scholarly journals A Mouse Model of Gestational Diabetes Mellitus Using the Combination of High Fat Diet and Low‐Moderate Dose of Streptozocin

2008 ◽  
Vol 22 (S1) ◽  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Mouse Model ◽  
Gestational Diabetes Mellitus ◽  
High Fat Diet ◽  
High Fat ◽  
Moderate Dose

scholarly journals Berberine elevates cardiolipin in heart of offspring from mouse dams with high fat diet-induced gestational diabetes mellitus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura K. Cole ◽  
Genevieve C. Sparagna ◽  
Marilyne Vandel ◽  
Bo Xiang ◽  
Vernon W. Dolinsky ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Mitochondrial Function ◽  
High Fat Diet ◽  
Fatty Acid Uptake ◽  
Isoquinoline Alkaloid ◽  
Acid Uptake ◽  
High Fat ◽  
Low Fat

AbstractBerberine (BBR) is an isoquinoline alkaloid from plants known to improve cardiac mitochondrial function in gestational diabetes mellitus (GDM) offspring but the mechanism is poorly understood. We examined the role of the mitochondrial phospholipid cardiolipin (CL) in mediating this cardiac improvement. C57BL/6 female mice were fed either a Lean-inducing low-fat diet or a GDM-inducing high-fat diet for 6 weeks prior to breeding. Lean and GDM-exposed male offspring were randomly assigned a low-fat, high-fat, or high-fat diet containing BBR at weaning for 12 weeks. The content of CL was elevated in the heart of GDM offspring fed a high fat diet containing BBR. The increase in total cardiac CL was due to significant increases in the most abundant and functionally important CL species, tetralinoleoyl-CL and this correlated with an increase in the expression of the CL remodeling enzyme tafazzin. Additionally, BBR treatment increased expression of cardiac enzymes involved in fatty acid uptake and oxidation and electron transport chain subunits in high fat diet fed GDM offspring. Thus, dietary BBR protection from cardiac dysfunction in GDM exposed offspring involves improvement in mitochondrial function mediated through increased synthesis of CL.

scholarly journals Global mRNA and Long Non-Coding RNA Expression in the Placenta and White Adipose Tissue of Mice Fed a High-Fat Diet During Pregnancy

2018 ◽  
Vol 50 (6) ◽  
pp. 2260-2271 ◽  
Author(s):  
Chen Huang ◽  
Bin-bin Huang ◽  
Jian-min Niu ◽  
Yan Yu ◽  
Xiao-yun Qin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Fat Diet ◽  
Differentially Expressed ◽  
High Fat ◽  
The Core ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Background/Aims: Gestational diabetes mellitus (GDM) is a common complication of pregnancy, but the mechanisms underlying the disorders remain unclear. The study aimed to identify mRNA and long non-coding RNA (lncRNA) profiles in placenta and gonadal fat of pregnant mice fed a high-fat diet and to investigate the transcripts and pathways involved in the development of gestational diabetes mellitus. Methods: Deep and broad transcriptome profiling was performed to assess the expression of mRNAs and lncRNAs in placenta and gonadal fat from 3 mice fed an HFD and chow during pregnancy. Then, differentially expressed mRNAs and lncRNAs were validated by quantitative real-time PCR. The function of the differentially expressed mRNAs was determined by pathway and Gene Ontology (GO) analyses, and the physical or functional relationships between the lncRNAs and the corresponding mRNAs were determined. Results: Our study revealed that 82 mRNAs and 52 lncRNAs were differentially expressed in the placenta of mice fed an HFD during pregnancy, and 202 mRNAs and 120 lncRNAs were differentially expressed in gonadal fat. GO and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed differentially expressed mRNAs of placenta were closely related to extracellular matrix interactions, digestion, adhesion, and metabolism, whereas the differentially expressed mRNAs in adipose tissue were related to metabolic and insulin signalling pathways. The gene network demonstrated that Actg2, Cnfn, Muc16, Serpina3k, NONMMUT068202, and NONMMUT068203, were the core of the network in placental tissue, and the genes Tkt, Acss2, and Elovl6 served as the core of the network in gonadal fat tissue. Conclusion: These newly identified key genes and pathways in mice might provide valuable information regarding the pathogenesis of GDM and might be used to improve early diagnosis, prevention, drug design, and clinical treatment.

scholarly journals Gestational Diabetes Mellitus-Associated Hyperglycemia Impairs Glucose Transporter 3 Trafficking in Trophoblasts Through the Downregulation of AMP-Activated Protein Kinase

2021 ◽  
Vol 9 ◽  
Author(s):  
Li Zhang ◽  
Xinyang Yu ◽  
Yue Wu ◽  
Huijia Fu ◽  
Ping Xu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Protein Kinase ◽  
Glucose Metabolism ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Fat Diet ◽  
Glucose Transporter ◽  
Ampk Activation ◽  
High Fat ◽  
Amp Activated Protein Kinase

AMP-activated protein kinase (AMPK) is an important regulator of glucose metabolism, and glucose transporter 3 (GLUT3) is an efficient glucose transporter in trophoblasts. Whether placental AMPK and GLUT3 respond accordingly to gestational diabetes mellitus (GDM) remains uncertain. Here, we explored the regulatory role of AMPK in the GLUT3-dependent uptake of glucose by placental trophoblasts and the viability of the cells. In this study, the level of glycolysis in normal and GDM-complicated placentas was assessed by LC-MS/MS. The trophoblast hyperglycemia model was induced by the incubation of HTR8/SVneo cells with a high glucose concentration. GDM animal models were generated with db/ + mice and C57BL/6J mice fed a high-fat diet, and AMPK was manipulated by the oral administration of metformin. The uptake of glucose by trophoblasts was assessed using 2-NBDG or 2-deoxy-D-[3H] glucose. The results showed that GDM is associated with impaired glycolysis, AMPK activity, GLUT3 expression in the plasma membrane (PM) and cell survival in the placenta. Hyperglycemia induced similar changes in trophoblasts, and these changes were rescued by AMPK activation. Both hyperglycemic db/ + and high-fat diet-induced GDM mice exhibited a compromised AMPK–GLUT3 axis and suppressed cell viability in the placenta as well as excessive fetal growth, and all of these effects were partially alleviated by metformin. Taken together, our findings support the notion that AMPK activation upregulates trophoblast glucose uptake by stimulating GLUT3 translocation, which is beneficial for viability. Thus, the modulation of glucose metabolism in trophoblasts by targeting AMPK might ameliorate the adverse intrauterine environment caused by GDM.

Nuciferine administration in C57BL/6J mice with gestational diabetes mellitus induced by a high-fat diet: the improvement of glycolipid disorders and intestinal dysbacteriosis

2021 ◽  
Author(s):  
Zhuohong Tang ◽  
Ting Luo ◽  
Peng Huang ◽  
Mi Luo ◽  
Jianghua Zhu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Fat Diet ◽  
High Fat ◽  
Intestinal Dysbacteriosis

Improvement of glycolipid disorders and gut dysbacteriosis by nuciferine in high-fat diet-induced gestational diabetes mellitus mice.

scholarly journals Anti-inflammatory activities of puerarin in high-fat diet-fed rats with streptozotocin-induced gestational diabetes mellitus

2020 ◽  
Vol 47 (10) ◽  
pp. 7537-7546 ◽  
Author(s):  
Wenting Xu ◽  
Mengyu Tang ◽  
Jiahui Wang ◽  
Lihong Wang
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Density Lipoprotein ◽  
Reproductive Organs ◽  
Control Group ◽  
High Fat ◽  
Adipose Tissues ◽  
Tnf Α

Abstract To investigate the effect of puerarin on insulin resistance and inflammation in rats with gestational diabetes mellitus (GDM). Gestational diabetic model rats were established by intraperitoneal injection of streptozotocin (25 mg/kg) combined with high-fat feeding and were randomly assigned to three groups: the control group, the GDM group, and the puerarin-treated group. Puerarin was intragastrically administered to rats daily until the offspring were born. The rats in both the GDM group and control group were administered the same volume of normal saline. Serum total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol in all groups of rats were measured. Haematoxylin and eosin staining was used to evaluate morphological changes in the liver, pancreas, and adipose tissues around the reproductive organs. Western blotting was carried out to measure the protein expression of IRS-1 and inflammatory factors, including TNF-α, TLR4, MyD88 and phosphorylated NF-κB, in the adipose tissues around the reproductive organs. Puerarin had preventive effects on GDM-induced pathological changes and ameliorated glucose and lipid metabolism disorders in GDM rats. Puerarin upregulated IRS-1 expression and decreased the protein expression of TNF-α, TLR4, and MyD88 as well as the levels of phosphorylated NF-κB in adipose tissues around the reproductive organs in GDM rats. This study indicated that puerarin exerts anti-inflammatory effects by downregulating the important TLR4/MyD88/NF-κB inflammatory signalling pathway. Therefore, puerarin can decrease the expression of TNF-α and ameliorate insulin resistance in GDM rats, suggesting the potential efficacy of puerarin in GDM treatment.

scholarly journals Renal microvascular damaged in diabetes mellitus with hyperlipidemia through the regulation of MAMs by PACS2 in endothelial cell

2021 ◽  
Author(s):  
Zhihao Shu ◽  
Shuhua Chen ◽  
Hong Xiang ◽  
Ruoru Wu ◽  
Shaoli Zhao ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Endothelial Cells ◽  
Fatty Acid ◽  
Endothelial Cell ◽  
Mouse Model ◽  
Vascular Permeability ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Kidney Tissue ◽  
High Fat

Abstract Background: The prevalence of diabetic vascular complications is rapidly increasing, especially in the diabetes mellitus with hyperlipidemia. Consistent hyperglycemia and hyperlipidemia impairs microvascular, but lack of effective intervention target to prevention or reduced the risk of serious bad ending. Methods: A mouse model of diabetes combined with hyperlipidemia were established by STZ injection and high fat diet to observe the possible damage of HGHF to renal blood vessels include vascular permeability, fibrosis and subcellular structure. Then, we replicated an in vitro endothelial cell injury model treated by 30mm Glucose and 0.1mm palmitic acid to verify its main functional changes. Proteomics and metabolomics were used to explore the molecular mechanisms behind diabetic microvascular damage. The mechanisms were further verified at siRNA interference and transgenic knockout mice. Results: We found that renal vascular permeability impaired and fibrosis increased significantly in the stz+HFD mice. In human umbilical vein endothelial cells (HUVECs) treated with high glucose/high fat (HGHF), the number of mitochondrial-associated membranes (MAMs) and the expression of phosphofurin acidic cluster sorting protein 2 (PACS2) increased. In particular, gene manipulation of PACS2 altered endothelial cell MAMs. Knocking down PACS2 restored the barrier function of HUVECs. In vivo, knocking out PACS2 ameliorated the kidney injury in diabetic mice induced by streptozotocin and fed with high-fat diet for up to 20 weeks. PACS2-/- mice leaked less vascular Evan’s blue and improved glomerular fibrosis in the kidney tissue of hyperglycemia and hyperlipidemia mouse model. We further observed the reduction of fatty acid β-oxidation (FAO), CPT1α expression, and NADPH production in endothelial cells induced by HGHF. These changes in fatty acid metabolism were rescued by silencing PACS2, but were blocked by the FAO inhibitor, etomoxir. Conclusion: PACS2 impacts the metabolic response of endothelial cells to HGHF through MAMs. Loss of PACS2 expression reduces glomerular endothelial cells barrier injury, induced by VE-Cadherin internalized under HGHF. PACS2 play a metabolism and MAMs regulators in the vascular endothelial cells of diabetes with hyperlipidemia.

scholarly journals Gestational diabetes mellitus: a (nearly) perfect mouse model

2019 ◽  
Vol 597 (18) ◽  
pp. 4689-4690
Author(s):  
N. Blysniuk ◽  
A. Visram ◽  
K. T. Lam
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Mouse Model ◽  
Gestational Diabetes Mellitus

scholarly journals Effects of Astaxanthin on Inflammation and Insulin Resistance in a Mouse Model of Gestational Diabetes Mellitus

Dose-Response ◽  
2020 ◽  
Vol 18 (2) ◽  
pp. 155932582092676
Author(s):  
Weihong Feng ◽  
Yanxia Wang ◽  
Na Guo ◽  
Pu Huang ◽  
Yang Mi
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Gestational Diabetes ◽  
Glucose Tolerance ◽  
Mouse Model ◽  
Gestational Diabetes Mellitus ◽  
The Body ◽  
Ros Generation

Gestational diabetes mellitus (GDM) is a condition in which a hormone made by the placenta prevents the body from using insulin effectively. It is important to find an effective treatment. A mouse model of GDM was used to testify the effects of astaxanthin on glucose tolerance and insulin sensitivity. Production of inflammatory cytokines, reactive oxygen species (ROS), and glucose transporter type 4 (GLUT4) translocation and insulin-related signaling were measured in the presence of astaxanthin both in vivo and in vitro. It was found that astaxanthin improved insulin sensitivity, glucose tolerance, and litter size of offspring and reduced birth weight of offspring and inflammation in GDM mouse. Moreover, astaxanthin increased GLUT4 translocating to membrane without altering its secretion/expression and glucose uptake and consumption in C2C12 skeletal muscle cells. Furthermore, ROS generation and insulin-related signaling inhibited by tumor necrosis factor α was restored by astaxanthin. It is concluded that astaxanthin has the potential to attenuate GDM symptoms by regulating inflammation and insulin resistance in skeletal muscle of pregnant mice. Our findings suggest that astaxanthin could be a promising and effective molecule to treat GDM.

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