Semaglutid 10mg we yu de yuz

▎ Di Strukchɔ we di Semaglutid gɛt

▎ Semaglutid Risach

Wetin na di risach bakgrɔn fɔ Semaglutid?

Semaglutid na hכman glukagכn lεk pεptida-1 (GLP-1) analכg, we dεn klas as GLP-1 rεsεptכr agonist. GLP-1 na nεchכral כmon we di intestinal sεl dεm de kכl afta dεn it. i de ple rol fכ mek insulin sekreshכn εn inhibit glukagon sekreshכn, we de rεgεl di blכd glukכs lεvεl. di divεlכpmεnt fכ Semaglutid kכmכt frכm dip εksplכreshכn fכ di fysiolojikal fכnshכn dεm fכ GLP-1. כltu, GLP-1 gεt rili sכt haf layf na di bכdi, we de las כnli lεk 1 to 2 minit, we dεn atribyut to in susεptibiliti fכ dεgradashכn bay dipeptidyl pεptidaz-4 (DPP-4) εnzym dεm na di bכdi. fכ כvakom dis limitεshכn, sayɛnsman dεm modify di strכkchכ fכ GLP-1 tru spεsifi k amino asid sכbstityushכn dεm εn di adishכn fכ protεktiv grup dεm, we de εnhans in rεsistεns to DPP-4 εnzym dεm εn so i de lכng di tεm we i de akshכn ^[1] . insay di strכkchכ fכ Semaglutid, alanin na di 8th posishכn de riples wit α-aminoisobutyric asid (Aib). dis chenj nכ de כnli impruv di stεbiliti fכ di dכg bכt i de strכng in binding to di GLP-1 rεsεpכta (Ma H, 2020). apat frכm dat, wan yכŋ fεt asid sayd chen we kכnekt to in C-tεrminus, we lεnk via γ-glutamine to laysin rεsidεns, de εksεnd di haf layf mכr, we de mek i ebul fכ injεkshכn wan tεm insay wik כ wan tεm evri de כral administreshכn ^[1] . fכs bays pan di risεch εn modifyushכn fכ nεchכral GLP-1, Semaglutid aim fכ gi mכr ifektiv tritmεnt opshכn fכ pasεnshכn wit tayp 2 mεtabolism ^{[1, 2]} . afta strכkchכral optimizεshכn, i de rεtεn di fysiolojikal aktiviti fכ GLP-1 we i de sכmtεm impruv in fכmakokinetik prכpati dεm, we de bi imכtant lכng-aktin GLP-1 rεsεptכr agonist. di risach εn divεlכpmεnt fכ Semaglutid na big minin fכ di tritmεnt fכ tayp 2 mεtabolism, we de gi nyu chכys to di sik pipul dεm. bay we i de optimiz di strכkchכ, i de כvakom di prכblεm fכ di sכt haf-layf fכ nεchכral GLP-1, we de εnhans di dכg in stεbiliti εn di tεm we i de akshכn.

Wetin na di we aw Semaglutid de wok?

Semaglutid na wan lכng-akt glukagon lεk pεptida-1 (GLP-1) rεsεpכta agonist, εn in mεkanism fכ akshכn na dis:

Blɔd Glukɔs Rɛgyuleshɔn: As wan nyu glukagɔn-layk pεptida-1 rεsεptכr agonist (GLP-1RA), Semaglutid de mεntal ridyus di sikman dεm we dεn want fכ it εn i de dכn dεn prεfrεns fכ it dεm we gεt hεy fεt bay we i de sכpres di apεtit. i de rεgεl di fכd sεnta na di haypothalamus, i de ridyus di it we yu de it, i de mek yu satisfay, i de mek di gεstrik εmpti, εn i de dכn di gεstrointestinal mכtiliti, so dat i de rich di gol fכ lכs di wet. we yu lכs di wet de εp fכ impruv di insulin rεsistεns εn i de rεgεl di blכd glukכs lεvεl mכr ^[3] (Kim HS, 2021). Semaglutid de mek di rodεnt dεm weit lכs tru di distributed nyural path dεm. stכdi dεn sho se Semaglutid de akt dayrekt pan εria dεm lεk di bren stεm, septal nyuklios, εn haypothalamus. pan tap we i nכ de kכros di bכdi-bren barεri, i de intarakt wit di bren tru di sכkכmvεntrikul כgan dεm εn spεshal rijyכn dεm nia di vεntrikl dεm. i de indyuz sεntri c-Fos aktibכshכn insay 10 bren rijyכn dεm, inklud di hindbren rijyכn dεm we Semaglutid de tכk dεm dεn wan dεm εn sεkכnd rijyכn dεm we nכ gεt dayrekt GLP-1R intarakshכn, lεk di lateral parabrachial nyuklios. כtomatכk analisis sho se di aktibכshכn kin riliyt to di tεrminεshכn fכ it we nyuron dεm we de na di lateral parabrachial nyuklios de kכntro, we de mek i de rεgεl di blכd glukכs lεvεl ^[4]..

di gεstrointestinal rεguleshכn: Semaglutid de akt pan GLP-1 rεsεpכta dεm na di gεstrointestinal trakt. tru di afferent path fכ di vagus nεv, i de akt pan εria dεm na di bren lεk di nyuklios fכ di solitary trakt εn di dכsal mכtal nyuklios fכ di vagus nεv fכ rεgεl di gεstrointestinal mכtiliti. i kin mek di gastric antrum kכntrakshכn, i kin mek di tεnshכn na di pyloric sphincter bכku, i kin mek di it fכ de insay di bεlε lכng, εn i kin delay fכ go insay di duodenum, we kin mek di blכd glukכs we dεn dכn it kwik kwik wan εn mek di bכdi glukכs chenj mכr stebul ^[5] (Katsurada K, 2016). apat frכm dat, Semaglutid de akt pan GLP-1 risεptor dεm na di sεntri nεv sεstem, mεntal wan na εria dεm lεk di arcuate nyuklios εn paraventricular nyuklios na di haypothalamus. i de inhεbit di rilis fכ di fכs tin dεm we de mek yu want fכ it lεk nyuropεptida Y (NPY) εn agouti-rεlatεd protin (AgRP), εn di sem tεm i de aktibכt di pro-opiomelanocortin (POMC) nyuron dεm, we de protεkt di sekreshכn fכ α-melanocyte-stimulating hormone (α-MSH) ^[5] . Dɛn tin ya kin mek pɔsin fil se i dɔn satisfay, i kin mek pɔsin nɔ angri, ɛn i kin mek i nɔ it bɛtɛ tin fɔ it, ɛn dis kin mek i gɛt fayn impak pan di kɔntrol we i gɛt pan di glukɔs na di blɔd.

di kכdivaskyul protεkshכn: Semaglutid kin protεkt di vaskulεr εndoteyl sεl dεm fכ rilis vasodilatory fכktכ dεm lεk nitric oxide (NO), we de εnhans di vaskulכr dilayshכn abiliti εn impruv di bכdi fכ fכlכ pεrfyushכn. di sem tεm, i de inhεbit di inflammatory rεspכns dεm εn כksidεtiv strεs, i de ridyus di damej to vaskulεr εndoteyl sεl dεm, εn i de lכs di risk fכ atεrosklεrosis. pan tap dat, bay we i de ridyus di apɛtit ɛn it we i de it, Semaglutid de ɛp fɔ lɔs di wet, i de ɛp fɔ mek di lipid mɛtabolism dizayd bɛtɛ, i de ridyus di lɛvɛl dɛn we di triglisɛrɛyd ɛn lɔw-dɛnsity lipoprotein kɔlɔstrel (LDL-C) de, ɛn i de mek di lɛvɛl fɔ di ay-dɛnsity lipoprotein kɔlɔstrel (HDL-C) go ɔp. i kin gεt bεnεfit ifekt dεm bak pan blכd prεshכn bay we i de rεgεl di rεnal hεmodaynamiks εn nyuroεndokrin fכnshכn dεm, we de rεdכks di risk fכ haypatεnshכn εn kכdivaskyul sik risk fכktכ dεm ^[6]..

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

Sos: PubMed ^{[12] we dɛn pul am.}

Wetin na di men ɛkspiriɛns ɛn stɔdi dɛn?

Disain εn Optimayzεshכn כf Kεmikכl Strכkchכ: We dεn bin de disayn Semaglutid, dεn bin adopt wan mεtכd fכ rivεrsibl binding to albumin fכ εksεnd di dכg in durεshכn fכ akshכn. bay we dεn de disayd di optimal kכmbaynshכn fכ fεt asid εn linka dεm, we dεn de mεnten di efikכs fכ di GLP-1 rεsεpכta (GLP-1R), di binding kapasiti to albumin bin maksimayz ^[7]..

Drug Aplikeshɔn: Semaglutid na glukagon lεk pεptida-1 rεsεptכr agonist (GLP-1 RA) wit rili lכng εliminεshכn haf-layf, we de alaw fכ wan tεm insay wik sכbkutan injεkshכn. pan di sik pipul dεm we gεt tayp 2 mεtabolism (T2DM), di weit lכs ifekt fכ wan tεm insay wik sכbkutan injεkshכn fכ Semaglutid bכku pas di wan fכ כda wan tεm insay wik GLP-1RA dεm. Insay wan faz II doz-ɛksplɔreshɔn trayal fɔ fat pasɛnt dɛn we nɔ gɛt T2DM, wan tɛm ɛvride sɔbkyutan injɛkshɔn fɔ Semaglutid sho bɛtɛ wet lɔs ifɛkt pas plasɛbo ɛn wan tɛm ɛvride 3.0 mg liraglutide. Di digri we Semaglutid dɔn mek pɔsin lɔs in wet na dis stɔdi pas di standad fɔ di mɛrɛsin dɛn we di Yuropian Mɛdisin Ajɛns (EMA) ɛn di US Food and Drug Administration (FDA) bin dɔn sɛt fɔ di wet lɔs, ɛn i sef, we sho se we pɔsin injɛkshɔn Semaglutid wan tɛm ɛvride ɔnda di bɔdi, i gɛt di potenshal fɔ bi mɛrɛsin we go mek pɔsin lɔs in wet tumara bambay ^[8]..

Tritmɛnt fɔ Kadiɔvaskyuɛl Diziz bay we dɛn de impruv di Kadyak Fɔnkshɔn: Di rizɔlt dɛn fɔ di STEP-HFpEF trayal sho se ay-dos antidiabetic glucagon-layk peptide 1 agonist Semaglutid signifyantli impruv di simptom dɛm we gɛt fɔ du wit at fayl wit prɛzɛv ejekshɔn frakshɔn (HFpEF) ɛn ridyus di lɛvɛl fɔ N-terminal pro-B-tayp natriuretic peptide (NT-proBNP) we dɛn kɔl). Risach tεst dεn fכnshכn se akyu tritmεnt wit Semaglutid kin inkrεs di tεnshכn fכ di hכman atrial trabekul dεm pas tri tεm insay wan dכz-dipεndεnt we, witout inkrεs tεndεns fכ aritmia. dis ifekt kin bi biכs fכ inkrεs pan di כptek fכ Ca2+ bay di sarkoplasmik rεtikul. Tritmεnt wit hεy dכz Semaglutid pan pasεn dεm we hat fεl kin bεtεh atria fכnshכn, dat kin mek dεn rεliv di simptom dεm ^[9]..

Semaglutid de ɔnda invɛstigeshɔn fɔ di tritmɛnt fɔ non-alcoholic steatohepatitis (NASH): Di rayshɔnal dizayn fɔ Semaglutid dɔn mek big kɔntribyushɔn fɔ impɔtant blɔd glukɔs kɔntrol, bɔdi wet, blɔd prɛshɔn, blɔd lipid, β-sɛl fɔ wok, ɛn di kadiovaskular sistɛm pan pasɛnt dɛn we gɛt tayp 2 mɛtabolism. apat frכm dat, di divεlכpmεnt fכ wan כral fכmyuleshכn fכ Semaglutid kin gi adishכnal advantej pan tεm fכ di sikman dεm in tritmεnt kכmplians ^[7]..

Wetin na di difrɛns pan di wet lɔs ifɛkt dɛm we Semaglutid gɛt bitwin difrɛn pipul dɛm?

Adult dεm we bin gεt kכdivaskyul sik dεm we bin de bifo, we dεn bin ova wet כ we fat bכt we nכ gεt mεtabolism: Insay di SELECT cardiovascular outcomes trial, Semaglutid bin rεdכks di big big advεs kכdivaskyul ivent dεm bay 20% pan 17,604 big pipul dεm we bin gεt kכdivaskyul sik dεm we bin de bifo, כva wet כ fat, εn we nכ gεt mεtabolism ^[10] (Ryan DH, 2024). Insay dis prɛ-spɛsifikɛd analisis, risach pipul dɛn bin ɛgzamin di ifɛkt dɛn we Semaglutid gɛt pan bɔdi wet, anthropometric autkam, sef, ɛn tolɛrabiliti akɔdin to di beslayn bɔdi mas indeks (BMI). Di pasɛnt dɛn we bin de tek Semaglutid bin gɛt kɔntinyu fɔ go dɔŋ pan dɛn bɔdi wet insay 65 wik, we bin las te to 4 ia. Na 208 wik, we yu kɔmpia am wit di plesibo grup, Semaglutid lid to wan avɛj ridɔkshɔn pan di bɔdi wet (-10.2%), wɛst sɛkɔnfɛreshɔn (-7.7 cm), ɛn wɛst-to-ayt rɛtɛshɔn (-6.9%), we di plasɛbo grup bin gɛt ridyushɔn pan (-1.5%, -1.3 cm, ɛn -1.0%) rispɛktvɔli, ɛn ɔl di kɔmpiashɔn dɛn wit di plesibo na bin statistically signifyant. Klinikli mininful weit lɔs bin apin pan man ɛn uman, ɔl etnik grup, bɔdi tayp, ɛn rijyɔn. Semaglutid bin gɛt fɔ du wit smɔl siriɔs bad bad tin dɛn we kin apin. Fɔ ɛni BMI kategori (<30, 30 to <35, 35 to <40, ɛn ≥40 kg/m²), di insidɛns fɔ siriɔs bad bad tin dɛn we apin to Semaglutid (nɔmba fɔ di tin dɛn we dɛn si pan ɛvri 100 pɔsin-ia) bin smɔl (43.23, 43.54, 51.07, ɛn 47.06 fɔ Semaglutid, ɛn 50.48, 49.66, 52.73, ɛn 60.85 fɔ di plesibo). Semaglutid bin asosiet wit wan inkrεs rεt fכ diskontinuεshכn כf di trayal prodakt. As di BMI kategori de dכn, di rεt fכ diskontinyu de inkrεs. Insay di SELECT trayal, na 208 wik, Semaglutid prodyuz signifyant klinik weit lɔs ɛn impruvmɛnt in anthropometrik valyu kɔmpia wit di plasɛbo, ɛn di wet lɔs bin kɔntinyu fɔ 4 ia.

Pipul dεm we fat כ ova wet bכt we nכ gεt mεtabolism: Wan sistamat rivyu evaluate di efficacy εn sef fכ Semaglutid pan pipul dεm we fat כ ova wet bכt we nכ gεt mεtabolism ^[11] . Dis rivyu sεntez di risכlt dεm fכ mכltipכl klinik trial dεm, we εnfaz di ifekt dεm we Semaglutid gεt pan weit lכs, mεtabolik paramita dεm, εn כvala hεlth autkam dεm. Di rizɔlt sho se Semaglutid bin gɛt fɔ du wit bɔku bɔku weit lɔs ɛn impɔtant tin dɛn we gɛt fɔ du wit wɛlbɔdi indikɛtɔ dɛn we gɛt fɔ du wit fat, ɛn i kin bi valyu tritmɛnt opshɔn fɔ di wan dɛn we fat.

Di wan dɛn we nɔ gɛt dayabitis (evidɛns frɔm bɔku RCT dɛn): Insay 4 randomized kɔntrol trayal dɛn, pasɛnt dɛn we gɛt beslayn bɔdi wet we na 96 to 105 kg bin gɛt 2.4 mg Semaglutid injɛkshɔn ɛvri wik sabkutanɛs ɛn layf stayl intavɛnshɔn (kɔnsɛl, it, ɛn fizik aktiviti) fɔ tritmɛnt fɔ lɔs dɛn wet. Wan randomized controlled trial fɔ non-diabetic patients (N = 1961) sho se afta 68 wik, di avrej weit lɔs na bin 15% (15 kg), we bin statistically signifyant difrɛn frɔm di 2% (3 kg) na di plasɛbo grup. Di prɔpɔshɔn fɔ di pasɛnt dɛn we gɛt wet lɔs we na ≥5% na bin 86% we yu kɔmpia am wit 32% na di plesibo grup, ɛn di nɔmba we dɛn nid fɔ trit (NNT) = 2; di prɔpɔshɔn fɔ di pasɛnt dɛn we gɛt wet lɔs ≥10% na bin 69% kɔmpia wit 12% na di plasɛbo grup, ɛn NNT = 2. Di wet lɔs lɛvɛl ɔf na lɛk 60 wik. Di insidɛns fɔ gastrointestinal advays ivin (AEs) na bin 74% kɔmpia wit 48% na di plasɛbo grup, ɛn di nɔmba we nid fɔ du bad (NNH) = 3. Di prɔpɔshɔn fɔ di pasɛnt dɛn we stɔp di tritmɛnt bikɔs ɔf di bad tin dɛn we apin na bin 7% kɔmpia wit 3% na di plasɛbo grup, ɛn NNH = 25. Insay wan ɔda randomized kɔntrol trial wit intensiv layf stayl intavɛnshɔn (N = 611), di wet lɔs na di Semaglutid grup na bin 16% (17 kg), we bin statistically signifyant difrɛn frɔm di 6% (6 kg) na di plasɛbo grup. Insay wan doz-ɛksplɔreshɔn randomiz kɔntrol trayal fɔ dayabitik pasɛnt dɛn (N = 1210), dɛn bin gi pasɛnt dɛn 2.4 mg Semaglutid ɛvri wik, 1.0 mg Semaglutid ɛvri wik, ɔ plasɛbo. Afta 68 wik, di avrej weit lɔs na bin 10% (2.4 mg), 7% (1.0 mg), ɛn 3% (plasɛbo) rispɛktvɔli. Di prɔpɔshɔn fɔ di pasɛnt dɛn we gɛt wet lɔs ≥5% na bin 69% (2.4 mg), 57% (1.0 mg) kɔmpia wit 29% na di plesibo grup. Fɔ di 2.4 mg ɛn 1.0 mg dos, NNT = 9. Di bad bad tin dɛn we apin bin simpul bitwin difrɛn doz dɛn. Insay wan weit mentenɛns randomiz kɔntrol trayal (N = 803), patisipan dɛn we nɔ gɛt dayabitis bin gɛt tritmɛnt ɛvri wik wit 2.4 mg Semaglutid fɔ 20 wik, ɛn afta dat dɛn bin sheb dɛn randomly insay wan grup we kɔntinyu fɔ trit Semaglutid ɔ wan plasɛbo grup. Afta 48 wik, di grup we kɔntinyu fɔ tek Semaglutid tritmɛnt lɔs 8% pan dɛn bɔdi wet, we di plesibo grup gɛt 7% pan dɛn bɔdi wet.

fכ kכnklud, Semaglutid na GLP-1 rεsεptכr agonist dכg wit aplikεshכn valyu insay mכltipכl fil dεm. insay di fild fכ mεtabolism tritmεnt, i de kכntro di bכdi glukכs lεvεl fayn fayn wan bay we i de biεn di GLP-1 rεsεpכta dεm, protεkt insulin sekreshכn, εn inhibit glukagon rilis, we de gi imכtant tritmεnt opshכn fכ di sik pipul dεm we gεt tayp 2 mεtabolism. Insay di aspek fɔ ɔbisiti tritmɛnt, Semaglutid de ridyus di ɛnaji we dɛn de it bɔku bɔku wan tru mɛkanism dɛn lɛk sɛntral apɛtit 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, Semaglutid de sho bak di pɔtɛnɛshɛl aplikeshɔn prɔspɛkt dɛm fɔ prɛvɛnshɔn ɛn tritmɛnt fɔ di sik dɛm we de kam pan di at ɛn di blɔd. di impruvmεnt we i de mek fכ di kכdivaskyul risk fכktכ dεm de gi nyu we fכ ridyus di insidεns fכ di kכdivaskyul ivent dεm.

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 ^[9]..

▎ 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 ɔ f di Pakistan Mɛdikal Assosiayshɔn, 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.

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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.