Type 2 Diabetic Rats on Diet Supplemented With Chromium Malate Show Improved Glycometabolism, Glycometabolism-Related Enzyme Levels and Lipid Metabolism

Feng, Weiwei; Zhao, Ting; Mao, Guanghua; Wang, Wei; Feng, Yongzeng; Li, Fang; Zheng, Donghai; Wu, Hui-Yu; Dun, Jin; Yang, Liuqing

doi:10.1371/journal.pone.0125952

Cited by 30 publications

(30 citation statements)

References 42 publications

(40 reference statements)

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“…Previous studies revealed the key role of chromium as a blood glucose and lipid regulator [17,18]. Both in a diabetic rodent model and patients, chromium supplementation could improve glucose and lipid metabolism [11,19,20,21]. …”

Section: Discussionmentioning

confidence: 99%

Maternal Chromium Restriction Leads to Glucose Metabolism Imbalance in Mice Offspring through Insulin Signaling and Wnt Signaling Pathways

Zhang

Sun

Xiao

et al. 2016

IJMS

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An adverse intrauterine environment, induced by a chromium-restricted diet, is a potential cause of metabolic disease in adult life. Up to now, the relative mechanism has not been clear. C57BL female mice were time-mated and fed either a control diet (CD), or a chromium-restricted diet (CR) throughout pregnancy and the lactation period. After weaning, some offspring continued the diet diagram (CD-CD or CR-CR), while other offspring were transferred to another diet diagram (CD-CR or CR-CD). At 32 weeks of age, glucose metabolism parameters were measured, and the liver from CR-CD group and CD-CD group was analyzed using a gene array. Quantitative real-time polymerase chain reaction (qPCR) and Western blot were used to verify the result of the gene array. A maternal chromium-restricted diet resulted in obesity, hyperglycemia, hyperinsulinemia, increased area under the curve (AUC) of glucose in oral glucose tolerance testing and homeostasis model assessment of insulin resistance (HOMA-IR). There were 463 genes that differed significantly (>1.5-fold change, p < 0.05) between CR-CD offspring (264 up-regulated genes, 199 down-regulated genes) and control offspring. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and STRING (Search Tool for the Retrieval of Interacting Genes/Proteins) analysis revealed that the insulin signaling pathway and Wnt signaling pathway were in the center of the gene network. Our study provides the first evidence that maternal chromium deficiency influences glucose metabolism in pups through the regulation of insulin signaling and Wnt signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Maternal Chromium Restriction Leads to Glucose Metabolism Imbalance in Mice Offspring through Insulin Signaling and Wnt Signaling Pathways

Zhang

Sun

Xiao

et al. 2016

IJMS

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“…In experimental models of diabetes, both a high-carbohydrate/high-fat diet and alloxan exert their toxic effects on the liver and other organs in addition to pancreatic β -cells. The insulin insufficiency and hyperglycemia that result from β -cell necrosis further augment liver damage through reactive free radical mediated lipid peroxidation of hepatocellular membrane [39, 40]. In this study, the diabetic hyperglycemia induced by HFD-alloxan treatment produced elevated levels of AST and ALT in the serum, which are considered highly indicative of liver dysfunction.…”

Section: Discussionmentioning

confidence: 84%

Quercetin Isolated from Toona sinensis Leaves Attenuates Hyperglycemia and Protects Hepatocytes in High-Carbohydrate/High-Fat Diet and Alloxan Induced Experimental Diabetic Mice

Zhang

Dong

Wang

et al. 2016

Journal of Diabetes Research

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The development of diabetes mellitus is related to oxidant stress induced by a high carbohydrate/high-fat diet (HFD). Quercetin, as a major bioactive component in Toona sinensis leaves (QTL), is a natural antioxidant. However, the exact mechanism by which QTL ameliorate diabetes mellitus is still unknown. In this study, we investigated the hypoglycemic effects and hepatocytes protection of QTL on HFD and alloxan induced diabetic mice. Intragastric administration of QTL significantly reduced body weight gain, serum glucose, insulin, total cholesterol, triglyceride, low density lipoprotein-cholesterol, alanine aminotransferase, and aspartate aminotransferase serum levels compared to those of diabetic mice. Furthermore, it significantly attenuated oxidative stress, as determined by lipid peroxidation, nitric oxide content, and inducible nitric oxide synthase activity and as a result attenuated liver injury. QTL also significantly suppressed the diabetes-induced activation of the p65/NF-κB and ERK1/2/MAPK pathways, as well as caspase-9 and caspase-3 levels in liver tissues of diabetic mice. Finally, micrograph analysis of liver samples showed decreased cellular organelle injury in hepatocytes of QTL treated mice. Taken together, QTL can be viewed as a promising dietary agent that can be used to reduce the risk of diabetes mellitus and its secondary complications by ameliorating oxidative stress in the liver.

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“…It has been reported that malate could improve the quality of life of patients with idiopathic arterial pulmonary hypertension and also reduce mean arterial pulmonary hypertension (Sharif Kashani et al, ). Moreover, elevation of malate improves mitochondrial functions of aged rats by reversing oxidative stress (Feng et al, ; Wu et al, ). Aspartate may also scavenge reactive oxygen species (Marquezi, Roschel, Dos, & Sawada, ; Yatzidis, ).…”

Section: Resultsmentioning

confidence: 99%

Combined metabolomic and correlation networks analyses reveal fumarase insufficiency altered amino acid metabolism

Hou

Liu

et al. 2018

Biomedical Chromatography

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Fumarase catalyzes the interconversion of fumarate and l-malate in the tricarboxylic acid cycle. Fumarase insufficiencies were associated with increased levels of fumarate, decreased levels of malate and exacerbated salt-induced hypertension. To gain insights into the metabolism profiles induced by fumarase insufficiency and identify key regulatory metabolites, we applied a GC-MS based metabolomics platform coupled with a network approach to analyze fumarase insufficient human umbilical vein endothelial cells (HUVEC) and negative controls. A total of 24 altered metabolites involved in seven metabolic pathways were identified as significantly altered, and enriched for the biological module of amino acids metabolism. In addition, Pearson correlation network analysis revealed that fumaric acid, l-malic acid, l-aspartic acid, glycine and l-glutamic acid were hub metabolites according to Pagerank based on their three centrality indices. Alanine aminotransferase and glutamate dehydrogenase activities increased significantly in fumarase deficiency HUVEC. These results confirmed that fumarase insufficiency altered amino acid metabolism. The combination of metabolomics and network methods would provide another perspective on expounding the molecular mechanism at metabolomics level.

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Type 2 Diabetic Rats on Diet Supplemented With Chromium Malate Show Improved Glycometabolism, Glycometabolism-Related Enzyme Levels and Lipid Metabolism

Cited by 30 publications

References 42 publications

Maternal Chromium Restriction Leads to Glucose Metabolism Imbalance in Mice Offspring through Insulin Signaling and Wnt Signaling Pathways

Maternal Chromium Restriction Leads to Glucose Metabolism Imbalance in Mice Offspring through Insulin Signaling and Wnt Signaling Pathways

Quercetin Isolated from Toona sinensis Leaves Attenuates Hyperglycemia and Protects Hepatocytes in High-Carbohydrate/High-Fat Diet and Alloxan Induced Experimental Diabetic Mice

Combined metabolomic and correlation networks analyses reveal fumarase insufficiency altered amino acid metabolism

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