Article

Correction: Hydrogen Improves Glycemic Control in Type1 Diabetic Animal Model by Promoting Glucose Uptake into Skeletal Muscle

Department of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
PLoS ONE (Impact Factor: 3.53). 04/2013; 8(1):e53913. DOI: 10.1371/journal.pone.0053913
Source: PubMed

ABSTRACT Hydrogen (H(2)) acts as a therapeutic antioxidant. However, there are few reports on H(2) function in other capacities in diabetes mellitus (DM). Therefore, in this study, we investigated the role of H(2) in glucose transport by studying cultured mouse C2C12 cells and human hepatoma Hep-G2 cells in vitro, in addition to three types of diabetic mice [Streptozotocin (STZ)-induced type 1 diabetic mice, high-fat diet-induced type 2 diabetic mice, and genetically diabetic db/db mice] in vivo. The results show that H(2) promoted 2-[(14)C]-deoxy-d-glucose (2-DG) uptake into C2C12 cells via the translocation of glucose transporter Glut4 through activation of phosphatidylinositol-3-OH kinase (PI3K), protein kinase C (PKC), and AMP-activated protein kinase (AMPK), although it did not stimulate the translocation of Glut2 in Hep G2 cells. H(2) significantly increased skeletal muscle membrane Glut4 expression and markedly improved glycemic control in STZ-induced type 1 diabetic mice after chronic intraperitoneal (i.p.) and oral (p.o.) administration. However, long-term p.o. administration of H(2) had least effect on the obese and non-insulin-dependent type 2 diabetes mouse models. Our study demonstrates that H(2) exerts metabolic effects similar to those of insulin and may be a novel therapeutic alternative to insulin in type 1 diabetes mellitus that can be administered orally.

0 Followers
 · 
214 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: We have found hydrogen (dihydrogen; H2) has beneficial lipid-lowering effects in high-fat diet-fed Syrian golden hamsters. The objective of this study was to characterize the effects of H2-rich water (0.9-1.0 L/day) on the content, composition, and biological activities of serum lipoproteins on 20 patients with potential metabolic syndrome. Serum analysis showed that consumption of H2-rich water for 10 weeks resulted in decreased serum total-cholesterol (TC) and low-density lipoprotein-cholesterol (LDL-C) levels. Western blot analysis revealed a marked decrease of apolipoprotein B100 (apoB100) and apoE in serum. Besides, we found H2 significantly improved high-density lipoprotein (HDL) functionality assessed in four independent ways, namely (i) protection against LDL oxidation, (ii) inhibition of TNF-α induced monocyte adhension to endothelial cells, (iii) stimulation of cholesterol efflux from macrophage foam cells, (iv) protection of endothelial cells from TNF-α induced apoptosis. Further, we found consumption of H2-rich water resulted in an increase in antioxidant enzyme superoxide dismutase and a decrease in thiobarbituric acid-reactive substances in whole serum and LDL. In conclusion, supplementation with H2-rich water appear to decrease serum LDL-C and apoB levels, improve dyslipidemia injured HDL functions, and reduce the oxidative stress and may have a beneficial role in prevention of potential metabolic syndrome.
    The Journal of Lipid Research 04/2013; DOI:10.1194/jlr.M036640 · 4.73 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Multiple parallel hits, including genetic differences, insulin resistance and intestinal microbiota, account for the progression of non-alcoholic steatohepatitis (NASH). Multiple hits induce adipokine secretion, endoplasmic reticulum (ER) and oxidative stress at the cellular level that subsequently induce hepatic steatosis, inflammation and fibrosis, among which oxidative stress is considered a key contributor to progression from simple fatty liver to NASH. Although several clinical trials have shown that anti-oxidative therapy can effectively control hepatitis activities in the short term, the long-term effect remains obscure. Several trials of long-term anti-oxidant protocols aimed at treating cerebrovascular diseases or cancer development have failed to produce a benefit. This might be explained by the non-selective anti-oxidative properties of these drugs. Molecular hydrogen is an effective antioxidant that reduces only cytotoxic reactive oxygen species (ROS) and several diseases associated with oxidative stress are sensitive to hydrogen. The progress of NASH to hepatocellular carcinoma can be controlled using hydrogen-rich water. Thus, targeting mitochondrial oxidative stress might be a good candidate for NASH treatment. Long term clinical intervention is needed to control this complex lifestyle-related disease.
    International Journal of Molecular Sciences 10/2013; 14(10):20704-20728. DOI:10.3390/ijms141020704 · 2.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sinapic acid is a hydroxycinnamic acid contained in plants. In an attempt to know the hyperglycemic effect of sinapic acid, this study applied streptozotocin (STZ) to induce type 1-like diabetic rats and fed fructose-rich chow to induce type 2-like diabetic rats. Sinapic acid dose-dependently reduced the hyperglycemia of STZ-diabetic rats (9.8 ± 1.8 %, 11.6 ± 0.7 %, and 19.4 ± 3.2 % at 5 mg/kg, 10 mg/kg and 25 mg/kg,). Also, sinapic acid attenuated the postprandial plasma glucose without changing plasma insulin in rats. Repeated treatment of sinapic acid increased the gene expression of GLUT 4 in soleus muscle of STZ-diabetic rats. Moreover, sinapic acid enhanced glucose uptake into isolated soleus muscle and L6 cells (337.0 ± 29.6 %). Inhibition of phospholipase C (PLC) using U73122 (1.00 ± 0.02 μg/mg protein) or protein kinase C (PKC) using chelerythrine (0.97 ± 0.02 μg/mg protein) attenuated the sinapic acid-stimulated glucose uptake (1.63 ± 0.02 μg/mg protein) in L6 cells. Otherwise, the reduced glucose infusion rate (GIR) in fructose-rich chow-fed rats was also raised by sinapic acid. Our results suggest that sinapic acid ameliorates hyperglycemia through PLC-PKC signals to enhance the glucose utilization in diabetic rats.
    Journal of Agricultural and Food Chemistry 11/2013; 61(49). DOI:10.1021/jf403092b · 3.11 Impact Factor

Preview

Download
4 Downloads
Available from