Semaglutid 5mg we yu de yuz

▎ Di Strukchɔ we di Semaglutid gɛt

▎ Semaglutid Risach

Wetin na di risach bakgrɔn fɔ Semaglutid?

Semaglutid na hכman glukagon lεk pεptida-1 (GLP-1) analכg, we de insay di klas fכ GLP-1 rεsεptכr agonist dכg dεm. GLP-1 na nכmal כmon we di intestinal sεl dεm de kכl afta yu it, we de mek insulin sekreshכn εn i de mek di glukכn kכmכt fכ rεgεl di blכd glukכs lεvεl. di divεlכpmεnt fכ Semaglutid kכmכt frכm dip risεch pan di fysiolojikal fכnshכn dεm fכ GLP-1. GLP-1 gεt sכt haf layf na di bכdi, lεk 1-2 minit, as i izi fכ dεgrεd bay dipεptidayl pεptidaz-4 (DPP-4) εnzym dεm na di bכdi. fכ כvakom dis limitεshכn, sayɛnsman dεm modify di strכkchכ fכ GLP-1, introdכks spεsifi k amino asid sכbstityushכn dεm εn ad protεktiv grup dεm fכ εnhans in rεsistεns to DPP-4 εnzym dεm, we de mek i lכng di tεm we i de akshכn na di bכdi ^[1] . insay di strכkchכ fכ Semaglutid, di alanin we de na posishכn 8 de riples am wit α-aminoisobutyric acid (Aib), we nכ de כnli impruv di stεbiliti fכ di dכg bכt i de εnhans in binding fכs wit GLP-1 rεsεpכta dεm ^[2] . wan yכŋ fεt asid sayd chen dεn ad to di C-tεrminus fכ Semaglutid, we kכnekt to wan laysin rεsidεns tru γ-glutamine, we de εksεnd di dכg in haf layf mכr εn alaw fכ injεkt am wan tεm insay di wik כ tek am bay mכt wan tεm insay di de ^[1] . Semaglutid bin fכs divεlכp bays pan risεch εn modifyushכn fכ nεchכral GLP-1, we aim fכ gi mכr ifektiv tritmεnt fכ pasεnshכn wit tayp 2 mεtabolism ^{[1, 2]} . tru dεn strכkchכral optimizεshכn dεm ya, Semaglutid nכ de כnli rεtεn di fysiolojikal aktiviti fכ GLP-1 bכt i de impruv in fכmakokinetik prכpati dεm bכku bכku wan, we de bi lכng-aktin GLP-1 rεsεptכr agonist we imכtant klinik valyu. di divεlכpmεnt fכ Semaglutid na wan imכtant achivmεnt, we de bכn nyu tritmεnt opshכn fכ pasεn dεm wit tayp 2 mεtabolism. bay we i de optimiz di strכkchכ fכ nεchכral GLP-1, i de כvakom di limitεshכn fכ in sכt haf-layf εn i de impruv di drog in stεbiliti εn di tεm we i de akshכn.

Wetin na di we aw Semaglutid de wok?

Semaglutid na lכng-akt glukagon lεk pεptida-1 (GLP-1) rεsεpכta agonist, εn in mεkanism fכ akshכn de mεnli achy tru di fכlכw aspek dεm:

Di we aw dɛn de rigul di glukɔs na di blɔd:

Semaglutid na wan nyu GLP-1 rεsεptכr agonist (GLP-1RA). di praymar mεkanism we i de du na fכ kכbכt di krayv fכ it bay we i de mek i nכ want fכ it, i de rεdכks di prεfrεns fכ it dεm we gεt hכy fεt, εn i de mכdulet di haypothalamic fכd sεnta fכ dכn di it we i de it. I de mek bak yu satisfay, i de delay di gastric ɛmti, ɛn i de ridyus di gastrointestinal motility, so dat i de mek yu nɔ gɛt bɔku bɔku wet. dis we aw dεn de ridyus di wet de mek di insulin sεnsitiviti bכku εn i de εp fכ rεgεl di blכd glukכs lεvεl ^[3] . Semaglutid de mek di rodεnt dεm weit lכs tru distribyut nyural path dεm. stכdi dεm sho se i de akt pan di bren stεm, septal nyuklios, εn haypothalamus bכt i nכ de kכros di bכdi-bren barεri. bifo dat, i de intarakt wit di bren tru di sεkכnvεntrikul כgan dεm εn di vεntrikul-prכksimal εria dεm. semaglutid de aktibכt c-Fos insay tεn bren rijyכn dεm, inklud di hindbren εria dεm we dεn tכk dεn tכk dεn wan dεm εn sεkכnd rijyכn dεm lεk di lateral parabrachial nyuklios we nכ gεt dayrekt GLP-1R intarakshכn. כtomatכk analisis dεn sho se aktibכshכn involv lateral parabrachial nyuklios nyuron dεm we de kכntro di it tεrminεshכn, so dat de rεgεl di blכd glukכs ^[4]. .

Gεstrointestinal rεgulεshכn:

semaglutid de akt pan GLP-1 risεptor dεm na di gכt, i de yuz di vagus nεv path fכ mכdulet di gεstrointestinal mכtiliti. i de sכpres di antral kכntrikshכn, i de bolst di pyloric sphincter tεnshכn, εn i de mek di gastric fכd rεtεnshכn lכng, i de delay di duodenal εntri εn i de mek di blכd glukכs spayk dεm afta it, we de mek di lεvεl dεm we de stebul ^[5] . apat frכm dat, Semaglutid de afekt sεntri GLP-1 rεsεpכta dεm, patikyular insay di haypothalamic arcuate εn paraventricular nyuklios. i de inhεbit fכs tin dεm we de mek yu want fכ it lεk nyuropεptida Y (NPY) εn agouti-rεlatεd protin (AgRP), we i de aktibכt proopiomelanocortin (POMC) nyuron dεm fכ bכst di alfa-melanosayt-stimulεt כmon (α-MSH) sekreshכn ^[5] . Dɛn akshɔn ya kin mek pɔsin satis, i kin mek i nɔ angri, ɛn i kin mek i nɔ it bɔku tin fɔ it, ɛn dis kin ɛp fɔ mek pɔsin ebul fɔ kɔntrol di wet ɛn indaykt wan i kin mek pɔsin kɔntrol di glukɔs na di blɔd fayn fayn wan.

Protɛkshɔn fɔ di at ɛn di blɔd dɛn:

semaglutid de mek di naytrik oksayd (NO) εn כda vasodilator dεm kכmכt frכm di vaskulεr εndoteyl sεl dεm, we de mek di vasodilayshכn εn bכdi fכ fכlכ bכku. i de inhεbit inflameshn εn כksidεtiv strεs bak, we de ridyus di εndoteyl dεm we de dכn εn di risk fכ atεrosklεrosis. bay we i de stɔp di apɛtit ɛn it, i de ɛp fɔ lɔs di wet, i de mek di lipid mɛtabolism bɛtɛ, i de mek di triglisɛrɛyd ɛn lɔw-dɛnsity lipoprotein kɔlɔstrel (LDL-C) dɔŋ, ɛn i de mek di ay-dɛnsity lipoprotein kɔlɔstrel (HDL-C) go ɔp. pan tap dat, i kin bεnεfit bכdi prεshכn bay we i de mכdulet di rεnal hεmodaynamik εn nyuroεndokrin fכnshכn, lכs di haypatεnshכn risk εn ridyus di kכdivaskyul sik risk fכktכ dεm ^[6]. .

Semaglutid εn transkripshכnal rεguleshכn fכ WAT to BAT kכnvכshכn εn BAT aktibכshכn.

Sos: PubMed ^{[13] we dɛn pul am.}

Ki ɛkspiriɛns ɛn risach

in tεm fכ kεmikכl strכkchכ disayn εn optimayzεshכn, di tεm we dεn de disayn di sεmaglutayd, wan mεtכd fכ rivεrsibl binding to albumin bin adopt fכ prolכng di tεm we di dכg de akshכn. bay we dεn dεtermin di optimal kכmbaynshכn fכ fεt asid εn linka dεm, di binding kapasiti to albumin bin maksimayz we dεn de mεnten di efikכs pan di GLP-1 rεsεptכr (GLP-1R) (Knudsen LB, 2019).

We i kam pan aw fɔ yuz drɔgs, semaglutide gɛt bɛtɛ wet lɔs ifɛkt. Semaglutid na glukagon lεk pεptida-1 rεsεptכr agonist (GLP-1 RA) wit lכng εliminεshכn haf-layf, we de alaw fכ injεkshכn sכbkutan ɛvri wik. Di we aw i de mek pɔsin nɔ gɛt bɔku bɔku bɔdi, rili wɔndaful. pan di sik pipul dεm we gεt tayp 2 mεtabolism (T2DM), i tan lεk se di wik sכbkutan injεkshכn fכ semaglutide de wok fכ lכs di wet pas כda wik GLP-1RA dεm. Insay wan faz II doz-fayndin trayal fɔ fat pasɛnt dɛn we nɔ gɛt T2DM, wan tɛm ɛvride sabkyutan injɛkshɔn fɔ semaglutayd bin mɔ ifɛktiv fɔ weit lɔs pas plasɛbo ɛn wan tɛm ɛvride 3.0mg liraglutide. Di wet we semaglutide mek na dis stɔdi pas di standad fɔ anti-obesity drugs we di European Medicines Agency (EMA) ɛn di US Food and Drug Administration (FDA) bin sɛt, wit nɔ sefty ishu, we sho se wan tɛm ɛvride sabkutan injɛkshɔn fɔ semaglutide gɛt di potenshal fɔ bi wan fiuja weit lɔs drɔg ^[7]. .

Semaglutid kin mek di at wok fayn ɛn dɛn kin yuz am fɔ trit di sik dɛn we de ambɔg di at ɛn di blɔd. di risalts fכ di STEP-HFpEF trayal bin anawns, we hεy-dos antidiabetik glukagon-layk pεptida 1 agonist semaglutide sכmtεm impruv di simptom dεm fכ hat fεil wit prεsiv εjεkshכn frakshכn (HFpEF) εn ridyus N-tεrminal pro-B-tayp natriuretik pεptida (NT-proBNP) lεvεl dεm. di stכdi tεst di ifekt we akyu semaglutayd tritmεnt gεt pan isolεt hυman rayt atrial trabekul dεm εn fכnshכn se semaglutide inkrεs di tεnshכn fכ hυman atrial trabεkul dεm pas tri tεm insay wan we we dipεnd pan dכz, witout inkrεs di tεndens fכ aritmia. dis ifekt de mכst lεk biכs fכ inkrεs pan sarkoplasmik rεtikulכm Ca2+ כptek. di tritmεnt we dεn gεt hεy dכz semaglutide pan pipul dεm we hat fεil kin mek di atria wok fayn εn dis kin mek dεn sכmtεm bεtεh ^[8]. .

Dɛn de stɔdi semaglutid fɔ di tritmɛnt fɔ nɔ-alkohol steatohepatitis (NASH). di rayshכnal disayn we i mek dεn dכn mek big kכntribyushכn fכ impruv di bכdi glukכs kכntrכl, wet, bכdi prεshכn, lipid, β-sεl fכnshכn, εn di kכdivaskyul sistεm insay di sik pipul dεm we gεt tayp 2 mεtabolism. pan tap dat, di divεlכpmεnt fכ wan כral fכmyuleshכn fכ semaglutide kin gi כda bεnεfit to di sik pipul dεm we i kam pan di tritmεnt we de fala ^[9]. .

Difrɛns pan di Weyt Lɔs Ifɛkt dɛm fɔ Semaglutid Across Populeshɔn dɛm

Di Ifekt dɛm fɔ Lɔs di Wɛt pan big pipul dɛm we gɛt di sik we de naw, we gɛt bɔku bɔku bɔdi ɔ we fat pasmak we nɔ gɛt Mɛtabolism: 

Insay di SELECT kadiovaskular autkam trayal, semaglutide ridyus di big big advεs kכdivaskyul ivent dεm (MACE) bay 20% pan 17,604 big pipul dεm we gεt kכdivaskyul sik we bin de, כva wet כ fat, εn nכ mεtabolism ^[10] . Insay dis prɛ-spɛsifikɛd analisis, risach pipul dɛn bin ɛgzamin di ifɛkt dɛn we semaglutide gɛt pan di wet, anthropometric autkam, sef, ɛn tolɛrabiliti bay beslayn bɔdi mas indɛks (BMI). Di pasɛnt dɛn we bin de tek semaglutide bin gɛt sɔstayn wet lɔs fɔ 65 wik, we bin kɔntinyu fɔ de te to 4 ia. Na 208 wik, semaglutide bin lid to signifyant big minin ridyushɔn pan wet (-10.2%), wɛst sɛkɔnfɛreshɔn (-7.7 cm), ɛn wɛst-to-ayt rɛsɛshɔn (-6.9%) kɔmpia to plasɛbo (-1.5%, -1.3 cm, ɛn -1.0%, rispɛktvɔli; ɔl di kɔmpiashɔn dɛn bin statistically signifyant. Klinikli mininful wet lɔs apin a krɔs man ɛn uman, ɔl di etnik grup dɛn, di kayn bɔdi dɛn, ɛn di rijyɔn dɛn Semaglutid bin gɛt fɔ du wit smɔl siriɔs advays ivin dɛn (<30, 30 to <35, 35 to <40, ɛn ≥40 kg/m²), semaglutide bin gɛt lɔwa siriɔs bad bad tin dɛn we apin. 43.54, 51.07, ɛn 47.06 vs. 50.48, 49.66, 52.73, ɛn 60.85 fɔ plasɛbo). anthropometric improvements kompare to plasebo na 208 wik, wit weit loss we sustain ova 4 ia.

Di Ifekt dɛm fɔ Lɔs di Wɛt pan pipul dɛm we fat ɔ we gɛt bɔku bɔku bɔdi we nɔ gɛt Mɛtabolism:  

wan sistamat rivyu evaluate di efficacy εn sefty fכ semaglutide in obese כ ovaweit pipul dεm we nכ gεt mεtabolism ^[11] . Dis rivyu sεntez di risכlt frכm mכltipכl klinik trial dεm, we hεlayt di impak we semaglutide gεt pan di wet lכs, mεtabolik paramita dεm, εn di כvala hεlth autkam dεm. Di tin dɛn we dɛn fɛn sho se semaglutide bin gɛt fɔ du wit signifyant weit lɔs ɛn impruvmɛnt pan ɔbisiti-rilayt wɛlbɔdi mɛtrik, we sho se i pɔtnɛshɛl as valyu tritmɛnt opshɔn fɔ fat pasɛnt dɛn. 

Weight Loss Effects in Non-Dabetic Patients (Evidɛns frɔm Bɔku RCT dɛn): 

Fo randomized controlled trials (RCTs) we involv pasεnshכn dεm wit beslayn wet 96–105 kg evaluate wik 2.4 mg sabkutan semaglutide plus layfstayl intavεnshכn (kכnsεl, it, fyzikal aktiviti) fכ weit lכs ^[12] . Wan RCT pan pipul dɛn we nɔ gɛt dayabitis (N = 1,961) ripɔt wan min weit lɔs fɔ 15% (15 kg) vs. 2% (3 kg) wit plasɛbo afta 68 wik (statistikal sifyukɛnt). Di prɔpɔshɔn fɔ di pasɛnt dɛn we ajɔst ≥5% wet lɔs na bin 86% vs. 32% (nɔmba we dɛn nid fɔ trit [NNT] = 2), ɛn ≥10% weit lɔs na bin 69% vs. 12% (NNT = 2). Weight loss plateaued na ~60 wiks. di gεstrointestinal advεs ivent (AE) dεm bin apin insay 74% vs. 48% (nכmba we nid fכ harm [NNH] = 3). Diskontinyueshɔn bikɔs ɔf AE dɛn na bin 7% vs. 3% (NNH = 25). Dɛn bin si di sem kayn rizɔlt insay ɔda RCT wit intensiv layf stayl intavɛnshɔn (N = 611): semaglutide indyuz 16% (17 kg) vs. 6% (6 kg) weit lɔs. Insay wan doz-ɛksplɔreshɔn RCT pan pasɛnt dɛn we nɔ gɛt dayabitis (N = 1,210), ɛvri wik 2.4 mg semaglutide, 1.0 mg semaglutide, ɔ plasɛbo bin gi min weit lɔs we na 10%, 7%, ɛn 3% afta 68 wik. Prɔpɔshɔn dɛn we ajɔst to ≥5% weit lɔs na bin 69% (2.4 mg), 57% (1.0 mg), ɛn 29% (plasɛbo). Fכ 2.4 mg vs. 1.0 mg, NNT = 9. AE profayl dεm bin sεm akrays dכz. Insay wan wet mentenɛns RCT (N = 803), patisipan dɛn we nɔ gɛt dayabitis bin gɛt 2.4 mg sɛmaglutayd ɛvri wik fɔ 20 wik, dɔn dɛn randomiz fɔ kɔntinyu sɛmaglutayd ɔ chenj to plasɛbo. Afta 48 wik, di wan dɛn we kɔntinyu fɔ yuz semaglutide lɔs 8% vs di wan dɛn we de yuz plasɛbo we gɛt 7%. 

in sכmari, semaglutide na GLP-1 rεsεptכr agonist wit mכlti-domεn aplikεshכn valyu. insay mεtabolism tritmεnt, i de biεn GLP-1 rεsεpכta dεm fכ protεkt insulin sekreshכn εn inhεbit glukagon rilis, i de kכntro di bכdi glukכs lεvεl fayn fayn wan εn gi wan siknifikant tritmεnt opshכn fכ pasεn dεm we gεt tayp 2 mεtabolism. Insay di fild fɔ tritmɛnt fɔ fat, semaglutide kin ridyus di ɛnaji we dɛn de tek tru mɛkanism dɛn lɛk sɛntral apɛtɛyt sɔpreshɔn ɛn dilay gastric ɛmti, we de ɛp di wan dɛn we fat fɔ lɔs dɛn wet ɛn impruv dɛn mɛtabolik stetɔs. Apat frɔm dat, semaglutide de sho pɔtɛnɛshɛl aplikeshɔn prɔspɛkt fɔ di prɛvɛnshɔn ɛn tritmɛnt fɔ di sik dɛm we de ambɔg di at ɛn di blɔd, ɛn di impɔtant tin dɛm we de mek di at ɛn di blɔd go bifo de gi nyu we fɔ ridyus di tin dɛm we kin apin to di at ɛn di blɔd. Di we aw semaglutide de kɔmɔt nɔ jɔs de mek di tritmɛnt we dɛn de yuz fɔ sik dɛn we gɛt fɔ du wit am, bɛtɛ bɔt i de briŋ nyu op fɔ mek di sikman dɛn kwaliti layf ɛn wɛlbɔdi bɛtɛ.

Bɔt di pɔsin we rayt di buk

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Sayɛns Jɔnal Author

Hegner P na wan risachman na di Yunivasiti ɔf Rɛgensbɔg. In wok de pan Kwɛstyɔn, Kadiɔvaskyuɛl Sistɛm, ɛn Kadiɔlɔji. Insay Kwɛstyɔn, i de ɛksplɔrɔ di riakshɔn dɛn we tay to di at ɛn di blɔd wɛlbɔdi. Insay di Kadiovaskyuɛl Sistɛm stɔdi, i de chɛk aw di at ɛn di vessel de wok, ɛn i de luk fɔ di tritmɛnt insayt. In Kadiɔlɔji risach de tɔk mɔ bɔt aw fɔ avɔyd at sik, aw fɔ no aw i gɛt am, ɛn aw fɔ trit am.

Di tin dɛn we Hegner bin du rili impɔtant. Di tin dɛn we i dɔn lan bɔt di kemikal dɛn dɔn mek i de mek nyu mɛrɛsin dɛn we de mek di at ɛn di blɔd. Di wok we i dɔn du pan di we aw at ɛn di vessel dɛn de wok dɔn mek pipul dɛn ɔndastand mɔ bɔt di sik dɛn we de ambɔg di at ɛn di blɔd. Na klinik, in risach dɔn mek dɛn ebul fɔ mɛn at sik dɛn fayn fayn wan, ɛn dis dɔn mek di standad fɔ kia fɔ di wan dɛn we sik go ɔp. Ɔl togɛda, di we aw Hegner de yuz bɔku difrɛn tin dɛn de mek di mɛrɛsin we dɛn kɔl kadiovaskular gɛt mɔ ɛn mɔ, ɛn i de gi op fɔ ridyus di prɔblɛm dɛn we di sik kin gɛt ɛn fɔ mek di pɔsin gɛt bɛtɛ tin fɔ du. Hegner P de list in di rεfrεns כf saytεshכn [8].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] Memon A, Tehrim M, Kumari B. Semaglutid: nyu dawn fɔ di wan dɛn we gɛt dayabitis[J]. J ɔ rnal ov di Pakistan Mɛdikal Asosieshɔn, 2023,73(3):721.DOI:10.47391/JPMA.7558.

[2] Ma H, Huang W, Wang X, ɛn ɔda pipul dɛn. strכkchכral insayt dεm fכ di aktibכshכn fכ GLP-1R bay wan sכm mכlikul agonist[J]. Sel Risach, 2020,30(12):1140-1142.DOI:10.1038/s41422-020-0384-8.

[3] Kim HS, Jung C H. Oral Semaglutid, di Fכs Ingestible Glucagon-Like Pεptid-1 Risεptor Agonist: I kin bi majik Bulet fכ Tayp 2 Mεtabolism?[J]. Int ɛ rnash ɔ nal J ɔ rnal ɔ f Mɔlikul Sayns, 2021,22(18).DOI:10.3390/ijms22189936.

[4] Gabery S, Salinas C. G., Pɔlsɛn S. J., ɛn ɔda pipul dɛn. semaglutid de lכs di bכdi wet insay rodεnt dεm via distribyut nyural path dεm[J]. Jci Insayt, 2020,5(6).DOI:10.1172/jci.insight.133429.

[5] Katsurada K, Yada T. Nyural ifekt dεm fכ gut- εn bren-dεriv glukagon-lεk pεptida-1 εn in rεsεptכr agonist[J]. J ɔ rnal ov M ɛ t abolism Inv ɛ stigesh ɔ n, 2016,7:64-69.DOI:10.1111/jdi.12464.

[6] Ryan D. H., Lingvay I, Kɔlɔhɔn H. M., ɛn ɔda pipul dɛn. Semaglutid Efεkt pan Kadivaskyul Autkam in Pipul dεm wit Ovaweit כ Obesity (SELECT) rεshכnal εn disayn[J]. Amɛrikan At Jɔnal, 2020,229:61-69.DOI:10.1016/j.ahj.2020.07.008.

[7] 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.

[8] Hegner P, Seitz S, Schopka S, ɛn ɔda pipul dɛn. semaglutid de impruv di kכntraktil fכnshכn insay isolεt hכman atrium[J]. Yuropian At Jɔnal, 2024,45.DOI:10.1093/eurheartj/ehae666.3729.

[9] Knudsen LB, Lau J. Di Diskכvri εn Divεlכpmεnt כf Liraglutide εn Semaglutid[J]. Frontiers in Ɛndokrinɔlɔji, 2019,10.DOI: 10.3389/fendo.2019.00155.

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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.