1. Effect of Konjac Mannan Oligosaccharides on Glucose Homeostasis via the Improvement of Insulin and Leptin Resistance In Vitro and In Vivo
- Author
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Qiaojuan Yan, Haijie Liu, Di Zhu, Li Yanxiao, Zhengqiang Jiang, and Jun Liu
- Subjects
Blood Glucose ,Leptin ,Male ,0301 basic medicine ,Glucose uptake ,medicine.medical_treatment ,Mannans ,0302 clinical medicine ,insulin resistance ,Homeostasis ,Insulin ,Glucose homeostasis ,Nutrition and Dietetics ,biology ,Chemistry ,Hep G2 Cells ,leptin resistance ,Liver ,lcsh:Nutrition. Foods and food supply ,hormones, hormone substitutes, and hormone antagonists ,Signal Transduction ,medicine.medical_specialty ,030209 endocrinology & metabolism ,lcsh:TX341-641 ,Carbohydrate metabolism ,Diet, High-Fat ,Article ,03 medical and health sciences ,Insulin resistance ,Internal medicine ,medicine ,Animals ,Humans ,Hypoglycemic Agents ,glucose homeostasis ,Glucose Metabolism Disorders ,Leptin receptor ,AMPK ,medicine.disease ,Mice, Inbred C57BL ,Disease Models, Animal ,konjac mannan oligosaccharides ,030104 developmental biology ,Endocrinology ,Dietary Supplements ,Hepatocytes ,biology.protein ,GLUT2 ,Biomarkers ,Food Science - Abstract
Functional oligosaccharides, particularly konjac mannan oligosaccharides (KMOS), can regulate glucose metabolism. However, the molecular mechanisms involved in the hypoglycemic effect of KMOS remain largely unknown. Here, the effect of KMOS supplementation on glucose homeostasis was evaluated in both high-fat diet (HFD)-fed C57BL/6J mice and high-glucosamine-induced HepG2 cells. KMOS supplementation remarkably ameliorated the fasting blood glucose, glucose tolerance, and insulin tolerance of HFD-fed mice. Abnormalities of triglyceride and glycogen metabolism in the liver induced by the HFD were reversed by KMOS supplementation. The insulin signaling pathway was activated by KMOS, with stimulation of GLUT2 membrane translocation and glucose uptake in HepG2 cells via the AMPK pathway. Moreover, KMOS suppressed p-mTOR expression and stimulated the GSK-3&beta, /CREB pathway via the AMPK pathway. KMOS significantly upregulated leptin receptor expression and downregulated PTP1B and SOCS3 levels in the liver and brain, with a decreased serum leptin concentration. Phosphorylation of JAK2 and STAT3 in the liver was activated by KMOS supplementation, while the expressions of Sirt1, Tfam, and Pgc1-&alpha, in the brain were elevated. Conclusively, KMOS attenuated HFD-induced glucose metabolism dysfunction through the regulation of insulin resistance and leptin resistance. This finding indicates that KMOS have potential value as an anti-hyperglycemic dietary supplement.
- Published
- 2019
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