/wjd.v14.i4.424.
[6] Hegner P, Seitz S, Schopka S, ɛn ɔda pipul dɛn. semaglutid de impruv di kכntraktil fכnshכn insay isolεt hכman atrium[J]. Yuropian Hat Jɔnal, 2024,45(Saplimɛnt_1):ehae666-ehae3729.DOI:10.1093/eurheartj/ehae666.3729.
[7] Tiba AT, Qassam H, Hadi N R. Semaglutid in rεnal ischemia-rεpεrfyushכn injεri in mays[J]. J Med Layf, 2023,16(2):317-324.DOI:10.25122/jml-2022-0291.
ƆL DI ATIKUL ƐN PRODƆKT INFƆMƐSHƆN WE DƐN GI NA DIS WƐBSAYT NA FƆ ƆL FƆ DI INFƆMƐSHƆN ƐN FƆ EDYUKESHƆN.
Di prɔdak dɛn we dɛn gi na dis wɛbsayt na fɔ in vitro risach nɔmɔ. in vitro risach (Latin: *in glas*, we min insay glas) dεn de du am ausayd mכtalman bכdi. Dɛn prɔdak ya nɔto famasitik, dɛn nɔ gɛt di aprɔval frɔm di US Food and Drug Administration (FDA), ɛn dɛn nɔ fɔ yuz dɛn fɔ protɛkt, trit, ɔ mɛn ɛni mɛrɛsin, sik, ɔ sik. Di lɔ nɔ gri fɔ mek dɛn put dɛn tin ya insay mɔtalman ɔ animal bɔdi ɛni we.