GLP-3 30mg

▎ GLP-3 Struktrɔ

▎ GLP-3 Risach

Wetin na di risach bakgrɔn fɔ GLP-3?

Fat pasmak dɔn bi wan pan di big big pɔblik wɛlbɔdi prɔblɛm dɛn na di sosayti tide. I kin gi bɔku bɔku wɛlbɔdi prɔblɛm dɛn lɛk tayp 2 mɛtabolism mɛlitɔs, sik dɛn we de ambɔg di at ɛn di blɔd, ay blɔd prɛshɔn, dislipidemia, ɛn di sik we nɔ gɛt rɔm we gɛt fat liva. Wit di kɔntinyu we di pipul dɛn we fat de bɔku, dɛn de nid fɔ gɛt nyu tritmɛnt dɛn we go ebul fɔ manej di bɔdi wet fayn fayn wan ɛn mek di wɛlbɔdi kɔndishɔn bɛtɛ ^[1] . Pan ɔl we di tin dɛn we pɔsin kin du fɔ liv in layf, lɛk fɔ mek i ebul fɔ du bɔku tin ɛn fɔ kɔntrol di it we i de it, na di men tin dɛn we dɛn kin du fɔ mek dɛn ebul fɔ kɔntrol dɛn wet, i rili at fɔ mek bɔku big pipul dɛn we fat pasmak fɔ mek dɛn kɔntinyu fɔ lɔs dɛn wet fɔ lɔng tɛm.

GLP-3, as nכvel tripl rεsεpכta agonist, kin akt pan di glukagכn lεk pεptida-1 rεsεpכta (

GLP-1R), glukכs-dipεndεnt insulinotropik pכlipεptida rεsεptכr (GIPR), εn glukכgכn rεsεptכr (GCGR). dis mכlti-rεsεptor mεkanism fכ akshכn de εndow am wit sכm advantej dεm na di fil fכ lכs weit. we yu kכmpεr wit di weit lכs dכg dεm we de akt pan wan rεsεpכta nכmכ, GLP-3 kin mכr kכmprεhεnsiv rεgεl di bכdi in mεtabolik prכsεs dεm ^[1] . GLP-3 de ajɔst di wet we i de lɔs bay we i de rigul bɔku ɔmon rεsεpכta dεm, nכto nכmכ de sho rεmarkabl efεktiv bכt i de gεt rεlatεvli mild gεstrointestinal sayd ifekt dεm. apat frכm dat, as tripl rεsεptכr agonist, GLP-3 gεt mכr pawaful weit lכs ifekt εn wan wayda rεnj כf aplikεbl populeshכn kכmpεr wit כda nyu weit lכs drog dεm.

Wetin na GLP-3?

GLP-3 na nכvel lכng-aktin glukagכn lεk pεptida-1 (GLP-1) rεsεptכr agonist. i de modify εn optimiz bays pan di strכkchכ fכ nεchכral GLP-1, εn i kin spεshal fכ biεn εn aktibכt di GLP-1 rεsεpכta, fכ εksyεrt fysiolojikal fכnshכn dεm we sכm kayn we lεk di nεchכral GLP-1, lεk fכ promuot insulin sekreshכn, inhεbit glukagon sekreshכn, delay gastric εmpti, rεdכks apεtit, εtk I gεt brayt aplikεshכn prכspεkt in di tritmεnt fכ mεtabolism εn weit mεnejmεnt.

Wetin na di mεkanism fכ akshכn fכ GLP-3?

di mεkanism fכ akshכn fכ GLP-3 kכmכt frכm in agonistik ifekt dεm pan mכltipכl rεsεpכta dεm. fכs, in agonistik ifekt pan di glukagon lεk pεptida-1 rεsεptכr (GLP-1R) kin inkrεs insulin sekreshכn, inhibit glukagon sekreshכn, lכs di bכdi glukכs lεvεl, εn di sem tεm delay di gεstrik εmpti, inkrεs di satiety, εn ridyus di it we yu de it ^[2] . sεkכn, in agonistik ifekt pan di glukכs-dipεndεnt insulinotropik polipεptida rεsεpכta (GIPR) kin promuot insulin sekreshכn, εnhans glukכs yutilizeshכn, εn afekt fεt mεtabolism, inhεbit lipolysis εn promuot fεt sεntesis ^[2] . pan tap dat, di agonistik ifekt we GLP-3 gεt pan di glukagon rεsεpכta (GCGR) kin כlwayz protεkt glycogenolysis εn gluconeogenesis insay di liva, we de inkrεs di bכdi glukכs lεvεl. כl di akshכn fכ GLP-3, dis glukכs-rayzin ifekt de כfset bay di ifekt dεm we di כda tu rεsεpכta dεm de gi, we i de protεkt lipolysis εn ridyus fεt akyumyuleshכn ^[2] . dis mכlti-target mכd fכ akshכn kin bi mכr ifektiv fכ trit fכ fat pas singl rεsεpכta agonist dεm.

bay we i de aktibכt dεn tri rεsεpכta dεm ya wan tεm, GLP-3 kin εksyεrt difrεn mεtabolik rεgεdyushכn ifekt dεm εn prodyuz tεrapi ifekt dεm pan fכ fat εn sik dεm we de rilet to am. pan tεm fכ rεgεl di blכd glukכs lεvεl, biכs di aktibכshכn fכ GLP-1R εn GIPR de protεkt insulin sekreshכn εn inhεbit glukagon sekreshכn, εn di aktibכshכn fכ GCGR de כfset bay di ifekt dεm we di כda tu rεsεpכta dεm de gi, GLP-3 kin rigul di blכd glukכs lεvεl fayn fayn wan, we na big minin fכ di tritmεnt fכ tayp 2 mεtabolism mεllitus ^{[1, 2]} . pan tεm fכ ridyus fεt akyumyuleshכn, di aktibכshכn fכ GCGR de promuot lipolysis εn ridyus fεt akyumyuleshכn, we di aktibכshכn fכ GLP-1R de inkrεs satiety εn ridyus fכd intake, we de ridyus fεt sεntesis mכr ^[1] . apat frכm dat, GLP-3 gεt impruv ifekt bak pan nכn-alkohol fεt liva sik. I kin mek di fat we de insay di liva nɔ bɔku ɛn i kin mek di liva wok fayn.

HbA1c, bɔdi wet, blɔd prɛshɔn, ɛn lipid dɛn Data na lɛst-skwea min (wit mistek bar dɛn we de sho SE dɛn) frɔm di ɛfifikɛshɔn analisis sɛt, pas nɔmɔ dɛn no ɔda we.

Sos:PubMed ^{[4] we dɛn pul am.}

Insay us aspek dɛn GLP-3 de sho in ifɛkt dɛn?

GLP-3 de sho signifyant ifekt in mכltipכl aspek dεm

Sigifikant weit lכs ifekt: GLP-3 dכn sho signifyant weit lכs ifekt in mכltipכl klinik trial dεm. Fɔ ɛgzampul, insay wan klinik stɔdi we involv 338 big pipul dɛn (Jastreboff AMM, 2023), pasɛnt dɛn we dɛn trit wit difrɛn doz dɛn fɔ GLP-3 bin gɛt bɔku bɔku wet lɔs we dɛn ol 48 wik. Na dɛn wan ya, di pasɛnt dɛn we bin de na di 12mg doz grup bin lɔs 24.2% pan dɛn bɔdi wet, ɛn wan ay pat pan di pasɛnt dɛn bin ajɔst di wet lɔs to difrɛn digri dɛn. Fɔ ɛgzampul, pan di pasɛnt dɛn we bin de tek 4mg, 8mg, ɛn 12mg dos, 92%, 100%, ɛn 100% pan di pasɛnt dɛn, rispɛktvɔli, lɔs 5% ɔ mɔ pan dɛn bɔdi wet. Insay wan ɔda stɔdi ^[3] , tu randomized kɔntrol trayal dɛn we involv 353 pasɛnt dɛn wit tayp 2 mɛtabolism mɛlitus sho se we dɛn kɔmpia am wit di plasɛbo, GLP-3 kin ridyus di bɔdi wet fɔ di pasɛnt dɛn bad bad wan bay 11.89kg, ɛn i kin ridyus bak di glycated hemoglobin (HbA1C). Apat frɔm dat, insay trayal fɔ big pipul dɛn we fat we nɔ gɛt mɛtabolism, GLP-3 mek di sik pipul dɛn lɔs 24.2% pan dɛn wet, ɛn 83% pan di pasɛnt dɛn lɔs 15% ɔ mɔ pan dɛn bɔdi wet we dɛn ol 48 wik. dis rizulεt dεm sho se GLP-3 gεt big pכtεnshal fכ lכs wet.

tritmεnt fכ tayp 2 mεtabolism mεlitus: GLP-3 de sho bak sכm pכtεnshal fכ di tritmεnt fכ tayp 2 mεtabolism mεlitus. insay sכm klinik trial dεm, GLP-3 dכn sho se di glycated hemoglobin (HbA1c) dεn dכn dכn εn di dכz-dipεndεnt we di wet lכs. fכ egzampl, insay wan stכdi, pan pasεnshכn dεm we gεt tayp 2 mεtabolism mεlitus, GLP-3 sho se i gεt bכku bכku blכd glukכs kכntrכl ifekt dεm. we yu kכmpεr wit di plasεbo, glycated hemoglobin dכn dכn bay 1.64% ^[3] . apat frכm dat, insay wan randomizεd, dכbl-blaynd, plasεbo εn aktv-kכntrol paralel-grup fεz 2 trayal, animal mכdel dεm wit tayp 2 mεtabolism mεlitus, afta dεn gεt GLP-3 tritmεnt, sho se di glycated hεmoglobin lεvεl dεm dכn sכmtεm, εn dεn bכdi wet dεn dכn dכn bak insay wan dכz-dipεndεnt mεnεj ^[4] . dis kin bi fכ di kכmprεhεnsiv ifekt dεm we di dכg gεt pan GLP-1, GCGR, εn GIPR, we de impruv glukכs mεtabolism εn εnεji bεlε.

di impruvmεnt fכ di kכdivaskyul risk fכktכ dεm: GLP-3 nכ kin כnli ridyus di bכdi wet bכt i kin impruv di kכdivaskyul risk fכktכ dεm, lεk di sεrum lipid profayl εn di glycated hemoglobin lεvεl. dis de sho se wan klos pathophysiological link de bitwin fat εn kכdivaskyul sik dεm, εn GLP-3 kin impruv di kכdivaskyul hεlth fכ di fat pasεnshכn dεm tru mכltipכl path dεm. fכ egzampl, fכ ridyus di nכn-HDL-C, apoB, εn LDLP lεvεl dεm kin ridyus di risk fכ atεrosklεrosis; fכ ridyus di glycated hεmoglobin lεvεl kin impruv di bכdi glukכs kכntrכl pan pasεn dεm we gεt mεtabolism, we de ridyus di risk fכ kכdivaskyul kכmplikεshכn dεm ^{[3, 5, 6].}.

Tritmεnt fכ nכn-alkoholik fεt liva sik (NAFLD): GLP-3 na nכvel tripl rεsεptכr agonist pεptida we de tכk to di glukagon rεsεptכr (GCGR), glukכs-dipεndεnt insulinotropik polipεptida rεsεptכr (GIPR), εn glukagon lεk pεptida-1 rεsεptכr (GLP-1R). stכdi dεn sho se GLP-3 gεt di potenshal fכ trit nכn-alkohol fεt liva sik. Insay wan stכdi, dεn bin kכnεkt wan randomizεd, dכbl-blaynd, plasεbo-kכntrol trial fכ 48 wiks pan patisipan dεm wit mεtabolik disfכnkshכn-asכsiet fεt liva sik εn liva fεt kכntεnt ≥10%. di risal sho se na 24 wik, di avrej rilitiv chenj dεm na di liva fεt frכm di beslayn insay patisipan dεm we dεn trit wit difrεn doz dεm fכ GLP-3 (1mg, 4mg, 8mg, εn 12mg) na -42.9%, -57.0%, -81.4%, εn -82.4%, rispεktivli, we di wan na di plasεbo grup na bin +0.3% ^[7] . dis sho se GLP-3 kin gεt sכm sכm tεrapi ifekt pan nכn-alkohol fεt liva sik.

fכ kכnklud, as nכvel tripl rεsεptכr agonist, GLP-3 sho big pכtεnshal fכ trit fכ fat εn sik dεm we de rilet to am. i kin rεgεl mכtalman mεtabolism frכm mכltipכl dimεnshכn dεm bay we i de aktibכt di glukagon rεsεpכta, glukכs-dipεndεnt insulinotropik polipεptida rεsεpכta, εn glukכs lεk pεptida-1 rεsεpכta, we de impruv di bכdi glukכs kכntrכl, ridyus di bכdi wet, εn rεgεl di lipid mεtabolism. Di we aw GLP-3 dɔn kam dɔn briŋ nyu tritmɛnt opshɔn fɔ di wan dɛn we fat, tayp 2 mɛtabolism mɛllitus, ɛn ɔda tin dɛn.Dɛn de op se i go brok di limiteshɔn dɛn we tradishɔnal singl riseptɔ agonist drɔgs dɛn gɛt, gi wan mɔ pawaful wɛpɔn fɔ sɔlv di prɔblɛm dɛn we de bɔku mɔ ɛn mɔ we gɛt fɔ du wit fat ɛn mɛtabolik sik dɛn, fɔ mek di divɛlɔpmɛnt go bifo pan di mɛdikal fild dɛn we gɛt fɔ du wit am, fɔ mek di kwaliti fɔ layf fɔ di sik pipul dɛn bɛtɛ, ɛn fɔ ridyus di soshal mɛdikal lod we dɛn kin du.

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

Rosenstock J na wan masta sabi bukman we gɛt bɔku pawa pan di mɛdikal fild, i de wok tranga wan wit institiushɔn dɛn lɛk di Yunivasiti ɔf Tɛksas Sawt Wɛstɛn Mɛdikal Sɛnta ɛn di Yunivasiti ɔf Tɛksas Dalas. I de du risach bak na sɛnta dɛn lɛk di Kanada VIGOR Senta ɛn Veloc Clin Res Ctr Med Siti. 

In risach de span endokrinoloji ɛn mɛtabolism, kadiovaskular sistɛm ɛn kadyolɔji, famakɔlɔji, ɛn ɛkspirimɛnt mɛrɛsin, wit fɔs fɔ mɛtabolism, fat, ɛn tritmɛnt dɛn we gɛt fɔ du wit am ɛn divɛlɔpmɛnt fɔ drɔgs. J Rosenstock dɔn gɛt bɔku sakrifays pan klinik mɛrɛsin, we dɛn kɔl am Highly Cited Researcher frɔm 2017 to 2024. Dis de sho di ay impak ɛn bɔku pipul dɛn we de no in wok. Tru kolaboreshɔn wit bɔku risach institiushɔn dɛm, i dɔn saksesfuli translet di bɛsis risach fayndin dɛm to klinik aplikeshɔn, bɛnifit pasɛnt dɛm wit mɛtabolik ɛn kadivaskyul sik dɛm ɛn advans mɛdikal sayɛns. Rosenstock J de list in di rεfrεns fכ saytεshכn [4].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] Kaur M, Misra S. Wan rivyu fɔ wan invɛstigeshɔn drɔg GLP-3, wan nyu triplɛ agonist ɛjɛn fɔ di tritmɛnt fɔ ɔbisiti[J]. Yuropian Jɔnal fɔ Klinik Famakɔlɔji, 2024,80(5):669-676.DOI:10.1007/s00228-024-03646-0.

[2] Jastreboff A. M., Kaplan L. M., Frias J. P., ɛn ɔda pipul dɛn. Tripl-Hכmon-Rεsεptor Agonist GLP-3 fכ Obesiti - Wan Faz 2 Trayal[J]. Nyu Ingland Jɔnal fɔ Mɛdisin, 2023,389(6):514-526.DOI:10.1056/NEJMoa2301972.

[3] Lopez D. C., Pajimna J. T., Milan M. D., ɛn ɔda pipul dɛn. 7792 Efficacy of GLP-3 fכ Weight Ridukshכn εn In Cardiometabolic Efεkt dεm bitwin Adult dεm: A Sistεmatik Rivyu εn Mεta-Analysis[J]. J ɔ rnal ov di Ɛndokrin Sɔsayti, 2024,8(1):163-749.DOI:10.1210/jendso/bvae163.749.

[4] Rosenstɔk J, Frias J, Jastrebɔf A. M., ɛn ɔda pipul dɛn. GLP-3, wan GIP, GLP-1 ɛn glukagon rεsεptכr agonist, fכ pipul dεm wit tayp 2 mεtabolism: wan randomizεd, dכbl-blaynd, plasεbo εn aktv-kכntrol, paralel-grup, fεz 2 trayal we dεn kכnεkt na di USA[J]. Lancet, 2023,402(10401):529-544.DOI:10.1016/S0140-6736(23)01053-X.

[5] Nicholls S, Pirro V, Lin Y, ɛn ɔda pipul dɛn. tripl-hכmon rεsεptכr agonist GLP-3 de impruv lipoprotein εn apolipoprotein profayl dεm sכmtεm insay patisipan dεm we fat כ ova wet[J]. Yuropian At Jɔnal, 2024,45.DOI:10.1093/eurheartj/ehae666.1501.

[6] Ray A. GLP-3: wan tripl inkrεtin rεsεptכr agonist fכ obesity mεnejmεnt[J]. Ekspɛkt Opinion Pan Investigeshɔn Drug, 2023,32(11):1003-1008.DOI:10.1080/13543784.2023.2276754.

[7] Sanyal A. J., Kaplan L. M., Frias J. P., ɛn ɔda pipul dɛn. Tripl hכmon rεsεptכr agonist GLP-3 fכ mεtabolik disfכnkshכn-asכsiet stεatotik liva sik: wan randomizεd fεz 2a trayal[J]. Nature Mεdisin, 2024,30 (7): 2037-2048.DOI: 10.1038/s41591-024-03018-2.

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.