| dc.description.abstract | Glucose uptake into skeletal muscle cells require insulin-dependent and insulin independent
signaling pathways, both leading to the translocation of glucose transporter-4 (GLUT4) to the
plasma membrane. Insulin resistance occurs due to failure of insulin signaling to translocate
GLUT4 resulting in the failure of glucose uptake and causing hyperglycemia. Cholecalciferol is
known to have a function in regulating calcium homeostasis was shown to increase the
synthesis of insulin and increasing insulin sensitivity. The purpose of this study is to explain the
role of cholecalciferol to decreased fasting blood glucose in streptozotocin-induced
hyperglyemia mice. 30 mice adapted for one week and then induced using 150mg/kgBW
streptozotocin (STZ) intraperitoneally, After experiencing hyperglycemia mice were divided into
5 groups (n=6 each), Group I (hyperglycemic control), group II (25ng cholecalciferol), group III
(50ng cholecalciferol), group IV (100ng cholecalciferol), and group V (metformin
300mg/kgBBB). Cholecalciferol given orally for 14th days. On day 15th the examination of
fasting blood sugar levels were taken and the mice. Fasting blood sugar levels measured using
a glucometer. Based on statistical analysis showed that there were significant differences in
fasting blood sugar levels between treatment groups (p<0,001). Based on univariate regression
analyses there was negative correlation of cholecalciferol with fasting blood glucose (p<0,001).
Cholecalciferol may lower fasting blood sugar levels in hyperglycemia mice models. | en_US |
