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

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

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

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Shuzhen Guo ◽  
Hongjian Lian ◽  
Wenjing Chuo ◽  
Xuanchao Feng
Keyword(s):  
Endothelial Cells ◽  
Glucose Metabolism ◽  
High Glucose ◽  
High Fat Diet ◽  
Area Under The Curve ◽  
Tolerance Test ◽  
High Fat ◽  
Response Gene ◽  
Metabolism Disorder ◽  
Glucose Metabolism Disorder

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.

scholarly journals Effects of the electric stress on insulin secretion and glucose metabolism in rats fed with a high fat diet.

1978 ◽  
Vol 25 (5) ◽  
pp. 415-422 ◽  
Author(s):  
KEIKO YAMAGUCHI ◽  
SHUNJI TAKASHIMA ◽  
TAKAKO MASUYAMA ◽  
AKIRA MATSUOKA
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
Electric Stress

scholarly journals The prolyl hydroxylase PHD3 maintains β-cell glucose metabolism during fatty acid excess

2020 ◽  
Author(s):  
Daniela Nasteska ◽  
Federica Cuozzo ◽  
Alpesh Thakker ◽  
Rula Bany Bakar ◽  
Rebecca Westbrook ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
Β Cells ◽  
Β Cell ◽  
Cell Glucose ◽  
Fuel Source

ABSTRACTThe alpha ketoglutarate-dependent dioxygenase, prolyl-4-hydroxylase 3 (PHD3), is a hypoxia-inducible factor target that uses molecular oxygen to hydroxylate proline. While PHD3 has been reported to influence cancer cell metabolism and liver insulin sensitivity, relatively little is known about effects of this highly conserved enzyme in insulin-secreting β-cells. Here, we show that deletion of PHD3 specifically in β-cells (βPHD3KO) is associated with impaired glucose homeostasis in mice fed high fat diet. In the early stages of dietary fat excess, βPHD3KO islets energetically rewire, leading to defects in the management of pyruvate fate and a shift away from glycolysis. However, βPHD3KO islets are able to maintain oxidative phosphorylation and insulin secretion by increasing utilization of fatty acids to supply the tricarboxylic acid cycle. This nutrient-sensing switch cannot be sustained and βPHD3KO islets begin to show signs of failure in response to prolonged metabolic stress, including impaired glucose-stimulated ATP/ADP rises, Ca2+ fluxes and insulin secretion. Thus, PHD3 might be a pivotal component of the β-cell glucose metabolism machinery by suppressing the use of fatty acids as a primary fuel source, under obesogenic and insulin resistant states.SIGNIFICANCE STATEMENTProlyl-4-hydroxylase 3 (PHD3) is involved in the oxygen-dependent regulation of cell phenotype. A number of recent studies have shown that PHD3 might operate at the interface between oxygen availability and metabolism. To understand how PHD3 influences insulin secretion, which depends on intact glucose metabolism, we generated mice lacking PHD3 specifically in pancreatic β-cells. These mice, termed βPHD3KO, are apparently normal until fed high fat diet at which point their β-cells switch to fatty acids as a fuel source. This switch cannot be tolerated and β-cells in βPHD3KO mice eventually fail. Thus, PHD3 maintains glucose-stimulated insulin secretion in β-cells during states of fatty acid excess, such as diabetes and obesity.

scholarly journals Effects of Antarctic krill oil on lipid and glucose metabolism in C57BL/6J mice fed with high fat diet

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Dewei Sun ◽  
Liang Zhang ◽  
Hongjian Chen ◽  
Rong Feng ◽  
Peirang Cao ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
High Fat Diet ◽  
Antarctic Krill ◽  
Krill Oil ◽  
High Fat ◽  
Antarctic Krill Oil

scholarly journals Vagotomy Reduces Insulin Clearance in Obese Mice Programmed by Low-Protein Diet in the Adolescence

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Camila Lubaczeuski ◽  
Luciana Mateus Gonçalves ◽  
Jean Franciesco Vettorazzi ◽  
Mirian Ayumi Kurauti ◽  
Junia Carolina Santos-Silva ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Insulin Clearance ◽  
Protein Diet ◽  
Low Protein Diet ◽  
High Fat ◽  
Insulin Degrading Enzyme ◽  
Low Protein

The aim of this study was to investigate the effect of subdiaphragmatic vagotomy on insulin sensitivity, secretion, and degradation in metabolic programmed mice, induced by a low-protein diet early in life, followed by exposure to a high-fat diet in adulthood. Weaned 30-day-old C57Bl/6 mice were submitted to a low-protein diet (6% protein). After 4 weeks, the mice were distributed into three groups: LP group, which continued receiving a low-protein diet; LP + HF group, which started to receive a high-fat diet; and LP + HFvag group, which underwent vagotomy and also was kept at a high-fat diet. Glucose-stimulated insulin secretion (GSIS) in isolated islets, ipGTT, ipITT, in vivo insulin clearance, and liver expression of the insulin-degrading enzyme (IDE) was accessed. Vagotomy improved glucose tolerance and reduced insulin secretion but did not alter adiposity and insulin sensitivity in the LP + HFvag, compared with the LP + HF group. Improvement in glucose tolerance was accompanied by increased insulinemia, probably due to a diminished insulin clearance, as judged by the lower C-peptide : insulin ratio, during the ipGTT. Finally, vagotomy also reduced liver IDE expression in this group. In conclusion, when submitted to vagotomy, the metabolic programmed mice showed improved glucose tolerance, associated with an increase of plasma insulin concentration as a result of insulin clearance reduction, a phenomenon probably due to diminished liver IDE expression.

scholarly journals IP6-assisted CSN-COP1 competition regulates a CRL4-ETV5 proteolytic checkpoint to safeguard glucose-induced insulin secretion

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hong Lin ◽  
Yuan Yan ◽  
Yifan Luo ◽  
Wing Yan So ◽  
Xiayun Wei ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
High Fat Diet ◽  
E3 Ligase ◽  
Human Islets ◽  
Cop9 Signalosome ◽  
Congenital Hyperinsulinism ◽  
High Fat ◽  
Transcriptional Suppressor

AbstractCOP1 and COP9 signalosome (CSN) are the substrate receptor and deneddylase of CRL4 E3 ligase, respectively. How they functionally interact remains unclear. Here, we uncover COP1–CSN antagonism during glucose-induced insulin secretion. Heterozygous Csn2WT/K70E mice with partially disrupted binding of IP6, a CSN cofactor, display congenital hyperinsulinism and insulin resistance. This is due to increased Cul4 neddylation, CRL4COP1 E3 assembly, and ubiquitylation of ETV5, an obesity-associated transcriptional suppressor of insulin secretion. Hyperglycemia reciprocally regulates CRL4-CSN versus CRL4COP1 assembly to promote ETV5 degradation. Excessive ETV5 degradation is a hallmark of Csn2WT/K70E, high-fat diet-treated, and ob/ob mice. The CRL neddylation inhibitor Pevonedistat/MLN4924 stabilizes ETV5 and remediates the hyperinsulinemia and obesity/diabetes phenotypes of these mice. These observations were extended to human islets and EndoC-βH1 cells. Thus, a CRL4COP1-ETV5 proteolytic checkpoint licensing GSIS is safeguarded by IP6-assisted CSN-COP1 competition. Deregulation of the IP6-CSN-CRL4COP1-ETV5 axis underlies hyperinsulinemia and can be intervened to reduce obesity and diabetic risk.

Micro-RNA 206 affects glucose induced insulin secretion under high-fat diet

2015 ◽  
Vol 241 (1) ◽  
pp. e83
Author(s):  
M. Vinod ◽  
J.V. Patankar ◽  
V. Sachdev ◽  
W.A.E.L. Al-Zoughbi ◽  
G. Höfler ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
High Fat Diet ◽  
Micro Rna ◽  
High Fat
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