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"Belum banyak studi mempelajari keterkaitan antara defisiensi vitamin B12 dan toksisitas homosistein. Hiperhomosisteinemia dikaitkan dengan penyakit selular terkait NAFLD. Toksisitas homosistein dapat berupa steatosis atau inflamasi sel hati. H. sabdariffa. dan konstituen aktifnya memiliki efek pencegahan terhadap cedera seluler. Ekstrak H. sabdariffa. diuji pada tikus Sprague-Dawley (SD) dalam penelitian ini.Penelitian ini untuk melihat efek H.sabdariffa terhadap peningkatan homosistein pada hati tikus SD yang diberikan diet resriksi vitamin B12.Penelitian ini merupakan penelitian in vivo yang dilakukan di Fakultas Kedokteran Universitas Indonesia. Sebanyak 30 ekor tikus SD dibagi menjadi enam kelompok sesuai waktu perlakuan di 8 dan 16 minggu sebagai berikut: Kelompok kontrol diberikan diet standar AIN-93M, kelompok restriksi vitamin B12 diberi diet AIN-93M dengan modifikasi pengurangan komponen vitamin B12 dan kelompok restriksi vitamin B12 diberi AIN-93M dengan modifikasi pengurangan komponen vitamin B12 ditambah ekstrak etanol H.sabdariffa (HSE). Setelah 8 dan 16 minggu, kadar vitamin B12 dan homosistein diukur. Peningkatan aktivitas toksisitas homosistein dilihat dari ekspresi protein GRP78, SREBP1c dan NF-kB. Aktivitas hepatoprotektif HSE dinilai menggunakan AST, ALT, GGT, dan NAFLD Activity Score (NAS).Kadar vitamin B12 pada 8 minggu (233 ± 10.8 vs 176 ± 5.4 pg/L; p < 0.001) dan 16 minggu (226 ± 13 vs 190 6 pg/L; p < 0,001), lebih tinggi secara bermakna pada kelompok restriksi vitamin B12 dengan diet HSE dibandingkan kelompok diet restriksi vitamin B12 tanpa HSE. Kadar plasma homosistein plasma lebih rendah secara bermakna pada kelompok restriksi vitamin B12 dengan HSE dibandingkan kelompok restriksi vitamin B12 tanpa HSE di usia perlakuan 8 minggu (2,25 ± 0,07 vs 2,63 ± 0,1 mol/L; p < 0,001) dan 16 minggu (2,18 ± 0,07 vs 2,64 ± 0,09 mol/L; p < 0,001). Aktivitas GGT plasma di usia 16 minggu perlakuan menurun secara bermakna pada kelompok restriksi vitamin B12 dengan HSE dibandingkan kelompok restriksi vitamin B12 tanpa HSE (14,5 ± 1,1 vs 22,9 ± 2,4 IU; p < 0,05). Ekspresi protein GRP78, SREBP1c, dan NfKB diukur menggunakan protein GADPH sebagai kontrol internal. Pada minggu ke-8 dan 16, ekspresi protein NF-kB lebih rendah pada kelompok restriksi vitamin B12 dengan HSE dibandingkan dengan grup restriksi vitamin B12 tanpa HSE (0,78 ± 0,08 vs 1,08 ± 0,06; p < 0,05). Ekspresi protein SREBP1c lebih rendah pada kelompok restriksi vitamin B12 dengan HSE dibandingkan dengan grup restriksi vitamin B12 tanpa HSE pada usia perlakuan 16 minggu (0,55 ± 0,03 vs 1,00 ± 0,02; p < 0,05). Kelompok restriksi vitamin B12 dengan HSE memiliki gambaran histopatologis steatosis, inflamasi, dan fibrosis lebih baik dibandingkan kelompok yang restriksi vitamin B12 tanpa HSE setelah 16 minggu perlakuan.Disimpulkan peningkatan homosistein akibat diet restriksi vitamin B12 pada tikus SD menyebabkan steatosis hati, inflamasi, dan fibrosis. Ekstrak etanol H.Sabdariffa memiliki efek pencegahan terhadap kondisi steatosis, inflamasi dan fibrosis akibat peningkatan homosistein pada tikus SD yang diberi diet restriksi vitamin B12.

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There haven't been many studies on the link between vitamin B12 deficiency and homocysteine toxicity. Homocysteine is linked to NAFLD-related cellular disease, and toxicity can manifest as steatosis or inflammation of the liver cells. H. sabdariffa. and its active constituents have a preventive effect against cellular injury. H. sabdariffa extract was tested on Sprague-Dawley (SD) rats with NAFLD in this study. This study aimed to examine the effect of H. sabdariffa on increasing homocysteine ​​in the liver of SD rats fed a vitamin B12 restriction diet.

This research is an in vivo study conducted at the Faculty of Medicine, University of Indonesia. 30 SD rats were divided into six groups based on treatment time at 8 and 16 weeks, with the following treatments: the control group received the standard AIN-93M diet, the vitamin B12 restriction group received the AIN-93M diet with a modified reduction of the vitamin B12 component, and the vitamin B12 restriction + HSE group received the AIN-93M diet with a modified reduction of the vitamin B12 component and an ethanol extract of H. sabdariffa (HSE). After 8 and 16 weeks, vitamin B12 and homocysteine ​​levels were measured. The increase in homocysteine ​​toxicity activity was seen from the expression of GRP78, SREBP1c, and NF-kB proteins. The hepatoprotective activity of HSE was assessed using the AST, ALT, GGT, and NAFLD Activity Score (NAS).

Vitamin B12 levels at 8 weeks (233 ± 10.8 vs 176 ± 5.4 pg/L; p < 0.001) and 16 weeks (226 ± 13 vs 190 6 pg/l; p < 0.001), significantly higher in the HSE group with a vitamin restriction diet. B12. Plasma homocysteine ​​levels were significantly lower in the vitamin B12 restriction group with HSE than in the vitamin B12 restriction group without extract at 8 weeks of age (2.25 ± 0.07 vs. 2.63 ± 0.1 mol/L; p < 0.001 ) and 16 weeks (2.18 ± 0.07 vs. 2.64 ± 0.09 mol/L; p < 0.001). Plasma GGT activity at 16 weeks of treatment decreased significantly in the vitamin B12-restricted group with HSE compared to the vitamin B12-restricted group without HSE (14.5 ± 1.1 vs. 22.9 ± 2.4 IU; p < 0.05). GRP78, SREBP1c, and NfKB protein expressions were measured using GADPH protein as an internal control. At weeks 8 and 16, NF-kB protein expression was lower in the vitamin B12 restriction group with HSE compared to the vitamin B12 restriction group without HSE (0.78 ± 0.08 vs. 1.08 ± 0.06; p < 0 ,05). SREBP1c protein expression was lower in the vitamin B12 restriction group with HSE compared to the vitamin B12 restriction group without HSE at 16 weeks of treatment (0.55 ± 0.03 vs. 1.00 ± 0.02; p < 0.05). The vitamin B12 restriction group with HSE had better histopathological features of steatosis, inflammation, and fibrosis than the vitamin B12 restriction group without HSE after 16 weeks of treatment.

It was concluded that the increase in homocysteine ​​due to dietary restriction of vitamin B12 in SD rats caused liver steatosis, inflammation, and fibrosis. The ethanolic extract of H. Sabdariffa had a preventive effect on steatosis, inflammation, and fibrosis due to increased homocysteine ​​in SD rats fed a vitamin B12 restriction diet."

"ABSTRAKDefisiensi vitamin B12 merupakan masalah kesehatan di negara maju dan berkembang. Penelitian ini menganalisis hubungan restriksi vitamin B12 dengan perubahan struktur dan fungsi ginjal. Tikus Sprague-Dawley 18 ekor dibagi menjadi tiga kelompok: 1 kontrol yang diberi pakan standar hewan coba AIN-93M selama 12 minggu; 2 perlakuan-1 P-1 diberi pakan AIN-93M modifikasi tanpa vitamin B12 selama 4 minggu; dan 3 perlakuan-2 P-2 selama 12 minggu. Vitamin B12 plasma total turun dari 529.17 166.51 pg/ml menjadi 426.33 60.59 pg/ml pada P-1 dan 708.70 124.35 pg/ml menjadi 519.16 84.96 pg/ml pada P-2, pada kelompok kontrol meningkat dari 567.79 102.52 pg/ml menjadi 650.26 193.12 pg/ml. Homosistein plasma meningkat pada kelompok perlakuan setelah 4 minggu kontrol vs P-1 = 351.05 110.69 pmol/ml vs 597.09 308.02 pmol/ml dan 12 minggu kontrol vs P-2 = 414.473 224.13 pmol/ml vs 1055.12 651.68 pmol/ml, p

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ABSTRACTVitamin B12 deficiency is still a health problem in both developed and developing countries. This study was conducted to explore possible relationship between vitamin B12 dietary restriction with kidney rsquo;s histological and physiological changes. Eighteen male Sprague Dawley rats were divided into three groups: 1 control group were fed with standard AIN-93M for 12 weeks; 2 1st treatment group P-1 were fed with cobalamin restricted AIN-93M for 4 weeks; and 3 2nd treatment group P-2 were fed with cobalamin restricted AIN-93M for 12 weeks. Vitamin B12 level decreased from 529.17 166.51 pg/ml to 426.33 60.59 pg/ml in P-1 group and from 708.70 124.35 pg/ml to 519.16 84.96 pg/ml in P-2 group, while it increased from 567.79 102.52 pg/ml to 650.26 193.12 pg/ml in control group after 12 weeks. Plasma Hcy increased in treatment group after 4 weeks control vs P-1 = 351.05 110.69 pmol/ml vs 597.09 308.02 pmol/ml and 12 weeks control vs P-2 = 414.473 224.13 pmol/ml vs 1055.12 651.68 pmol/ml; p"

"ABSTRACTLatar Belakang: Defisiensi vitamin B12 belum diketahui secara jelas insidensi dan prevalensinya di seluruh dunia dan hanya terdapat penelitian di daerah-daerah tertentu. Terdapat indikasi defisiensi asam folat dan vitamin B12 menjadi masalah kesehatan masyarakat dalam beberapa negara. Dalam beberapa penelitian, ditemukan bahwa kadar vitamin B12 yang rendah berhubungan dengan terjadinya perlemakan hati. Kondisi perlemakan hati memiliki spektrum yang luas, dari perlemakan hati sederhana, steatohepatitis, fibrosis, hingga sirosis hati. Tujuan: Penelitian ini bertujuan untuk mengetahui perubahan gambaran histopatologi perlemakan hati pada tikus dengan diet restriksi vitamin B12 dalam durasi waktu tertentu. Metode: Penelitian dilakukan dengan 18 ekor tikus Sprague-Dawley yang terbagi dalam 3 kelompok: (1) kelompok kontrol dengan diet normal selama 16 minggu; (2) kelompok perlakuan dengan diet restriksi vitamin B12 selama 8 minggu; dan (3) kelompok perlakuan dengan diet restriksi vitamin B12 selama 16 minggu. Setelah masa perlakuan selesai, hewan coba didekapitasi dan diambil jaringan hati dan dilakukan pemeriksaan histopatologi dengan pewarnaan Hematoxylin-Eosin untuk diamati perlemakan hati yang terjadi.Hasil: Ditemukan steatosis mikrovesikular pada ketiga kelompok. Hanya sedikit ditemukan steatosis markovesikular, inflamasi lobular, dan pembengkakan hepatiosit pada kelompok perlakuan. Pemberian diet restriksi vitamin B12 menunjukkan perbedaan yang bermakna ketika dilihat melalui persentase pelemakan hati yang terjadi (p=0,001). Analisis post-hoc dilakukan dan didapatkan hasil yaitu terdapat perbedaan perlemakan hati yang bermakna pada kelompok kontrol dibandingkan kelompok perlakuan 8 minggu dan pada kelompok kontrol dibandingkan kelompok perlakuan 16 minggu. Kesimpulan: Diet restriksi vitamin B12 menunjukkan adanya perbedaan gambaran perlemakan hati yang bermakna yang terlihat pada gambaran histologi jaringan hati setelah perlakuan 8 dan 16 minggu.

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ABSTRACTIntroduction: Vitamin B12 deficiencys incidence and prevalence throughout the world are still unknown  and studies only found in certain areas. There is an indication that folate and vitamin B12 deficiency will be global health problem in some countries. In some research, it was found that low level of serum vitamin B12 was associated with non-alcoholic fatty liver disease (NAFLD). NAFLD has a broad spectrum, from simple steatosis, steatohepatitis, fibrosis, until cirrhosis. Objective: This research aimed to investigate the histopathological changes of steatosis in rats induced with vitamin B12 restriction diet within observation period. Method: This experimental study was conducted with 18 Sprague-Dawley rats that were divided equally in 3 groups: (1) control group with normal diet for 16 weeks; (2) treatment group with vitamin B12 restriction diet for 8 weeks; and (3) treatment group with vitamin B12 restriction diet for 16 weeks. After observation period was finished, decapitation was performed to obtain rats liver tissue. Liver tissue then stained with Hematoxylin-Eosin to observe the steatosis percentage. Result: Microvesicular steatosis was observed in all groups. There were a little macrovesicular steatosis, lobular inflammation, and hepatic ballooning in treatment group. Steatosis percentage showed significant result when all groups were compared (p=0,001). Post-hoc analysis then performed; there was significant difference of steatosis percentage of control group compared with 8 weeks treatment group and control group compared with 16 weeks treatment group. Conclusion: Vitamin B12 restriction diet showed significant difference of steatosis showed in liver tissue after 8 and 16 weeks of treatment."

"Background. Metformin is the first-line oral antidiabetic agent used in the treatment of diabetes mellitus. One of the adverse reactions of the long term use of metformin is cobalamin malabsorption. Clinical and laboratory findings are important in the diagnosis of cobalamin deficiency.Objective. This study aimed to evaluate the risk of cobalamin deficiency symptoms related to long-term use of metformin in type 2 diabetes mellitus patients at Pasar Rebo General Hospital in Jakarta.Setting. This quantitative, observational study with retrospective cohort design was conducted in outpatient department Pasar Rebo General Hospital November 2015 until January 2016.Methods. 200 subjects were recruited and divided into two groups, patients who had been taking metformin for 1-3 years and patients who had been taking metformin for more than 3 years. Each patient was assessed for thepresence of cobalamin deficiency symptoms. Main outcome measure. Cobalamin deficiency symptoms evaluated were symptoms of neuropathy(measured by DN4 questionnaire) and hematologic abnormalities associated to cobalamin deficiency, i.e. macrocytic erythrocyte, hypersegmented neutrophils, and giant bands.Results. There are significant differences in the proportions of neuropathy symptoms (RR 2.36, 95%, p=0.000) and hematologic abnormalities (RR 1.5, 95%, p=0.007) between the two groups.Conclusions. Long-term use of metformin (≥3 years) may increase the risk of cobalamin deficiency symptoms in type 2 diabetes mellitus patients."