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All Journal The Indonesian Biomedical Journal GANESHA MEDICINA
Budhiarta, Anak Agung Gde
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Biochemistry, Genetics & Molecular Biology Health Professions Medicine & Pharmacology Public Health

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DIABETES INSIPIDUS PADA PASIEN DENGAN CEDERA KEPALA SEDANG S., Hantono; Gotera, Wira; Suastika, Ketut; Budhiarta, Anak Agung Gde; Saraswati, Made Ratna; Dwipayana, I Made Pande; Semadi, I Made Siswadi; Nugraha, Ida Bagus Aditya
Ganesha Medicina Vol. 4 No. 1 (2024)
Publisher : Universitas Pendidikan Ganesha

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.23887/gm.v4i1.75553

Abstract

Diabetes Insipidus (DI) adalah suatu sindrom yang ditandai dengan ekskresi urin dalam jumlah besar yang tidak normal (poliuria) disertai peningkatan asupan cairan sebagai kompensasinya (polidipsia). Hal ini disebabkan oleh penurunan sekresi (DI sentral/neurogenik) atau kerja (DI nefrogenik) dari Hormon Antidiuretik. Hormon ini diproduksi oleh neuron hipotalamus di nukleus supraoptik dan paraventrikular dan disekresikan ke sirkulasi bila ada rangsangan. Cedera kepala merupakan salah satu penyebab mortalitas dan morbiditas terbanyak pada generasi muda terutama laki-laki. Salah satu dampaknya adalah disfungsi hormonal pada hipofisis anterior dan posterior. Angka kejadian DI setelah cedera kepala berkisar 1-2,9%. Dalam kasus tertentu, keadaan ini hanya terjadi sementara namun dapat juga menjadi permanen. Dalam laporan kasus ini, dilaporkan laki-laki berusia 28 tahun dengan DI setelah mengalami cedera kepala. Pasien menjalani kraniektomi dekompresi dengan osteoplasti. Selama perawatan, pasien didiagnosa dengan Diabetes Insipidus dari gejalanya, osmolalitas urin yang rendah, osmolalitas plasma yang tinggi, dan hipernatremia, kemudian ditangani dengan rehidrasi dan pemberian injeksi vasopresin 5 IU secara intramuskular serta pemantauan ketat terhadap keseimbangan cairan setiap hari. Selama beberapa hari berikutnya, setelah keseimbangan cairan normal, vasopresin dihentikan dan keseimbangan cairan masih dalam batas normal.
Diabetes Risk Allele of Transcription Factor 7-like 2 (TCF7L2) Polymorphisms is Associated with Higher Glucagon-like Peptide 1 (GLP1) and Lower Insulin Secretion Saraswati, Made Ratna; Suastika, Ketut; Budhiarta, Anak Agung Gde; Oktavianthi, Suksma; Malik, Safarina G.
The Indonesian Biomedical Journal Vol 16, No 5 (2024)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v16i5.3202

Abstract

BACKGROUND: The most influential susceptible gene associated with diabetes, transcription factor 7-like 2 (TCF7L2), has been observed in diverse populations. TCF7L2 influences type 2 diabetes risk through glucagon-like peptide 1 (GLP1) production. The presence of risk allele of TCF7L2 leads to the alteration of gene expression in pancreatic beta cells; however, how the mechanism is related with GLP1 remains unclear. This study was conducted to explore the variations of GLP1 increment and insulin secretion between individuals with and without diabetes risk allele of single nucleotide polymorphisms (SNPs) in TCF7L2.METHODS: A cross-sectional analytic study was conducted involving individuals subjects who harbored known variants of SNPs in the TCF7L2: heterozygote or mutant of rs12255372 (GT or TT), rs7903146 (CT or TT), rs10885406 (AG or GG); as well as control subjects with wild type of rs12255372 (GG), rs7903146 (CC), and rs10885406 (AA). Anthropometric parameters, blood glucose, insulin, and GLP1 were measured; and homeostasis model assessment-beta cell (HOMA-%B) index was calculated.RESULTS: The GLP1 increment response was higher in subjects carrying the diabetes risk allele (0.34±0.80 ng/mL) than those with the wild type (-0.04±0.57 ng/mL) (p=0.041). The HOMA-%B was reduced in subjects carrying the diabetes risk allele (71.64±24.72) than those with the wild type (103.23±68.00) (p=0.011). Among individuals carrying the diabetes risk allele, the likelihood of GLP1 increment with high response was twice as high (p=0.007), while the occurrence of low HOMA-%B was 1.47 more frequent (p=0.011).CONCLUSION: TCF7L2 polymorphisms were associated with the GLP1 increment response and reduced HOMA-%B, which might be potentially contributing to GLP1 resistance in patients with diabetes risk factors.KEYWORDS: diabetes risk, TCF7L2, GLP1, HOMA-%B
Co-Authors I Ketut Suastika I Made Pande Dwipayana I Made Siswadi Semadi Ida Bagus Aditya Nugraha MADE RATNA SARASWATI . Malik, Safarina G. Oktavianthi, Suksma S., Hantono Wira Gotera