Background: Identification of appropriate biomarker involved in the pathophysiology of diabetes-associated cognitive decline in animal model is necessary. Glucose transporter 4 (GLUT4) is the component of insulin-dependent neuronal signaling pathway needed for maintaining cognitive function. It is highly expressed in hippocampal neurons. Objective: To investigate the effect of GLUT4 expression in hippocampal neurons on the spatial memory of diabetes-induced Rattus novergicus. Methods: This experimental study used 24 male Rattus novergicus divided into control groups terminated on day-0 (C0), 14 (C1) and 28 (C2) and diabetic groups terminated on day-0 (D0), 14 (D1) and 28 (D2). Diabetes was induced using streptozotocin injections intraperitoneally. Spatial memory (travel time) of rats was assessed on day-14 and 28. Brain tissue sampling was performed for assessment of GLUT4 expression using immunohistochemical methods. Significant differences in means of GLUT4 expression and travel time between groups on day-0, 14 and 28 as well as correlation between means of GLUT4 expression and travel time in D1 and D2 were analyzed statistically. Results: The mean of GLUT4 expression in diabetic group was significantly higher compared to control on day-14, but not on day-0 and 28. The immunohistochemical examination confirmed this results. There were no significant differences in mean of travel time between control and diabetic groups on day-14 and 28. There were no significant correlation between means of GLUT4 expression and travel time in diabetic groups on day-14 and 28. Conclusion: The GLUT4 expression of hippocampal neurons did not significantly affect spatial memory of diabetes-induced Rattus novergicus.

Latar Belakang : Diabetes melitus (DM) merupakan penyakit degeneratif yang ditandai dengan kondisi hiperglikemia. Data Riset Kesehatan Dasar tahun 2018, menunjukan peningkatan prevalensi DM di Indonesia selama 5 tahun terakhir dengan 6,9% pada tahun 2013 menjadi 8,5% di tahun 2018. Ekspresi reseptor insulin pankreas dapat menjadi marker untuk menilai keberadaan sel ?, produksi dan sekresi dari insulin. Insulin berperan dalam menyebabkan GLUT4 ditranslokasikan ke membran sel neuron hipokampus. Pada kondisi DM, dapat terjadi perubahan ekspresi reseptor insulin pankreas yang disertai dengan perubahan ekspresi GLUT4 neuron hipokampus.   Metode : Penelitian eksperimental ini menggunakan 16 ekor tikus putih (Rattus Novergicus) yang dibagi secara acak menjadi 4 kelompok yaitu 2 kelompok kontrol (A0 dan A1), dan 2 kelompok perlakuan (B0 dan B1). Kelompok perlakuan diinduksi diabetes dengan nikotinamid 110 mg/kgBB dan streptozotocin 70 mg/kgBB dosis tunggal secara intraperitoneal. Data penelitian diperoleh dari pemeriksaan imunohistokimia jaringan pankreas dan hipokampus.   Hasil : Rerata ekspresi reseptor insulin pankreas kelompok tikus diabetik lebih tinggi tetapi tidak signifikan pada pengamatan hari ke-14 dibandingkan hari ke-0 (p>0,05), sedangkan rerata ekspresi GLUT4 neuron hipokampus signifikan lebih tinggi pada pengamatan hari ke-14 dibandingkan hari ke-0 (p<0,05). Hasil Uji korelasi tidak menunjukkan hasil yang signifikan pada pengamatan hari ke-0 maupun hari ke-14 untuk masing-masing kelompok (p>0,05).   Kesimpulan : Tidak terdapat pengaruh yang signifikan dari ekspresi reseptor insulin pankreas terhadap ekspresi GLUT4 neuron hipokampus pada tikus model diabetes.

Vitamin D has a number of roles in various body systems with receptors scattered in many organs,1,2 showing a link between vitamin D and several chronic diseases such as cancer, diabetes and autoimmune disease.3,4 Several studies have shown the role of vitamin D in type 2 diabetes in controlling blood sugar levels and HbA1c levels. Vitamin D plays a role in increasing insulin sensitivity and secretion and suppressing inflammation in type 2 diabetes. Vitamin D has a protective role in various complications of type 2 diabetes, including diabetic nephropathy, diabetic neuropathy and diabetic retinopathy.5 Monitoring of vitamin D levels and vitamin D supplementation have a therapeutic role to controlling glycemic blood glucose and prevent complications in type 2.6