Abstract
The aim of this study was to determine the effects of balanced deep-sea water (BDSW) on hyperglycemia and glucose intolerance in streptozotocin (STZ)-induced diabetic mice. BDSW was prepared by mixing DSW mineral extracts and desalinated water to yield a final hardness of 1000–4000 ppm. Male ICR mice were assigned to 6 groups; mice in each group were given tap water (normal and STZ diabetic groups) or STZ with BDSW of varying hardness (0, 1000, 2000, and 4000 ppm) for 4 weeks. The STZ with BDSW group exhibited lowered fasting plasma glucose levels than the STZ-induced diabetic group. Oral glucose tolerance tests showed that BDSW improves impaired glucose tolerance in STZ-induced diabetic mice. Histopathological evaluation of the pancreas showed that BDSW restores the morphology of the pancreatic islets of Langerhans and increases the secretion of insulin in STZ-induced diabetic mice. Quantitative real-time PCR assay revealed that the expression of hepatic genes involved in gluconeogenesis, glucose oxidation, and glycogenolysis was suppressed, while the expression of the genes involved in glucose uptake, β-oxidation, and glucose oxidation in muscle were increased in the STZ with BDSW group. BDSW stimulated PI3-K, AMPK, and mTOR pathway-mediated glucose uptake in C2C12 myotubes. BDSW increased AMPK phosphorylation in C2C12 myotubes and improved impaired AMPK phosphorylation in the muscles of STZ-induced diabetic mice. Taken together, these results suggest that BDSW is a potential anti-diabetic agent, owing to its ability to suppress hyperglycemia and improve glucose intolerance by modulating glucose metabolism, recovering pancreatic islets of Langerhans and increasing glucose uptake.
Highlights
In recent years, the number of diabetes patients has steadily increased worldwide
Food intake did not differ between STZ and STZ with balanced deep-sea water (BDSW) groups; there was a difference in BDSW intake between the BDSW groups
These findings indicate that BDSW has strong anti-hyperglycemic potential in STZ-induced diabetic mice
Summary
The number of diabetes patients has steadily increased worldwide. The pathologic mechanisms of this disease are mainly attributed to impaired insulin secretion by pancreatic b-cells and insulin resistance in target tissues, including skeletal muscle and the liver, which leads to hyperglycemia. The available diabetic therapies include insulin and several oral anti-diabetic agents such as sulfonylureas, thiazolidinediones, and a-glucosidase inhibitors; these drugs can be used as a monotherapy or in combination, to achieve optimal glycemic control. Studies of both basic sciences and clinical trials indicate that sulfonylureas cause hypoglycemic symptoms associated with persistent insulin secretion. These effects are not dependent on blood glucose levels and attenuate the efficacy of long-term diabetes treatments. Most oral anti-diabetic agents are associated with many serious adverse effects [2]
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