GLP-3 10mg

▎ GLP-3 Struktrɔ

▎ GLP-3 Risach

Wetin na di risach bakgrɔn fɔ GLP-3?

Fɔ fat pasmak na wan pan di big prɔblɛm dɛn we de mit pipul dɛn tide. If pɔsin fat, i kin mek i gɛt difrɛn difrɛn wɛlbɔdi prɔblɛm dɛn, lɛk di kayn we aw i de wok na di bɔdi, di sik dɛn we de na di at ɛn di blɔd, ay blɔd prɛshɔn, dislipidemia, ɛn di sik we de na di liva we nɔ gɛt rɔm. Wit di kɔntinyu we di pipul dɛn we fat de bɔku, pipul dɛn de aks fɔ nyu tritmɛnt dɛn we go ebul fɔ manej di bɔdi wet fayn fayn wan ɛn mek di wɛlbɔdi biznɛs bɛtɛ ^[1] . Pan ɔl we fɔ chenj di we aw pɔsin de liv in layf, lɛk fɔ du mɔ bɔdi wok ɛn fɔ ridyus di it we dɛn de it, na di men we fɔ mek dɛn nɔ gɛt bɔku bɔku bɔdi, fɔ mek dɛn nɔ gɛt bɔku bɔku bɔdi fɔ lɔng tɛm stil na prɔblɛm fɔ bɔku big pipul dɛn we di sik dɔn afɛkt. GLP-3 na nכvel tripl rεsεpכta agonist we de akt pan di glukכgכn lεk pεptida-1 rεsεpכta (GLP-1R), glukכs-dipεndεnt insulinotropik polipεptida rεsεpכta (GIPR), εn glukagכn rεsεpכta (GCGR). dis mכlti-rεsεptor mεkanism fכ akshכn de gi am yכnik advantej dεm fכ lכs weit. we yu kכmpεr wit di weit lכs dכg dεm we de akt pan wan rεsεpכta, GLP-3 kin mכr kכmprεhεnsiv rεgεl di bכdi in mεtabolik prכsεs dεm ^[1] . GLP-3 de mek yu lכs di wet bay we i de rεgεl mכltipכl כmon rεsεpכta dεm. I nɔ jɔs gɛt signifyant weit lɔs ifɛkt bɔt i gɛt rili mild gastrointestinal sayd ɛfɛkt. apat frכm dat, we yu kכmpεr wit כda nyu weit lכs drog dεm, GLP-3, as tripl rεsεptכr agonist, gεt mכr pawaful weit lכs ifekt εn wan big rεnj כf aplikεbl populeshכn.

Wetin na di mεkanism fכ akshכn fכ GLP-3?

di mεkanism fכ akshכn fכ GLP-3 mεnli kכmכt frכm in agonistik ifekt dεm pan mכltipכl rεsεpכta dεm. fכs, in agonistik ifekt pan di glukagon lεk pεptida-1 rεsεpכta (GLP-1R) de inkrεs insulin sekreshכn, inhεbit glukagon sekreshכn, rεdכks di blכd glukכs lεvεl, εn di sem tεm i de delay di gεstrik εmpti, i de inkrεs di satiety, εn i de ridyus di it we yu de it ^[2] . sεkכn, in agonistik ifekt pan di glukכs-dipεndεnt insulinotropik polipεptida rεsεptכr (GIPR) kin promuot insulin sekreshכn, εnhans glukכs yutilizeshכn, εn gεt impak pan fεt mεtabolism, inhεbit lipolysis εn protεkt fεt sεntesis ^[2] . pan tap dat, pan כl we di agonistik ifekt we GLP-3 gεt pan di glukagon rεsεpכta (GCGR) kin כlwayz fכ protεkt glycogenolysis εn gluconeogenesis insay di liva, we de inkrεs di blכd glukכs lεvεl, כnda di akshכn fכ GLP-3, dis ifekt we de inkrεs di bכdi glukכs de כfset bay di ifekt dεm we di כda tu rεsεpכta dεm de gi. di sem tεm, i de mek di lipolysis kכmכt εn i de ridyus di fεt we de kכmכt ^[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 fכ di aktibכshכn fכ GLP-1R εn GIPR we de promuot insulin sekreshכn εn inhibit glukagon sekreshכn, εn di aktibכshכn fכ GCGR we 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 ^{[1, 2]} . pan tεm fכ ridyus fεt akyumyuleshכn, di aktibכshכn fכ GCGR de promuot lipolysis εn ridyus fεt akyumyuleshכn. di sem tεm, di aktibכshכn fכ GLP-1R de inkrεs di satεti εn ridyus di it we yu de it, we de ridyus di fεt sεntesis mכr ^{[1, 2]} . apat frכm dat, GLP-3 gεt bεnεfit 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. Wan randomized, double-blind, placebo-controlled trial sho se di avrej rilitiv chenj na di liva fat na di GLP-3 tritmɛnt grup na 24 wiks bin rili smɔl pas di wan na di plasɛbo grup ^[3]..

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.}

aw εksakכt GLP-3 de rεgεl di glukכs mεtabolism afta i aktibכt di tri rεsεpכta dεm?

GLP-3 de rεgεl di bכdi glukכs tru mכltipכl mεkanism dεm, we inklud fכ aktibכt GLP-1 εn GIP rεsεpכta dεm, fכ mek insulin sekreshכn, inhibit glukagon sekreshכn, delay di gεstrik εmpti, rεgεl di fεt mεtabolism, εn fכ ridyus di ANGPTL3/8 lεvεl dεm. we i kam pan bכdi glukכs rεguleshכn, GLP-3 de akt pan GLP-1 εn GIP rεsεpכta dεm, i de protεkt di sεnsitiviti fכ di pankrεas β sεl dεm to glukכs, i de sεntez εn rilis insulin, εn afta dat i de protεkt di כptek εn yutilizeshכn fכ glukכs bay tisu dεm, we de achy di ifekt fכ ridyus di glukכs na di bכdi ^{[4, 5]} .In wan stכdi we dεn du pan tayp 2 mεtabolism pasεnshכn dεm, GLP-3 sho wan siknifikant ifekt fכ ridyus glycated hemoglobin (HbA1c), we bכku bεnεfit frכm in rol fכ stimulat insulin sekreshכn (Rosenstock J, 2023). di sem tεm, we dεn aktibכt di GLP-1 rεsεpכta kin inhεbit di sekreshכn fכ glukagon bay pankrεas α sεl dεm, we de mek di bכdi glukכs nכ tu hכy. insay klinik stכdi dεm, dεn si se di glukכn lεvεl fכ di pasεn dεm we de yuz GLP-3 dכn dכn, we in tכn de εp fכ mεnten di stεbiliti fכ di blכd glukכs ^{[4, 5]} . fכ aktibכt GLP-1 εn GIP rεsεpכta dεm kin delay bak di rεt fכ εmpti di gεstrik, slo dכn di dijeshכn εn absכpshכn fכ it, εn rεdכks di shap rise in postprandial bכdi glukכs. stכdi dεn sho se di gastric εmpti tεm fכ di pasεn dεm we dεn trit wit GLP-3 de sכmtεm lכng afta dεn it, we de rεdכks di pik valyu fכ di postprandial bכdi glukכs ^[4]..

di rεguleshכn fכ fεt mεtabolism bay GLP-3 de afekt glukכs mεtabolism bak indaykt wan. fכ egzampl, insay stכdi dεm pan pipul dεm we fat, dεn fכnshכn se GLP-3 kin ridyus di lεvεl dεm fכ triglisεrayd (TG), lכw dεnsiti lipoprotein (LDL), εn vεri lכw dεnsiti lipoprotein (VLDL) kכlestכl ^{[2, 6]} . dis impruvmεnt na di lipid mεtabolism kin riliyt to di impruvmεnt fכ insulin sεnsitiviti, we de kכntribyut fכ kכntrכl glukכs na di bכdi. sכm spεshal, afta GLP-3 tritmεnt, di plasma 3-haydroksibutyrik asid (3-HB) de inkrεs, we de kכmpan wit inkrεs pan 3-haydroksibutyrilkarnitin (C ₄OH), di rεshכn fכ asetilkarnitin to fri kכnitin (C ₂/C ₀), εn mεdiכm-chεn asilkarnitin, we de sho se lipolysis de εnhans insay adipos tisu εn inkrεs dipεndεns pan fεt ɔksidɛshɔn.

GLP-3 kin ridyus di tכtal dihaydroseramid dεm (DhCers), εn dis chenj de sho se di insulin sεnsitiviti dεm we de rεdכks, rεdכks di hεpatik stεatosis, εn sistεmik inflameshn ^[6] .At di sem tεm, GLP-3 kin ridyus di kכnsantreshכn fכ di ANGPTL3/8 kכmpleks bak na di sεrum fכ di tayp 2 mεtabolism pasεnshכn dεm, we de rεgεl glukכs mεtabolism ^[7] . ANGPTL3/8 na di mכst ifektiv sεkyulayt inhibito fכ lipoprotein lipase (LPL), εn in sεrum lεvεl de rilayt dairekt to TG εn lכw-dεnsiti lipoprotein kכlestכl (LDL-C). GLP-3 de ridyus di lεvεl fכ ANGPTL3/8, we kin rεgεl di glukכs mεtabolism bay we i de ridyus di triglisεrayd-rich lipoprotein dεm ^[7]. .

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

Impɔtant ifɛkt we pɔsin kin gɛt we i de lɔs yu wet: 

GLP-3 dɔn sho signifyant weit lɔs ifɛkt dɛn insay bɔku klinik trayal dɛn. fכ egzampl, insay wan klinik stכdi we involv 338 big pipul dεm ^[2] , di pasεn dεm we dεn trit wit difrεn dos dεm fכ GLP-3 bin gεt bכku weit lכs we dεn bin de 48 wik. Na dɛn wan ya, di pasɛnt dɛn we bin de na di 12mg doz grup bin gɛt wet lɔs we na 24.2%, ɛn wan ay prɔpɔshɔn 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 bin lɔs 5% ɔ mɔ pan dɛn bɔdi wet, rispɛktvɔli. Insay wan ɔda stɔdi ^[8] , tu randomized kɔntrol trial we involv 353 tayp 2 mɛtabolism pasɛnt dɛn 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 ridyus glycated hemoglobin (HbA1C). Apat frɔm dat, insay wan trayal pan big pipul dɛn we nɔ gɛt dayabitik we fat, GLP-3 bin mek 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.

Tritmɛnt fɔ tayp 2 mɛtabolism : . 

GLP-3 de sho bak sכm pכtεnshal fכ di tritmεnt fכ tayp 2 mεtabolism. 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, insay tayp 2 mεtabolism pasεnshכn dεm, GLP-3 sho wan siknifikant blכd glukכs kכntrכl ifekt, we ridyus glycated hεmoglobin bay 1.64% kכmpεr wit di plasεbo ^{[4, 8]} . apat frכm dat, insay wan randomizεd, dכbl-blaynd, plasεbo, εn aktv-kכntrol paralel-grup fεz 2 trayal, animal mכdel dεm wit tayp 2 mεtabolism sho wan sכm rεdukshכn pan glycated hεmoglobin lεvεl εn wan dכz-dipεndεnt weit lכs afta dεn gεt GLP-3 tritmεnt ^[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.

Impruvmɛnt fɔ di tin dɛn we kin mek pɔsin gɛt prɔblɛm wit di at ɛn di blɔd: 

GLP-3 nכ kin כnli ridyus di bכdi wet bכt i kin impruv di kכdivaskyul risk fכktכ dεm, lεk di sεrum lipid profayl εn glycated hεmoglobin lεvεl. dis de sho se wan klos pathophysiological kכnεkshכn 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 in mεtabolism pasεnshכn dεm, we de ridyus di risk fכ kכdivaskyul kכmplikεshכn dεm ^[8-10]. .

Tritmɛnt fɔ di sik we dɛn kɔl fat liva we nɔ gɛt rɔm (NAFLD): 

GLP-3 na nכvel tripl rεsεptכr agonist pεptida we de tכk to di glukagכn rεsεpכta (GCGR), glukכs-dipεndεnt insulinotropik polipεptida rεsεpכta (GIPR), εn glukagכn lεk pεptida-1 rεsεpכta (GLP-1R). stכdi dεn sho se GLP-3 gεt pכtεnshal fכ trit nכn-alkohol fεt liva sik. Insay wan stכdi, dεn bin kכnεkt wan randomizεd, dכbl-blaynd, plasεbo-kכntrol trial we las 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 chenj dεm na di liva fεt rεlatεv to di beslayn in 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% ^[3] . 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 aktibכt di glukoz rεsεpכta, glukכs-dipεndεnt insulinotropik polipεptida rεsεpכta, εn glukכn lεk pεptida-1 rεsεpכta, kכmprεhεnsivli rεgεl di bכdi in mεtabolism frכm mכltipכl dimεnshכn dεm, impruv bכdi glukכs kכntrכl, ridyus di bכdi wet, εn rεgεl di lipid mεtabolism. Di we aw GLP-3 kɔmɔt de briŋ nyu tritmɛnt opshɔn fɔ di wan dɛn we fat, tayp 2 mɛtabolism, ɛn ɔda sik dɛn. Dɛn de op se i go brok di limiteshɔn dɛm fɔ tradishɔnal singl riseptɔ agonist drɔgs, gi wan mɔ pawaful wɛpɔn fɔ sɔlv di siriɔs prɔblɛm dɛm we de bɔku mɔ ɛn mɔ fɔ fat ɛn mɛtabolik sik dɛm, fɔ mek dɛn divɛlɔp mɔ di rilayt mɛdikal fil dɛm, impruv di kwaliti fɔ layf fɔ di sik pipul dɛm, ɛn ridyus di soshal mɛdikal lod.

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-A Faz 2 Trayal[J]. Nyu Ingland Jɔnal fɔ Mɛdisin, 2023,389(6):514-526.DOI:10.1056/NEJMoa2301972.

[3] 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.

[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] Brzozowska P, Frańczuk A, Nowinska B, ɛn ɔda pipul dɛn. GLP-3 - rivכlyushכn rεsεntli divεlכp GLP agonist - litεrachכ rivyu[J]. Kwaliti in Spɔt, 2024.DOI: 10.12775/qs.2024.15.52125.

[6] Pirro V, Piɔsɔn M. J., Lin Y, ɛn ɔda pipul dɛn. Efεkt dεm we Tripl-Hכmon Rεsεptor Agonist GLP-3 gεt pan Lipid Prכfaylin in Patisipεnt dεm wit Obesiti[J]. Dayabitis, 2024,73.DOI: 10.2337/db24-117-OR.

[7] Wen Y, Lemen D, Chen Y, ɛn ɔda pipul dɛn. rεdukshכn fכ triglisεrayd-rich lipoprotein wit GLP-3 in tayp 2 mεtabolism kin εksplen bay kכnכrεnt rεdukshכn in ANGPTL3/8 lεvεl[J]. Yuropian At Jɔnal, 2024,45.DOI:10.1093/eurheartj/ehae666.2862.

[8] 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.

[9] 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.

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

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.