Xylobiose, an Alternative Sweetener, Ameliorates Diabetes-Related Metabolic Changes by Regulating Hepatic Lipogenesis and miR-122a/33a in db/db Mice
- Nutrients. 2016 Dec 5;8(12):791. doi: 10.3390/nu8120791.
- 1. Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea. [email protected].
- 2. Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea. [email protected].
- 3. Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea. [email protected].
- 4. Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea. [email protected].
- 5. Department of Biomedical Laboratory Science, Eulji University, Seongnam-si, Gyunggi-do 13135, Korea. [email protected].
- 6. Department of Biomedical Laboratory Science, Eulji University, Seongnam-si, Gyunggi-do 13135, Korea. [email protected].
- 7. R&D Center, TS Corporation, Incheon 22300, Korea. [email protected].
- 8. Department of Food Science & Biotechnology, and Carbohydrate Bioproduct Research Center, Sejong University, Seoul 05006, Korea. [email protected].
- 9. Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea. [email protected].
Type 2 diabetes is a major public health concern worldwide. Xylobiose (XB) consists of two molecules of d-xylose and is a major disaccharide in xylooligosaccharides that are used as prebiotics. We hypothesized that XB could regulate diabetes-related metabolic and genetic changes via MicroRNA expression in db/db mice. For six weeks, C57BL/KsJ-db/db mice received 5% XB as part of the total sucrose content of their diet. XB supplementation improved glucose tolerance with reduced levels of OGTT AUC, fasting blood glucose, HbA1c, Insulin, and HOMA-IR. Furthermore, XB supplementation decreased the levels of total triglycerides, total Cholesterol, and LDL-C. The expression levels of miR-122a and miR-33a were higher and lower in the XB group, respectively. In the liver, expressions of the lipogenic genes, including, fatty acid synthase (FAS), peroxisome proliferator activated receptor γ (PPARγ), sterol regulatory element-binding protein-1C (SREBP-1C), sterol regulatory element-binding protein-2 (SREBP-2), Acetyl-CoA Carboxylase (ACC), HMG-CoA reductase (HMGCR), ATP-binding cassette transporter G5/G8 (ABCG5/8), Cholesterol 7 alpha-hydroxylase (CYP7A1), and sterol 12-alpha-hydroxylase (CYP8B1), as well as oxidative stress markers, including superoxide dismutase 1 (SOD1), superoxide dismutase 2 (SOD2), Glutathione Peroxidase (GPX), and catalase, were also regulated by XB supplementation. XB supplementation inhibited the mRNA expressions levels of the pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1, as well as phosphorylation of c-Jun N-terminal kinase/stress activated protein kinase (JNK/SAPK), p38 mitogen-activated protein kinases (MAPK), and extracellular signal-regulated kinases 1/2 (ERK1/2). These data demonstrate that XB exhibits anti-diabetic, hypolipogenic, and anti-inflammatory effects via regulation of the miR-122a/33a axis in db/db mice.
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