GLP-1 5mg

▎ GLP-1 Struktrɔ

▎ GLP-1 Risach

Wetin na di risach bakgrɔn fɔ GLP-1?

GLP-1 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 glukagon sekreshכn fכ rεgεl di blכd glukכs lεvεl. di divεlכpmεnt fכ GLP-1 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 GLP-1, di alanin na posishכn 8 de riples am wit α-aminoisobutyric acid (Aib), we nכ de nכmכ de impruv di stεbiliti fכ di drog bכt i de εnhans in binding fכs wit GLP-1 rεsεpכta dεm ^[2] . wan yunik fεt asid sayd chen de ad to di C-tεrminus fכ GLP-1, 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] . GLP-1 bin divεlכp fכs bays pan risεch εn modifyushכn fכ nεchכral GLP-1, we dεn aim fכ gi mכr ifektiv tritmεnt fכ pasεn dεm wit tayp 2 dayabεtis ^{[1, 2]} . tru dεn strכkchכral optimizεshכn dεm ya, GLP-1 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 divɛlɔpmɛnt fɔ GLP-1 na impɔtant tin we dɛn dɔn du, we de briŋ nyu tritmɛnt opshɔn fɔ di wan dɛn we gɛt tayp 2 dayabitis. 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 mεkanism fכ akshכn fכ GLP-1?

GLP-1 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:

GLP-1 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 ridyus 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] . GLP-1 de indyuz weit lכs in rodεnt tru distribyut nyural path dεm. stכdi dεn 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. GLP-1 de aktibכt c-Fos insay tεn bren rijyכn dεm, inklud di hindbren εria dεm we dεn tכk dεn tכk bכt 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:

GLP-1 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 bolster di pyloric sphincter tεnshכn, εn i de mek di gastric fכd rεtεnshכn lכng, i de delay di duodenal εntri εn i de mek di bכdi glukכs spayk dεm afta it, we de mek di lεvεl dεm we de stebul ^[5] . apat frכm dat, GLP-1 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 bɛtɛ 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:

GLP-1 de promuot di rilis fכ naytrik oksayd (NO) εn כda vasodilator dεm frכm vaskulεr εndoteyl sεl dεm, we de εnhans vasodilayshכn εn bכdi fכ fכlכ. i de inhεbit inflameshn εn כksidεtiv strεs bak, we de ridyus di εndoteyl dεmεj εn atεrosklεrosis risk. We i de stɔp di apɛtit ɛn it, i de ɛp fɔ lɛ pɔsin nɔ gɛt bɔku bɔku bɔdi, i de mek di lipid dayabitis bɛtɛ, i de mek di triglisɛrɛyd ɛn lɔw-dɛnsity lipoprotein kɔlɔstrel (LDL-C) go 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 rεdכks di kכdivaskyul sik risk fכktכ dεm ^[6]. .

GLP-1 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 כptimayzεshכn, di tεm we dεn de disayn GLP-1, dεn bin adopt wan mεtכd fכ rivεrsibl binding to albumin fכ prolכng di durεshכn fכ akshכn fכ di dכg. 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, GLP-1 gɛt bɛtɛ wet lɔs ifɛkt. GLP-1 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 dayabεtis (T2DM), i tan lεk se dεn injεkshכn GLP-1 we dεn de injεkt GLP-1 insay di wik εvri wik, i bεtεh fכ lכs di wet pas כda GLP-1RA dεm we dεn de gi dεm ɛvri wik. Insay wan faz II doz-fayndin trayal fɔ fat pasɛnt dɛn we nɔ gɛt T2DM, wan tɛm ɛvride sabkyutan injɛkshɔn fɔ GLP-1 bin mɔ ifɛktiv fɔ weit lɔs pas plasɛbo ɛn wan tɛm ɛvride 3.0mg liraglutide. Di wet we GLP-1 mek insay dis stɔdi pas di standad fɔ anti-obesity drɔgs 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 subkutan injɛkshɔn fɔ GLP-1 gɛt di potenshal fɔ bi wan fiuja weit lɔs drɔg ^[7]. .

GLP-1 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-dכz antidiabetik glukagon-lεk pεptida 1 agonist GLP-1 sכmtεm impruv di simptom dεm fכ hat fεil wit prεsiv εjεkshכn frakshכn (HFpEF) εn rεdכks N-tεrminal pro-B-tayp natriuretik pεptida (NT-proBNP) lεvεl dεm. di stכdi tεst di ifekt we akyu GLP-1 tritmεnt gεt pan isolεt hυman rayt atrial trabεkul dεm εn fכnshכn se GLP-1 inkrεs di tεnshכn fכ hυman atrial trabεkul dεm pas tri tεm insay wan dכz-dipεndεnt we, witout inkrεs di tεndens fכ aritmia. dis ifekt de mכst lεk fכ inkrεs sarkoplasmik rεtikul Ca2+ כptek. hεy dכz GLP-1 tritmεnt pan pipul dεm we hat fεil kin impruv atria fכnshכn εn dis kin mek dεn sכmtεm sכmtεm sכmtεm dεm ^[8]. .

GLP-1 de stכdi fכ di tritmεnt fכ nכn-alkohol stεatohepatitis (NASH). I rayshɔnal dizayn dɔn mek big kɔntribyushɔn fɔ impɔtant blɔd glukɔs kɔntrol, wet, blɔd prɛshɔn, lipid, β-sɛl fɔ wok, ɛn di kadiovaskular sistɛm pan pasɛnt dɛn we gɛt tayp 2 dayabitis. pan tap dat, di divεlכpmεnt fכ wan כral fכmyuleshכn fכ GLP-1 kin gi כda bεnεfit to di sik pipul dεm we i kam pan di tritmεnt kכmplians ^[9]. .

Difrɛns pan di Weyt Lɔs Ifɛkt dɛn we GLP-1 gɛt akɔdin to pipul dɛn

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 dayabitis: 

Insay di SELECT kadiɔvaskyuɛl autkam trayal, GLP-1 ridyus di big big advays kadiɔvaskyuɛl ivin dɛm (MACE) bay 20% pan 17,604 big pipul dɛm we gɛt kadiɔvaskyuɛl sik we dɔn de, we gɛt bɔku bɔku bɔdi ɔ we fat pasmak, ɛn we nɔ gɛt dayabitis ^[10] . Insay dis prɛ-spɛsifikɛd analisis, risach pipul dɛn bin ɛgzamin di ifɛkt dɛn we GLP-1 gɛt pan wet, anthropometric autkam, sef, ɛn tolɛrabiliti bay beslayn bɔdi mas indɛks (BMI). Di pasɛnt dɛn we bin de gɛt GLP-1 bin gɛt sɔstayn wet lɔs fɔ 65 wik, we bin kɔntinyu fɔ de te to 4 ia. Na 208 wik, GLP-1 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 across man ɛn uman, ɔl di etnik, bɔdi tayp, ɛn rijyɔn dɛn GLP-1 bin gɛt fɔ du wit smɔl siriɔs bad bad tin dɛn we apin Fɔ ɛni BMI kategori (<30, 30 to <35, 35 to <40, ɛn ≥40 kg/m²), GLP-1 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 plesibo). impruvmεnt dεm kכmpεr to plasεbo na 208 wik, wit weit lכs we dεn sכstayn ova 4 ia.

Di tin dɛn we kin apin we pɔsin we fat ɔ we gɛt bɔku bɔku bɔdi we nɔ gɛt dayabitis:  

Wan sistamat rivyu bin evaluate di efficacy ɛn sef fɔ GLP-1 insay pipul dɛn we fat ɔ we gɛt bɔku bɔku bɔdi we nɔ gɛt dayabitis ^[11] . Dis rivyu sεntez di risכlt frכm mכltipכl klinik trial dεm, we hεlayt GLP-1 in impak pan weit lכs, mεtabolik paramita, εn כvala hεlth autkam. Di tin dɛm we dɛn fɛn sho se GLP-1 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 dɛm. 

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 sabkyutan GLP-1 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): GLP-1 indyuz 16% (17 kg) vs. 6% (6 kg) weit lɔs. Insay wan doz-ɛksplɔreshɔn RCT insay pasɛnt dɛn we nɔ gɛt dayabitis (N = 1,210), ɛvri wik 2.4 mg GLP-1, 1.0 mg GLP-1, 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). Fɔ 2.4 mg vs. 1.0 mg, NNT = 9. AE profayl dɛn bin simpul akɔdin to di doz dɛn. Insay wan wet mentenɛns RCT (N = 803), patisipan dɛn we nɔ gɛt dayabitis bin gɛt 2.4 mg GLP-1 ɛvri wik fɔ 20 wik, dɔn dɛn bin randomiz fɔ kɔntinyu GLP-1 ɔ chenj to plesibo. Afta 48 wik, di wan dɛn we kɔntinyu fɔ yuz GLP-1 lɔs 8% vs di wan dɛn we yuz plasɛbo we gɛt 7%. 

in sכmari, GLP-1 na GLP-1 rεsεptכr agonist wit mכlti-dכmεn aplikεshכn valyu. Insay dayabitis tritmɛnt, i de tay to GLP-1 riseptɔ fɔ mek insulin sekreshɔn ɛn inhibit glukagon rilis, i de kɔntrol di blɔd glukɔs lɛvɛl fayn fayn wan ɛn gi wan impɔtant tritmɛnt opshɔn fɔ di wan dɛn we gɛt tayp 2 dayabitis. Insay di fil fɔ tritmɛnt fɔ fat, GLP-1 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, GLP-1 de sho di pɔtɛnɛshɛl aplikeshɔn prɔspɛkt dɛm fɔ prɛvɛnshɔn ɛn tritmɛnt fɔ di sik dɛm we de kam pan 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 GLP-1 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 sik pipul dɛn kwaliti layf ɛn wɛlbɔdi bɛtɛ.

Bɔt di pɔsin we rayt di buk

Di tin dɛm we wi dɔn tɔk bɔt, na ɔl di tin dɛm we Cocer Peptides dɔn du risach, ɛdit ɛn kɔmpilayt.

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 if 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 pɔsin in 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 du bɔku tin dɛn de ɛnrich di mɛrɛsin we de mek di at ɛn di blɔd, we 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. GLP-1: 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 GLP-1, di Fכs Ingεstibl Glukagon-Lεk Pεptid-1 Risεptor Agonist: I kin bi Mεjik Bulet fכ Tayp 2 dayabεtis?[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. GLP-1 de lכs 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 ɔ f dayabitis 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. GLP-1 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. GLP-1 as wan prɔmis antiɔbesiti drɔg[J]. Obesiti Rivyu, 2019,20 (6): 805-815.DOI: 10.1111/obr.12839.

[8] Hegner P, Seitz S, Schopka S, ɛn ɔda pipul dɛn. GLP-1 de impruv 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 GLP-1[J]. Frɔntiers in Ɛndokrinɔlɔji, 2019,10.DOI: 10.3389/fendo.2019.00155.

[10] Ryan D. H., Lingvay I, Dinfild J, ɛn ɔda pipul dɛn. Lכng tεm weit lכs ifekt dεm fכ GLP-1 pan fכ fat we nכ gεt dayabεtis insay di SELECT trayal[J]. Nature Mεdisin, 2024,30 (7): 2049-2057.DOI: 10.1038/s41591-024-02996-7.

[11] Alanazi M, Alshahrani J. A., Aljaberi A. S., ɛn ɔda pipul dɛn. Efεkt we GLP-1 gεt pan pipul dεm we fat כ ova wet witout dayabεtis[J]. Cureus Jɔnal fɔ Mɛdikal Sayns, 2024,16(8).DOI:10.7759/cureus.67889.

[12] Ojeniran M, Dube B, Pej A, ɛn ɔda pipul dɛn. GLP-1 fכ weit lכs[J]. Kanada Famili Dɔktɔ, 2021,67(11):842.DOI:10.46747/cfp.6711842.

[13] Papakonstantinou I, Tsioufis K, Katsi V. Spɔtlayt pan di Mɛkanism fɔ Akshɔn fɔ GLP-1[J]. Kɔrɛnt Isyu dɛn na Mɔlikul Bayoloji, 2024,46(12):14514-14541.DOI:10.3390/cimb46120872.

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.