GLP-3 40 mg

▎ GLP-3 Structure

Source: PubChem

Sequence: YA⊃1;QGTFTSDYSI-L⊃2;LDKK⁴AQA⊃1;AFIEYLLEGGPSSGAPPPS⊃3; Molecular Formula: C 221H 342N 46O68 Molecular Luj: 4731 g / mol CAS Nr .: 2381089-83-2 PubChem CID: 171390338 Cov ntsiab lus: LY3437943

▎ GLP-3 Kev Tshawb Fawb

Dab tsi yog qhov kev tshawb fawb keeb kwm yav dhau rau GLP-3?

Lub ntiaj teb no muaj feem ntau ntawm kev rog rog thiab hom 2 metabolism tseem nce ntxiv, ua rau muaj kev sib tw tseem ceeb rau pej xeem kev noj qab haus huv. Cov tshuaj uas twb muaj lawm ib leeg lossis ob lub hom phiaj muaj kev txwv hauv kev ua tau zoo thiab kev nyab xeeb. Raws li txoj kev xav ntawm ntau lub hom phiaj kev sib koom ua ke ntawm kev ua haujlwm ntawm lub plab zom mov insulin axis, kev tshawb fawb tau qhia txog lub luag haujlwm ntawm GLP-1, GIP, thiab glucagon hauv cov txheej txheem metabolic, muab lub hauv paus theoretical rau kev txhim kho ntau cov receptor agonists.

Tsim los ntawm kev paub txog kev tsim tshuaj thib ob lub hom phiaj ua ntej, cov kws tshawb fawb tau tsim thiab ua kom zoo dua GLP-3 raws li cov yam ntxwv ntawm cov qauv thiab cov kev taw qhia cov txheej txheem ntawm cov receptors triple. Los ntawm kev ua haujlwm ib txhij GLP-1R, GIPR, thiab GCGR, nws ua tiav ntau lub zog glycemic tswj thiab txo qhov hnyav.

Dab tsi yog qhov txheej txheem ntawm kev txiav txim rau GLP-3?

Receptor Agonism

GLP-3 ua haujlwm raws li triple receptor agonist tsom GLP-1, GCGR, thiab GIP receptors ^[1].

GLP-1 receptor agonism: GLP-1 yog incretin hormone secreted los ntawm txoj hnyuv L hlwb. Raws li kev khi rau GLP-1 receptors, GLP-3 txhawb nqa insulin secretion hauv cov piam thaj-concentration-dependent yam. Thaum lub sij hawm hyperglycemia, GLP-3 khi rau GLP-1 receptors, ua kom cov kev taw qhia qis qis uas ua rau cov kab mob pancreatic β-hlwb kom zais cov tshuaj insulin thiab txo cov ntshav qabzib. Nws kuj tseem inhibits glucagon secretion thiab txo cov piam thaj hauv siab, ua kom cov ntshav qabzib ruaj khov ntxiv. GLP-1 receptor agonism tseem ua rau lub plab zom mov, ua kom satiety, thiab txo cov zaub mov noj, pab tswj kev hnyav ^[2].

GCGR receptor agonism: Glucagon feem ntau ua thaum lub sijhawm hypoglycemia kom nce qib ntshav qabzib. GLP-3's agonist action ntawm GCGR yog qhov nyuaj. Nyob rau hauv cov ntaub so ntswg adipose, nws txhawb lipolysis thiab tsub kom fatty acid oxidation, yog li pab txhawb kev siv zog. Hauv daim siab, nruab nrab GCGR agonism tuaj yeem tswj cov txheej txheem zoo li gluconeogenesis, ua kom lub siab ua haujlwm metabolic. Qhov no tiv thaiv ntau dhau ntawm gluconeogenesis los ntawm kev ua rau hyperglycemia thaum tswj cov ntshav qabzib txaus kom ua tau raws li lub cev xav tau lub zog ^[1].

GIP receptor agonism: GIP, lwm yam tshuaj incretin, yog zais los ntawm K hlwb hauv duodenum thiab jejunum tom qab noj mov. GLP-3's GIP receptor agonism txhim kho insulin secretion, sib koom ua ke nrog GLP-1 txhawm rau txhim kho kev tswj cov piam thaj. Hloov pauv, GIP receptor activation tuaj yeem cuam tshuam lipid metabolism thiab lub zog sib npaug. Brzozowska P txoj kev tshawb fawb qhia tias GIP txhawb nqa cov piam thaj thiab lipid synthesis hauv adipocytes. Txawm li cas los xij, raws li GLP-3 lub hwj chim, GIP signaling yog hloov kho kom zoo dua kev siv hluav taws xob ntau dua li tsuas yog txhawb nqa cov roj cia, yog li pab tswj qhov hnyav ^[1].

Daim duab 1 GLP-3's mechanisms of action ^[3].

Kev tswj hwm ntawm cov txheej txheem metabolic

Kev Tswjhwm Mob Ntshav Qab Zib Zog: Los ntawm kev ua kom peb lub receptors tau hais los saum toj no, GLP-3 tau tswj hwm lub zog metabolism. Nws txhawb lipolysis, nce fatty acid nkag mus rau hauv mitochondria rau β-oxidation thiab txhawb zog siv nyiaj. Nws txo lipogenesis los ntawm inhibiting fatty acid uptake thiab triglyceride synthesis nyob rau hauv adipocytes, yog li hloov lub cev lub zog cia thiab tshuav nyiaj li cas los pab kom poob ceeb thawj. Hauv kev tshawb fawb txog tsiaj txhu thiab kev sim tshuaj los ntawm Jastreboff AM, GLP-3 kev tswj hwm tau nce kev siv hluav taws xob ntau ntxiv thiab txo qis lub cev rog cov ntsiab lus hauv cov rog rog ^[4].

Glucose Diabetes Regulation: GLP-3 modulates ntshav qabzib los ntawm ntau txoj hauv kev. Tshaj li stimulating insulin secretion ntawm GLP-1 thiab GIP receptor activation, nws cuam tshuam rau cov piam thaj hauv siab los ntawm kev tswj GCGR. Nws inhibits ntau dhau ntawm hepatic gluconeogenesis, txo cov piam thaj tso zis, thiab ib txhij txhim kho peripheral cov ntaub so ntswg glucose uptake thiab siv, yog li tswj cov ntshav qabzib ib txwm. Qhov no yog qhov tseem ceeb tshwj xeeb rau cov neeg mob rog rog nrog hom 2 metabolism, tswj cov ntshav qabzib zoo thiab txhim kho cov mob ntshav qab zib ^[2].

Kev tswj hwm lub siab: Hauv daim siab, GLP-3 tsis tsuas yog hloov pauv cov piam thaj metabolism, tab sis kuj cuam tshuam cov lipid metabolism. Nws txo qis triglyceride synthesis thiab tsub zuj zuj ntawm hepatic triglycerides, txhim kho hepatic steatosis, thiab tuav cov nqi kho mob rau cov kab mob uas tsis yog-alcoholic fatty siab (NAFLD). Hauv kev sim tshuaj uas koom nrog cov neeg koom nrog kev ua haujlwm tsis zoo ntawm cov kab mob metabolic-uas cuam tshuam nrog cov kab mob rog rog (MDAFLD), GLP-3 txo qis cov rog rog hauv lub siab, ua kom pom nws cov txiaj ntsig zoo ntawm cov metabolism hauv hepatic ^[5].

 Qhov cuam tshuam rau kev ua haujlwm ntawm plab hnyuv

GLP-3 ncua lub plab khoob los ntawm kev ua kom GLP-1 receptors. Lub plab zom mov qeeb qeeb ua rau lub sijhawm noj zaub mov nyob hauv lub plab, ua kom muaj kev txaus siab thiab txo qis kev noj zaub mov ntxiv. Nyob rau tib lub sijhawm, nws tuaj yeem cuam tshuam rau lub plab hormonal secretion thiab plab hnyuv motility, ntxiv regulating gastrointestinal digestion thiab assorption txheej txheem, yog li muaj kev cuam tshuam rau lub zog noj thiab lub cev hnyav ^[2].

Dab tsi yog qhov sib koom ua ke ntawm GLP-3's agonistic teebmeem ntawm GLP-1, GCGR, thiab GIP receptors?

Synergy hauv Energy Diabetes Regulation

Kev siv hluav taws xob ntau ntxiv: Ua kom GCGR txhawb nqa glycogenolysis thiab gluconeogenesis kom nce qib ntshav qabzib. Nws kuj tseem txhim kho kev siv hluav taws xob los ntawm kev ua kom cov lipid metabolism thiab txo qis kev noj zaub mov los ntawm qhov nruab nrab satiety. GLP-1R agonists txhawb nqa cov tshuaj insulin tso tawm thiab tawm dag zog cardioprotective thiab neuroprotective cuam tshuam, thaum tseem txo qis zog noj los ntawm kev ncua lub plab zom mov thiab txo qis qab los noj mov. Thaum GIPR ua rau hauv cov ntaub so ntswg adipose txhawb lipid tsub zuj zuj, nws lub hauv paus ua kom txo tau cov zaub mov noj thiab txo qhov hnyav nce. GLP-3 ib txhij lub hom phiaj no peb receptors, tsim kom muaj qhov sib npaug tshiab ntawm kev siv zog thiab kev siv nyiaj. Qhov no zoo dua ua tiav lub zog tsis txaus, yog li yooj yim rau kev poob phaus.

Kev tswj cov lipid metabolism: GCGR agonism txhim kho lipid metabolism, thaum GIPR ua rau hauv cov ntaub so ntswg adipose kuj cuam tshuam lipid metabolism. GLP-1R agonists tuaj yeem cuam tshuam ncaj qha rau lipid metabolism los ntawm cov txheej txheem xws li kev txhim kho insulin rhiab heev. Lawv cov synergistic ua haujlwm zoo dua tswj cov roj synthesis, tawg, thiab thauj, txo cov rog thiab txhim kho lub cev rog. Piv txwv li, kev tshawb fawb hauv cov neeg mob rog rog tau pom tias tom qab siv GLP-3 rau ib lub sijhawm, qhov feem pua ​​​​ntawm cov rog hauv lub cev tau txo qis thiab cov lipid profile tau txhim kho rau qee qhov, qhia txog nws cov txiaj ntsig zoo hauv kev tswj cov roj metabolism ^[6].

Synergistic Effects hauv Glucose Regulation

Enhanced Insulin Secretion: GLP-1R agonists txo cov ntshav qabzib los ntawm kev khi rau GLP-1 receptors thiab txhawb kev tso tawm insulin. GIP zoo ib yam ua rau cov kab mob pancreatic β-hlwb los tsim cov tshuaj insulin secretion zoo ib yam li cov neeg raug ntxias los ntawm kev noj haus. GLP-3, uas ib txhij ua rau GLP-1R thiab GIPR, txhim kho cov tshuaj insulin secretion, yog li txo cov ntshav qabzib ntau dua. Txawm hais tias GCGR feem ntau cuam tshuam nrog cov ntshav qabzib siab, nws cov teebmeem-xws li txhawb kev siv hluav taws xob- tuaj yeem ua rau tsis muaj zog rau cov piam thaj hauv lub cev thaum sib koom ua ke nrog cov receptors zoo li GLP-1R. Tsis tas li ntawd, kev siv ua ke ntawm GLP-1 thiab GCGR xaiv tawm tsam qhov kev pheej hmoo hyperglycemic tshwm sim los ntawm GCGR, ua kom muaj kev tswj hwm cov piam thaj ntau dua thiab zoo.

Regulating Glucose Homeostasis: Lub synergistic activation ntawm peb receptors txuas ntxiv tshaj li cov tshuaj insulin tso tawm kom suav nrog kev tswj hwm cov piam thaj hauv homeostasis. Los ntawm kev cuam tshuam cov piam thaj, kev siv, thiab kev khaws cia thoob plaws ntau cov ntaub so ntswg nrog rau daim siab, cov leeg, thiab adipose, GLP-3 tswj cov ntshav qabzib nyob rau hauv qhov chaw ruaj khov, tiv thaiv kev hloov pauv loj. Hauv kev tshawb fawb los ntawm Nicholls S cuam tshuam nrog hom 2 cov neeg mob metabolism, GLP-3 kev tswj hwm tau ua rau txo qis glycated hemoglobin qib, qhia txog nws qhov kev cuam tshuam zoo rau kev tswj glycemic mus sij hawm ntev thiab ua kom pom kev sib koom ua ke ntawm peb receptors hauv kev tswj cov piam thaj homeostasis ^[6].

Synergistic Activation of Signal Transduction Pathways

Kev Ua Haujlwm Zoo Tshaj Plaws: GLP-1R, GCGR, thiab GIPR feem ntau teeb liab los ntawm G (Gαs) cov proteins. Thaum GLP-3 ua rau peb cov receptors no, nws sib sau ua ke los ua kom muaj kev sib koom ua ke xws li cAMP-PKA txoj hauv kev. Txoj kev sib koom ua ke no txhim kho cov teeb liab transduction efficiency thiab potency, amplifying kev tswj cov teebmeem ntawm cellular metabolism thiab physiological functions.

Kev sib koom ua ke ntawm txoj kev sib txawv: Thaum sib koom txoj hauv kev, txhua tus neeg txais txiaj ntsig kuj tseem ua kom muaj kev sib txuas lus tshwj xeeb. GLP-3 modulates cov kev sib txawv no synergistically thaum lub sij hawm receptor activation, ua kom muaj kev sib koom ua ke ntawm cov txheej txheem metabolic.

Synergistic Regulation of Gastrointestinal Function

Influencing Gastrointestinal Hormone Secretion: GLP-1R agonists txhawb nqa GLP-1 secretion, thaum GIPR agonists tswj GIP tso tawm. Cov tshuaj hormones digestinal no ua lub luag haujlwm tseem ceeb hauv kev hloov pauv ntawm lub plab zom mov, kev zom zaub mov, thiab kev nqus. Los ntawm tib lub sijhawm ua rau ob qho tib si receptors, GLP-3 muab kev tswj hwm ntau dua ntawm cov tshuaj hormones hauv plab hnyuv, yog li cuam tshuam rau kev ua haujlwm ntawm plab hnyuv. Nws tuaj yeem txo qis kev nqus sai sai los ntawm kev hloov pauv ntawm lub plab zom mov thiab lub plab zom mov, pab kom hnyav thiab tswj ntshav qabzib.

Txhim kho lub plab zom mov Metabolic ib puag ncig: Los ntawm kev tswj cov kab mob hauv plab hnyuv, GLP-3 kuj txhim kho cov metabolism hauv ib puag ncig hauv plab hnyuv. Nws txhawb txoj kev loj hlob thiab cov metabolism ntawm cov kab mob hauv plab uas muaj txiaj ntsig zoo thiab hloov cov kab mob plab hnyuv ua haujlwm. Cov kev hloov pauv no tuaj yeem cuam tshuam ntxiv rau lub cev tag nrho cov metabolic xeev. Ua haujlwm synergistically nrog cov teebmeem ntawm lub zog metabolism thiab kev tswj cov ntshav qabzib, cov txheej txheem no sib sau ua ke rau kev kho mob los tiv thaiv kev rog rog thiab cuam tshuam txog cov kab mob metabolic.

Dab tsi yog cov ntawv thov ntawm GLP-3?

Kev kho mob rog

Qhov Teebmeem Tseem Ceeb Tseem Ceeb: Ntau qhov kev sim tshuaj xyuas pom tau tias GLP-3 qhov ua tau zoo hauv kev kho mob rog. Hauv Phase 2 ob qhov muag tsis pom kev, randomized, placebo-tswj sim los ntawm Jastreboff AM nrog rau 338 tus neeg laus, cov neeg koom tau txais GLP-3 txhua lub lim tiam ntawm kev sib txawv ntawm koob tshuaj lossis placebo rau 48 lub lis piam. Cov txiaj ntsig tau pom tias nyob rau lub lim tiam 24, pawg 1mg ua tiav qhov hnyav nruab nrab ntawm 7.2%, pawg 4mg ua ke poob 12.9%, pawg 8mg ua ke poob 17.3%, thiab 12mg pawg poob 17.5%, thaum pawg placebo poob tsuas yog 1.6%. Los ntawm lub lim tiam 48, pawg 1mg ua tiav qhov hnyav nruab nrab ntawm 8.7%, pawg 4mg ua ke poob 17.1%, pawg 8mg ua ke poob 22.8%, 12mg pawg poob 24.2%, thiab pawg placebo poob 2.1%. Ntawm cov neeg koom tau txais 4mg, 8mg, thiab 12mg GLP-3, 92%, 100%, thiab 100% ua tiav 5% lossis ntau dua qhov hnyav, feem. 75%, 91%, thiab 93% ua tiav 10% lossis ntau dua qhov hnyav. thiab 60%, 75%, thiab 83% ua tiav 15% lossis ntau dua qhov hnyav, piv rau 27%, 9%, thiab 2% hauv pawg placebo. Cov ntaub ntawv no qhia tau hais tias GLP-3 qhov ua tau zoo hauv kev txo qhov hnyav rau cov neeg mob rog ^[4].

Kev kho mob ntshav qab zib hom 2

Glycemic Control Efficacy: Kev tshawb fawb los ntawm Lopez DC thiab al. qhia GLP-3 zoo cuam tshuam glycemic tswj hauv hom 2 cov neeg mob metabolism. Hauv kev sim nrog 353 tus neeg koom, GLP-3 txo glycated hemoglobin (HbA1c) los ntawm 1.64% piv rau cov placebo. Qhov no qhia tau hais tias GLP-3 qhov ua tau zoo hauv kev txo cov ntshav qabzib hauv cov neeg mob ntshav qab zib hom 2, yog li pab txhawb kev kho mob tau zoo ^[7].

Combined Mechanism Advantage: GLP-3 ua rau ntau tus receptors, muab qhov zoo dua qub rau ib leeg-receptor agonists los ntawm nws cov txheej txheem ua ke agonist. Nws tsis tsuas yog txo cov ntshav qabzib los ntawm kev tsim cov tshuaj insulin secretion, tab sis kuj tseem txhim kho cov insulin rhiab heev, ua rau lub cev hlwb siv cov tshuaj insulin zoo dua rau kev tswj hwm glycemic. Nws cov txiaj ntsig txo qhov hnyav ntxiv txhim kho cov txheej txheem metabolic hauv cov neeg mob ntshav qab zib hom 2, vim tias rog rog yog qhov tseem ceeb ntawm kev pheej hmoo rau tus mob thiab kev poob phaus pab tswj ntshav qabzib zoo ^[5].

Kev kho mob uas tsis yog-Alcoholic Fatty Liver Disease

Txo cov roj ntsha hauv siab: GLP-3 tau pom tias muaj peev xwm txo qis cov roj siab hauv cov neeg mob uas muaj cov kab mob metabolic dysfunction-associated fatty siab kab mob (MDAFLD) thiab siab rog cov ntsiab lus ≥10%. Hauv kev sib tw randomized, ob-dig muag, kev sim tshuaj placebo, 98 tus neeg koom tau raug xaiv kom tau txais kev txhaj tshuaj subcutaneous txhua lub lim tiam ntawm GLP-3 (1mg, 4mg, 8mg, lossis 12mg) lossis placebo rau 48 lub lis piam. Cov txiaj ntsig tau pom tias nyob rau lub lim tiam 24, qhov kev hloov pauv hauv cov rog hauv siab txheeb ze rau cov hauv paus ntsiab lus yog -42.9% hauv pawg 1mg, -57.0% hauv pawg 4mg, -81.4% hauv pawg 8mg, thiab -82.4% hauv pawg 12mg, piv rau +0.3% hauv pawg placebo. Cov kev tshawb pom no qhia tias GLP-3 txo qis cov rog rog hauv siab, ua kom pom qhov muaj peev xwm kho tau rau cov kab mob tsis muaj dej cawv fatty siab ^[8].

Txhim kho Hepatic Metabolic Function: GLP-3 txhim kho daim siab metabolic muaj nuj nqi los ntawm kev tswj lub zog thiab lipid metabolism. Nws txhawb kev oxidation thiab rhuav tshem cov rog rog, txo cov rog hauv daim siab, hloov cov lus teb inflammatory thiab oxidative kev ntxhov siab nyob rau hauv daim siab, thiab ua rau muaj qee yam inhibitory cuam tshuam rau kev nce qib ntawm NAFLD, yog li tiv thaiv cov neeg mob lub siab noj qab haus huv.

Xaus

Raws li ib tug triple receptor agonist ntawm GLP-1R / GIPR / GCGR, GLP-3 exerts metabolic regulatory teebmeem los ntawm ntau lub hom phiaj synergistic mechanism. Nws cov teebmeem encompass activating GLP-1R los suppress qab los noj mov thiab ncua lub plab khoob, yog li txo lub zog kom tsawg; activating GIPR los txhim kho insulin secretion thiab txhim kho cov tshuaj insulin rhiab heev; thiab ua kom GCGR txhawb lipolysis thiab kev siv hluav taws xob thaum tswj cov piam thaj hauv siab thiab lipid metabolism kom txo cov rog. Qhov kev sib koom ua ke triple no ua tiav cov txiaj ntsig zoo suav nrog kev tswj hwm glycemic muaj zog, txo qhov hnyav, thiab txhim kho lipid thiab cov rog rog metabolism. Nws cov txiaj ntsig tseem ceeb yog nyob rau hauv kev kho mob rog, ua kom tau txais koob tshuaj raws li qhov hnyav txo nrog qhov siab tshaj 48 lub lis piam poob ntawm 24.2%. Rau hom 2 metabolism, nws txo qis glycated hemoglobin thiab txhim kho glycemic homeostasis. Hauv metabolic dysfunction-associated fatty daim siab kab mob, nws txo qis cov rog hauv siab, ua kom pom kev ua tau zoo ntawm ntau yam kab mob metabolic.

Hais Txog Tus Sau

Cov ntaub ntawv hais saum toj no yog txhua yam tshawb fawb, kho thiab sau los ntawm Cocer Peptides.

Scientific Journal Author

Arun J. Sanyal yog kws kho mob hepatologist thiab kws tshawb fawb tshwj xeeb hauv cov kab mob siab, tshwj xeeb tshaj yog cov kab mob tsis muaj dej cawv fatty siab (NAFLD) thiab tsis muaj dej cawv steatohepatitis (NASH). Nws koom nrog Virginia Commonwealth University Tsev Kawm Ntawv Tshuaj Kho Mob, qhov chaw uas nws tau ua tus kws qhia ntawv txij li xyoo 1989. Sanyal tau sau kwv yees li 1,000 cov ntawv tshaj tawm hauv cov ntawv xov xwm xws li Cell Diabetes, Nature Medicine, The New England Journal of Medicine, thiab The Lancet. Nws txoj haujlwm tau raug suav hais tias ntau dua 104,000 lub sijhawm, qhia txog nws qhov cuam tshuam tseem ceeb hauv thaj tsam ntawm hepatology. Nws tau txais nyiaj tsis tu ncua los ntawm National Institutes of Health txij li xyoo 1995 thiab yog tus kws tshawb fawb tseem ceeb ntawm plaub qhov nyiaj pabcuam NIH. Sanyal kuj tau lees paub rau nws cov thawj coj hauv kev tshawb fawb soj ntsuam thiab nws txoj kev koom tes rau kev txhim kho cov tswv yim kho mob rau cov kab mob siab. Arun J. Sanyal tau teev nyob rau hauv qhov kev siv ntawm cov ntaub ntawv pov thawj [5].

▎ Cov Lus Qhia Tseem Ceeb

[1] Brzozowska P, Frańczuk A, Nowińska B, Makłowicz A, Palacz KA, Lenartowicz I. GLP-3 - revolutionary nyuam qhuav tsim GLP agonist - ntaub ntawv tshuaj xyuas. Zoo hauv Sport 2024. https://api.semanticscholar.org/CorpusID: 271031379.

[2] Doggrel SA. GLP-3 qhia kev cog lus hauv kev rog (thiab hom 2 metabolism). Cov Kws Tshaj Lij Tshaj Tawm Txog Kev Tshawb Fawb Tshuaj 2023; 32(11): 997-1001.DOI: 10.1080/13543784.2023.2283020.

[3] Katsi V, Koutsopoulos G, Fragoulis C, Dimitriadis K, Tsioufis K. GLP-3—A Game Changer in Obesity Pharmacotherapy. Biomolecules 2025; 15(6).DOI: 10.3390/biom15060796.

[4] Jastreboff AM, Kaplan LM, Frías JP, et al. Triple-hormone-Receptor Agonist GLP-3 rau Obesity - Theem 2 Kev sim. New England Journal of Medicine 2023; 389(6): 514-526. DOI: 10.1056/NEJMoa2301972.

[5] Sanyal AJ, Kaplan LM, Frias JP, et al. Triple Hormone receptor agonist GLP-3 rau metabolic dysfunction-associated steatotic siab kab mob: randomized theem 2a sim. Ntuj Tshuaj 2024; 30: 2037-2048. https://api.semanticscholar.org/CorpusID:270378167.

[6] Nicholls S, Pirro V, Lin Y, et al. Triple-hormone receptor agonist GLP-3 txhim kho lipoprotein thiab apolipoprotein profiles hauv cov neeg koom nrog rog lossis rog. European Heart Journal 2024; 45(Supplement_1): ehae666-ehae1501.DOI:10.1093/eurheartj/ehae666.1501.

[7] Lopez DC, Pajimna JT, Milan MD, et al. 7792 Kev Ua Tau Zoo ntawm GLP-3 rau Kev Txo Nyhav thiab Nws Cov Teebmeem Cardiometabolic Ntawm Cov Neeg Laus: Kev Ntsuam Xyuas Txheej Txheem thiab Kev Ntsuas Meta. Phau ntawv Journal of the Endocrine Society 2024; 8(Supplement_1): bvae163-bvae749.DOI: 10.1210/jendso/bvae163.749.

[8] Naeem M, Imran L, Banatwala U. Unleashing lub hwj chim ntawm GLP-3: Ib tug muaj peev xwm kov yeej kev rog thiab rog: Ib tsab ntawv. Kev Tshawb Fawb Txog Kev Noj Qab Haus Huv 2024; 7(2): e1864.DOI: 10.1002/hsr2.1864.

Tag nrho cov kab lus thiab cov ntaub ntawv ntawm cov khoom lag luam muab rau ntawm lub vev xaib no tsuas yog rau cov ntaub ntawv tshaj tawm kev tshaj tawm thiab cov hom phiaj kev kawm.  

Cov khoom muab rau hauv lub vev xaib no yog npaj tshwj xeeb rau kev tshawb fawb hauv vitro. Kev tshawb fawb hauv vitro (Latin: * hauv iav *, lub ntsiab lus hauv iav) yog ua los ntawm tib neeg lub cev. Cov khoom no tsis yog tshuaj, tsis tau txais kev pom zoo los ntawm US Food and Drug Administration (FDA), thiab yuav tsum tsis txhob siv los tiv thaiv, kho, lossis kho txhua yam mob, kab mob, lossis mob. Nws raug txwv nruj raws li txoj cai los qhia cov khoom no rau hauv tib neeg lossis tsiaj lub cev hauv txhua daim ntawv.