Effects of chromium malate on glycometabolism, glycometabolism‐related enzyme levels and lipid metabolism in type 2 diabetic rats: A dose–response and curative effects study

Feng, Weiwei; Mao, Guanghua; Li, Qian; Wang, Wei; Chen, Yao; Zhao, Ting; Li, Fang; Zou, Ye; Wu, Hui-Yu; Yang, Liuqing

doi:10.1111/jdi.12350

Cited by 25 publications

(17 citation statements)

References 39 publications

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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%

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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%

“…[10]. Chromium can reduce fasting blood glucose levels in diabetic patients and diabetic rodent models [11], and enhance insulin action, including activation of insulin receptor sites [12]. Diabetic animals [13] and patients [14,15] have lower chromium levels than that of controls.…”

Section: Introductionmentioning

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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“…It is known that trace elements, especially chromium (Cr), play a significant role in the metabolism of lipids and carbohydrates (Feng et al, 2015). Chromium as a cofactor of chromodulin, a low molecular weight oligopeptide, by attaching to the β-subunit of the insulin receptor and activating tyrosine kinase, increases the effect of insulin.…”

Section: Discussionmentioning

confidence: 99%

Influence of chromium citrate on oxidative stress in the tissues of muscle and kidney of rats with experimentally induced diabetes

Sushko¹,

Iskra²,

Ponkalo³

2019

Regul. Mech. Biosyst.

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Chromium is one of the important trace elements that is essential for carbohydrate, protein and lipid metabolism. Chromium improves glucose metabolism and reduces insulin resistance due to increased insulin sensitivity. Therefore, it is important to consider the use of chromium citrate as a nutritional supplement with potential hypoglycemic and hypolipidemic effects. In this research work, we investigated the activity of the antioxidant system and the level of lipid hydroperoxides in the tissues of skeletal muscles and kidneys of experimental diabetic rats and for rats which received in their daily diet chromium citrate in the amounts 0.1 and 0.2 μg/mL of water. We induced the experimental model of diabetes by intraperitoneal injection of alloxan in the amount 150 mg/kg of body weight of the animals. We monitored glucose levels by measuring daily glucose levels with a portable glucose meter. For research, we selected animals with a glucose level > 11.1 mmol/L. We monitored the body weight of rats. On the 40th day of the study, we withdrew the animals from the experiment by decapitation. We selected the tissue for research, namely skeletal muscles and kidneys. In samples of the tissue homogenates, we measured the activity of antioxidant enzymes and the content of lipid peroxide oxidation products. As a result of our research, we found that the products of lipid peroxide oxidation and glutathione peroxidase activity increased in skeletal muscle of animals with diabetes mellitus. The activity of glutathione reductase, catalase, superoxide dismutase, and the content of reduced glutathione decreased at the same time. In the kidneys of diabetic rats, the activity of glutathione peroxidase, glutathione reductase, catalase and content of lipid hydroperoxides increased but the activity of superoxide dismutase and the content of reduced glutathione decreased. The addition of chromium citrate to the diet of animals in amounts 0.1 and 0.2 μg/mL led to the suppression of oxidative stress. The activity of catalase, glutathione peroxidase and the content of lipid hydroperoxides, TBA-positive substances decreased. Also, the activity of superoxide dismutase increased with the addition of chromium citrate. These results indicate normalization of antioxidant defense in the skeletal muscle and kidneys of experimental rats with experimental diabetes given chromium citrate in the amount 0.1 mg/mL of water.

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“…Chromium supplementation can significantly cut down total cholesterol (TC) and low-density lipoprotein (LDL) levels in Type 2 diabetes (T2D) subjects [7–10], women with polycystic ovary syndrome [11] and high fat diet rats [12,13]. The suggested minimum daily intake of chromium is 30 μg.…”

Section: Introductionmentioning

confidence: 99%

The effect of maternal chromium status on lipid metabolism in female elderly mice offspring and involved molecular mechanism

et al. 2017

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Maternal malnutrition leads to the incidence of metabolic diseases in offspring. The purpose of this project was to examine whether maternal low chromium could disturb normal lipid metabolism in offspring, altering adipose cell differentiation and leading to the incidence of lipid metabolism diseases, including metabolic syndrome and obesity. Female C57BL mice were given a control diet (CD) or a low chromium diet (LCD) during the gestational and lactation periods. After weaning, offspring was fed with CD or LCD. The female offspring were assessed at 32 weeks of age. Fresh adipose samples from CD–CD group and LCD–CD group were collected. Genome mRNA were analysed using Affymetrix GeneChip Mouse Gene 2.0 ST Whole Transcript-based array. Differentially expressed genes (DEGs) were analysed based on gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis database. Maternal low chromium irreversibly increased offspring body weight, fat-pad weight, serum triglyceride (TG) and TNF-α. Eighty five genes increased and 109 genes reduced in the offspring adipose of the maternal low chromium group. According to KEGG pathway and String analyses, the PPAR signalling pathway may be the key controlled pathway related to the effect of maternal low chromium on female offspring. Maternal chromium status have long-term effects of lipid metabolism in female mice offspring. Normalizing offspring diet can not reverse these effects. The potential underlying mechanisms are the disturbance of the PPAR signalling pathway in adipose tissue.

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Effects of chromium malate on glycometabolism, glycometabolism‐related enzyme levels and lipid metabolism in type 2 diabetic rats: A dose–response and curative effects study

Cited by 25 publications

References 39 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

Influence of chromium citrate on oxidative stress in the tissues of muscle and kidney of rats with experimentally induced diabetes

The effect of maternal chromium status on lipid metabolism in female elderly mice offspring and involved molecular mechanism

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