Abstract Aims/hypothesis: Type 1 di

Abstract Aims/hypothesis: Type 1 diabetes is widely held
to result from an irreversible loss of insulin-secreting beta
cells. However, insulin secretion is detectable in some peo-
ple with long-standing type 1 diabetes, indicating either a
small population of surviving beta cells or continued re-
newal of beta cells subject to ongoing autoimmune de-
struction. The aim of the present study was to evaluate these
possibilities. Materials and methods: Pancreatic sections
from 42 individuals with type 1 diabetes and 14 non-dia-
betic individuals were evaluated for the presence of beta
cells, beta cell apoptosis and replication, T lymphocytes and
macrophages. The presence and extent of periductal fibrosis
was also quantified. Results: Beta cells were identified in
88% of individuals with type 1 diabetes. The number of beta
cells was unrelated to duration of disease (range 4–67 years)
or age at death (range 14–77 years), but was higher (p

Hasil (Bahasa Indonesia) 1:

Abstract Aims/hypothesis: Type 1 diabetes is widely heldto result from an irreversible loss of insulin-secreting betacells. However, insulin secretion is detectable in some peo-ple with long-standing type 1 diabetes, indicating either asmall population of surviving beta cells or continued re-newal of beta cells subject to ongoing autoimmune de-struction. The aim of the present study was to evaluate thesepossibilities. Materials and methods: Pancreatic sectionsfrom 42 individuals with type 1 diabetes and 14 non-dia-betic individuals were evaluated for the presence of betacells, beta cell apoptosis and replication, T lymphocytes andmacrophages. The presence and extent of periductal fibrosiswas also quantified. Results: Beta cells were identified in88% of individuals with type 1 diabetes. The number of betacells was unrelated to duration of disease (range 4–67 years)or age at death (range 14–77 years), but was higher (p<0.05)in individuals with lower mean blood glucose. Beta cellapoptosis was twice as frequent in type 1 diabetes as incontrol subjects (p<0.001), but beta cell replication was rarein both groups. The increased beta cell apoptosis in type 1diabetes was accompanied by both increased macrophagesand T lymphocytes and a marked increase in periductalfibrosis (p<0.001), implying chronic inflammation overmany years, consistent with an ongoing supply of beta cells.Conclusions/interpretation: Most people with long-stand-ing type 1 diabetes have beta cells that continue to be de-stroyed. The mechanisms underlying increased beta celldeath may involve both ongoing autoimmunity and glucosetoxicity. The presence of beta cells despite ongoing apoptosis implies, by definition, that concomitant new betacell formation must be occurring, even after long-standingtype 1 diabetes. We conclude that type 1 diabetes may bereversed by targeted inhibition of beta cell destruction.Keywords Autoimmunity . Beta cell apoptosis . Insulinsecretion . Islet regeneration . Type 1 diabetesAbbreviations AMCA: [6-((7-amino-4-methylcoumarin-3-acetyl)amino)hexanoic acid] . DAPI: 4′,6-diamidino-2-phenylindole . FITC: fluorescein-5-isothiocyanate .TUNEL: terminal deoxynucleotidyl transferasebiotin-dUTP nick end-labelling

Hasil (Bahasa Indonesia) 2:

Abstrak Tujuan / hipotesis: Diabetes tipe 1 banyak diadakan
hasil dari kerugian ireversibel beta insulin mensekresi
sel. Namun, sekresi insulin terdeteksi dalam beberapa peo-
ple dengan diabetes lama tipe 1, yang menunjukkan baik
populasi kecil sel beta yang masih hidup atau terus kembali
newal sel beta tunduk berlangsung de- autoimun
struction. Tujuan dari penelitian ini adalah untuk mengevaluasi
kemungkinan. Bahan dan metode: bagian pankreas
dari 42 individu dengan diabetes tipe 1 dan 14 non-Dialog
individu betic dievaluasi untuk kehadiran beta
sel, apoptosis sel beta dan replikasi, limfosit T dan
makrofag. Kehadiran dan tingkat fibrosis periductal
juga diukur. Hasil: Sel Beta diidentifikasi di
88% dari individu dengan diabetes tipe 1. Jumlah beta
sel tidak berhubungan dengan durasi penyakit (kisaran 4-67 tahun)
atau usia saat kematian (kisaran 14-77 tahun), tetapi lebih tinggi (p <0,05)
pada individu dengan rata-rata glukosa darah. Sel beta
apoptosis adalah dua kali lebih sering terjadi pada diabetes tipe 1 seperti pada
subyek kontrol (p <0,001), tetapi replikasi sel beta jarang
pada kedua kelompok. Peningkatan apoptosis sel beta di tipe 1
diabetes didampingi oleh peningkatan makrofag
dan limfosit T dan peningkatan yang ditandai dalam periductal
fibrosis (p <0,001), menyiratkan peradangan kronis selama
bertahun-tahun, konsisten dengan pasokan yang berkelanjutan sel beta.
Kesimpulan / interpretasi : Kebanyakan orang dengan lama-siaga
diabetes tipe 1 memiliki ing sel beta yang terus menjadi de-
hancur. Mekanisme yang mendasari peningkatan sel beta
kematian mungkin melibatkan baik autoimunitas yang sedang berlangsung dan glukosa
toksisitas. Kehadiran sel beta meskipun apoptosis berlangsung menyiratkan, menurut definisi, bahwa beta bersamaan baru
pembentukan sel harus terjadi, bahkan setelah berdiri lama
diabetes tipe 1. Kami menyimpulkan bahwa diabetes tipe 1 dapat
dibalik dengan penghambatan target kerusakan sel beta.
Kata kunci Autoimunitas. Apoptosis sel beta. Insulin
sekresi. Regenerasi Islet. Diabetes tipe 1
Singkatan AMCA: [6 - ((7-amino-4-methylcoumarin-
3-asetil) amino) asam hexanoic]. DAPI: 4 ', 6-diamidino-2-
phenylindole. FITC:. Fluorescein-5-isothiocyanate
TUNEL: terminal deoxynucleotidyl transferase
biotin-dUTP nick end-label