Abstract 089: Response Gene To Complement 32 Is Involved In Glucose Metabolism Disorder In Endothelial Cells And Mediated By P53

Response gene to complement 32 (RGC-32) was considered as an apoptosis-promoting factor. To explore the novel functions of RGC-32, a DNA array analysis was performed in Human Microvascular Endothelial Cells (HMEC) treated with SiRNA, which showed that glucose metabolism was one of most dramatically changed biological process. qPCR analysis also proved that many glucose metabolism related genes were changed dramatically in RGC32 o/e HMEC, one of which was Insulin-like growth factor binding protein 4(IGFBP4). We propose that RGC-32 may be a potential factor involved in the cycle of endothelial glucose metabolism besides glucose induced apoptosis. Then we found that expression of RGC-32 was dramatically increased in mice hearts and adipose tissue after high fat diet treatment, as well as in HMEC after high glucose (30mM) treatment. In high fat diet treated endothelial specific RGC-32 transgenic mice (VE-Cad/RGC-32), decreases in area under the curve (AUC) of glucose tolerance test were observed when compared to their wild type littermates. Upregulated P53 and downregulated IGFBP4 mRNA expression level were also observed in the heart of VE-Cad/RGC-32 mice.Furthermore, we found that P53 was upregulated in RGC-32 o/e HMEC and blocking of p53 was able to decrease the RGC-32-related induction of apoptotic cells. We also observed that RGC-32 can not only decrease IGFBP4 but also reverse the decrease of IGFBP4 in high glucose or insulin condition. Interestingly, after treated the cells with pifithrin-a, a specific P53 inhibitor, decreased IGFBP4 by RGC-32 was rescued. These results demonstrate that RGC-32 may have some kind of connections with glucose metabolism besides its well-known apoptosis-promoting characters and P53 may be a mediator of RGC-32 related glucose metabolism disorder as well as apoptosis.These findings will provide some clues for novel insights into the functions of RGC-32.

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Lactobacillus acidophilus NX2-6 Improved High-Fat Diet-Induced Glucose Metabolism Disorder Independent of Promotion of Insulin Secretion in Mice

Journal of Agricultural and Food Chemistry ◽

10.1021/acs.jafc.1c05948 ◽

2021 ◽

Author(s):

Chao Tang ◽

Gang Cao ◽

Wen Zhao ◽

Xiaomei Bie ◽

Fengxia Lu ◽

...

Keyword(s):

Insulin Secretion ◽

Glucose Metabolism ◽

Lactobacillus Acidophilus ◽

High Fat Diet ◽

High Fat ◽

Metabolism Disorder ◽

Glucose Metabolism Disorder

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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Journal of Visualized Experiments ◽

10.3791/56672 ◽

2018 ◽

Cited By ~ 13

Author(s):

Csörsz Nagy ◽

Elisa Einwallner

Keyword(s):

Glucose Metabolism ◽

High Fat Diet ◽

Glucose Tolerance Test ◽

Tolerance Test ◽

Insulin Tolerance Test ◽

Oral Glucose ◽

Oral Glucose Tolerance ◽

High Fat ◽

Insulin Tolerance

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Effect of Forskolin on Body Weight, Glucose Metabolism and Adipocyte Size of Diet-Induced Obesity in Mice

Animals ◽

10.3390/ani11030645 ◽

2021 ◽

Vol 11 (3) ◽

pp. 645

Author(s):

Jing-Yi Chen ◽

Shao-Yu Peng ◽

Yeong-Hsiang Cheng ◽

I-Ta Lee ◽

Yu-Hsiang Yu

Keyword(s):

Body Weight ◽

Glucose Metabolism ◽

Dimethyl Sulfoxide ◽

High Fat Diet ◽

Tolerance Test ◽

Cell Diameter ◽

High Fat ◽

Fat Cell ◽

Glucose Levels ◽

Insulin Tolerance

The purpose of this study was to investigate the effects of forskolin on body weight, glucose metabolism and fat cell diameter in high-fat diet-induced obese mice. Four-week-old male mice (C57BL/6) were randomly assigned to 1 of 3 treatment groups: a high-fat diet plus 5% dimethyl sulfoxide (vehicle), high-fat diet plus 2 mg/kg of forskolin (dissolved in 5% dimethyl sulfoxide) and high-fat diet plus 4 mg/kg of forskolin (dissolved in 5% dimethyl sulfoxide). Forskolin or dimethyl sulfoxide was administered intraperitoneally every two days. The results indicated that no significant difference was observed in the body weight, feed intake and serum lipid parameters among groups at 20 weeks of age. The blood glucose levels were significantly reduced in the groups treated with 2 mg/kg of forskolin before glucose tolerance test. Forskolin administration linearly decreased blood glucose levels of high-fat diet-fed mice at 90 min and total area under curve (AUC) after insulin tolerance test. The subcutaneous adipocyte diameter was significantly reduced in the groups treated with 2 mg/kg of forskolin. Forskolin administration linearly reduced the gonadal adipocyte diameter of high-fat diet-fed mice. Forskolin significantly reduced the differentiation of murine mesenchymal stem cells into adipocytes and this was accompanied by a decrease in intracellular triglyceride content and an increase in glycerol concentration in the culture medium. The subcutaneous adipocyte diameter, gonadal adipocyte diameter and total AUC of insulin tolerance test were moderately negatively correlated with the concentration of forskolin in the high-fat diet-induced obese model. These results demonstrate that forskolin can regulate glucose metabolism and reduce fat cell diameter of high-fat diet-fed mice and inhibit the adipocyte differentiation of murine mesenchymal stem cells.

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Elevated hepcidin, ferroportin associated with glucose metabolism disorder in midpregnancy

10.21203/rs.3.rs-18111/v1 ◽

2020 ◽

Author(s):

Ziwen Ma ◽

Yan Cheng ◽

Qingying Zhang ◽

Kui Wu ◽

Tingting Li ◽

...

Keyword(s):

Diabetes Mellitus ◽

Glucose Metabolism ◽

Iron Metabolism ◽

Plasma Glucose ◽

Tolerance Test ◽

Control Group ◽

Oral Glucose ◽

Model Assessment ◽

Metabolism Disorder ◽

Glucose Metabolism Disorder

Abstract [Objective]: Hepcidin and ferroportin are major regulators of iron metabolism. Although many previous studies have shown that iron metabolism disorder may contribute to the pathogenesis of Type 2 diabetes mellitus (DM), few studies have investigated hepcidin and other iron metabolism parameters in women with gestational diabetes mellitus (GDM). The purpose of this study was to determine the relationship between hepcidin, ferroportin and GDM. [Methods]: A case-control study was conducted in 85 women with GDM and 85 women without GDM (controls) who received regular prenatal care at the Obstetrics and Gynecology Hospital of Fudan University from October 2015 to May 2016. Serum ferritin (SF), hepcidin (Hepc), ferroportin (FPN), and soluble transferrin receptor (sTfR), as well as other clinical parameters, were detected and analyzed in all groups. [Results]: The levels of fasting plasma glucose (FPG), oral glucose tolerance test (OGTT) 1-h and 2-h plasma glucose, glycated hemoglobin (HbA1c), SF, Hepc, FPN and sTfR as well as homeostasis model assessment for insulin resistance (HOMA-IR) were significantly higher in the GDM group (P<0.05 for all). In the GDM group, FPN was positively correlated OGTT-1 h and OGTT-2 h In the control group, only sTfR was positively correlated with OGTT-1 h. There was no correlation between the iron metabolism indicators in both GDM and control group.[Conclusion]: Hepc, FPN sRfR and SF levels were higher in the GDM group. Elevated Hepc and FPN are associated with glucose metabolism disorder and may play an important role in GDM.

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miR-22-3p is involved in gluconeogenic pathway modulated by 3,5-diiodo-L-thyronine (T2)

Scientific Reports ◽

10.1038/s41598-019-53019-2 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 3

Author(s):

Rosalba Senese ◽

Federica Cioffi ◽

Giuseppe Petito ◽

Pieter de Lange ◽

Aniello Russo ◽

...

Keyword(s):

Glucose Metabolism ◽

Glucose Homeostasis ◽

High Fat Diet ◽

Molecular Mechanisms ◽

Metabolic Diseases ◽

Tolerance Test ◽

High Fat ◽

Beneficial Effects ◽

Insulin Tolerance

Abstract The 3,5-diiodo-L-thyronine (T2) has emerged as an active iodothyronine and its beneficial effects on glucose metabolism including glucose tolerance and insulin resistance is well established. However, little is known about its molecular mechanisms. Given the emerging importance of microRNAs in various metabolic diseases, in this study a possible link between the effects of T2 on glucose metabolism and miRNA expression was investigated by using an in vivo model in which T2 was administered in rats receiving a high fat diet, a condition known to impair glucose homeostasis. The results showed that T2-treated rats had a better tolerance to glucose load and a better performance at the insulin tolerance test in comparison to high fat diet animals. Interestingly, in the serum of the animals treated with T2 there was a general decrease of miRNAs with miR-22a-3p, miR-34c-5p and miR-33a-3p significantly downregulated. Furthermore, miR-22a-3p had the largest variation pointing toward its preeminent role in T2 metabolic effect. In fact, in liver there was an up-regulation of its target (Transcription Factor 7) Tcf7, which had an important impact on gluconeogenesis. This study provide, for the first time, evidences that miRNAs are involved in the effects exerted by T2 on glucose homeostasis.

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