scholarly journals Emodin Attenuated the Kidney Damage of High-Fat-Diet Mice via the Upregulation of Glucagon-Like Peptide-1 Receptor

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jinlei Liu ◽  
Yao Sun ◽  
Hongwei Zheng ◽  
Jing Wang ◽  
Lili Liu ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
High Fat Diet ◽  
Cell Damage ◽  
Kidney Tissue ◽  
Kidney Damage ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Ppar Γ ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Objective. Secretion of glucagon-like peptide 1 (GLP-1) and its effect on target organs were impaired in individuals with obesity. However, its mechanism needs to be further studied. We aim to explore the roles of the receptor of GLP-1 (GLP-1R) involved in high-fat-diet- (HFD-) induced kidney damage improved by emodin. Methods. Male C57bl/6 mice were fed with HFD diet and therapied by emodin. NRK-52E cells were cultured and treated with palmitic acid or low-density lipoprotein cholesterol (LDL-C). Emodin was used to remedy the NRK-52E cell damage. GW9662 was administrated to block the function of peroxisome proliferator-activated receptor γ (PPAR-γ). GLP-1 in the plasma was measured by ELISA. PPAR-γ and GLP-1R in the kidney and NRK-52E cells were detected by western blotting. The interaction between PPAR-γ protein and GLP-1R promoter regions was observed by chromatin immunoprecipitation (ChIP). Results. Postprandial GLP-1 levels in plasma, as well as PPAR-γ and GLP-1R, decreased in kidney tissue of HFD mice, while they were reserved by emodin treatment. Although PPAR-γ and GLP-1R were not downregulated by LDL-C, they were suppressed by palmitic acid. Interestingly, GLP-1R mRNA was detected by PCR in the mixture pulled down with PPAR-γ antibody. Additionally, downregulation of PPAR-γ and GLP-1R by palmitic acid was remanded by emodin. Moreover, GW9662, an inhibitor of PPAR-γ, abolished the protective effect of emodin. Conclusion. The kidney damage of HFD mice seems to be alleviated by emodin via the upregulation of GLP-1R in kidney tissue.

Effects of glucagon-like peptide-1 analog liraglutide on the systemic inflammation in high-fat-diet-induced mice

Endocrine ◽  
2019 ◽  
Vol 66 (3) ◽  
pp. 494-502 ◽  
Author(s):  
Sha Sha ◽  
Xiaoming Liu ◽  
Ruxing Zhao ◽  
Li Qing ◽  
Qin He ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
High Fat Diet ◽  
High Fat ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

MiR-425-5p Regulates Glucagon-like Peptide-1 Production and Affects Blood Glucose Levels in High-fat Diet-fed Mice

2021 ◽  
Author(s):  
Lirui Wei ◽  
Xuenan Zhao ◽  
Feng Guo ◽  
Fengjiao Huang ◽  
Yanyan Zhao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Protein Level ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Tolerance Test ◽  
Control Group ◽  
High Fat ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract BackgroundIn modern society, obesity has become a global problem with resulting in metabolic disorders and poses high risk for type 2 diabetes mellitus (T2DM). The glucagon-like peptide-1 (GLP-1) has been taken as an effective drug for the therapy of T2DM and obesity. In the present study, the regulatory roles and molecular mechanisms of miR-425-5p in GLP-1 secretion in high-fat diet (HFD)-induced diabetic mice were explored. MethodsOral glucose tolerance test and insulin tolerance test were performed to assess glucose metabolism and GLP-1 and LPS levels. Quantitative real time polymerase chain reaction (qRT-PCR) was employed to detect the expression of LPS, GLP-1, GLP-1 receptors, miR-425-5p, phosphatase and tensin homology (PTEN), proglucagon, p65 and β-catenin. Western blot was performed to determine the expression of proglucagon, p65, β-catenin and PTEN. ResultsThe results showed that plasma GLP-1 level was negatively correlated with plasma LPS level in HFD-fed mice, and miR-425-5p expression and LPS level were up-regulated in the ileal fluid compared with control groups. LPS injection boosted miR-425-5p expression in ileum. MiR-425-5p ameliorated glucose intolerance and insulin resistance in HFD-fed mice by increasing GLP-1 secretion. Furthermore, p65 protein level in the cytoplasmic and nuclear in the ileum of HFD-fed mice was increased compared with the control group. MiR-425-5p agomir elevated nuclear β-catenin protein level, but reduced PTEN protein level in HFD-fed mice compared with HFD-fed mice treated with the miR-425-5p antagomir. ConclusionsOur results suggest that miR-425-5p promotes GLP-1 secretion and improves glucose tolerance and insulin resistance in high-fat diet-fed mice.

scholarly journals Oligofructose Promotes Satiety in Rats Fed a High-Fat Diet: Involvement of Glucagon-Like Peptide-1

2005 ◽  
Vol 13 (6) ◽  
pp. 1000-1007 ◽  
Author(s):  
Patrice D. Cani ◽  
Audrey M. Neyrinck ◽  
Nicole Maton ◽  
Nathalie M. Delzenne
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Time-dependent therapeutic roles of nitazoxanide on high-fat diet/streptozotocin-induced diabetes in rats: effects on hepatic peroxisome proliferator-activated receptor-gamma receptors

2018 ◽  
Vol 96 (5) ◽  
pp. 485-497 ◽  
Author(s):  
Samah M. Elaidy ◽  
Mona A. Hussain ◽  
Mohamed K. El-Kherbetawy
Keyword(s):  
High Fat Diet ◽  
Time Dependent ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Liver And Kidney ◽  
Kidney Functions ◽  
Dm Type 2

Targeting peroxisome proliferator-activated receptor-gamma (PPAR-γ) is an approved strategy in facing insulin resistance (IR) for diabetes mellitus (DM) type 2. The PPAR-γ modulators display improvements in the insulin-sensitizing and adverse effects of the traditional thiazolidinediones. Nitazoxanide (NTZ) is proposed as a PPAR-γ receptor ligand with agonistic post-transcriptional effects. Currently, NTZ antidiabetic activities versus pioglitazone (PIO) in a high-fat diet/streptozotocin rat model of type 2 diabetes was explored. Diabetic adult male Wistar rats were treated orally with either PIO (2.7 mg·kg−1·day−1) or NTZ (200 mg·kg−1·day−1) for 14, 21, and 28 days. Body masses, fasting blood glucose, IR, lipid profiles, and liver and kidney functions of rats were assayed. Hepatic glucose metabolism and PPAR-γ protein expression levels as well as hepatic, pancreatic, muscular, and renal histopathology were evaluated. Significant time-dependent euglycemic and insulin-sensitizing effects with preservation of liver and kidney functions were offered by NTZ. Higher hepatic levels of glucose-6-phosphatase and glucose-6-phosphate dehydrogenase enzymes and PPAR-γ protein expressions were acquired by NTZ and PIO, respectively. NTZ could be considered an oral therapeutic strategy for DM type 2. Further systematic NTZ/PPAR-γ receptor subtype molecular activations are recommended. Simultaneous use of NTZ with other approved antidiabetics should be explored.

scholarly journals Brain Glucagon-Like Peptide 1 Signaling Controls the Onset of High-Fat Diet-Induced Insulin Resistance and Reduces Energy Expenditure

Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 4768-4777 ◽  
Author(s):  
Claude Knauf ◽  
Patrice D. Cani ◽  
Afifa Ait-Belgnaoui ◽  
Alexandre Benani ◽  
Cédric Dray ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Carbon Dioxide Production ◽  
High Fat ◽  
Ambulatory Activity ◽  
Ucp2 Expression ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 (GLP-1) is a peptide released by the intestine and the brain. We previously demonstrated that brain GLP-1 increases glucose-dependent hyperinsulinemia and insulin resistance. These two features are major characteristics of the onset of type 2 diabetes. Therefore, we investigated whether blocking brain GLP-1 signaling would prevent high-fat diet (HFD)-induced diabetes in the mouse. Our data show that a 1-month chronic blockage of brain GLP-1 signaling by exendin-9 (Ex9), totally prevented hyperinsulinemia and insulin resistance in HFD mice. Furthermore, food intake was dramatically increased, but body weight gain was unchanged, showing that brain GLP-1 controlled energy expenditure. Thermogenesis, glucose utilization, oxygen consumption, carbon dioxide production, muscle glycolytic respiratory index, UCP2 expression in muscle, and basal ambulatory activity were all increased by the exendin-9 treatment. Thus, we have demonstrated that in response to a HFD, brain GLP-1 signaling induces hyperinsulinemia and insulin resistance and decreases energy expenditure by reducing metabolic thermogenesis and ambulatory activity.

scholarly journals A High-Fat Diet Increases Activation of the Glucagon-Like Peptide-1-Producing Neurons in the Nucleus Tractus Solitarii: an Effect that is Partially Reversed by Drugs Normalizing Glycemia

2021 ◽  
Author(s):  
Grazyna Lietzau ◽  
Stelia Ntika ◽  
Hiranya Pintana ◽  
Linda Tracy ◽  
Thomas Klein ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Nucleus Tractus Solitarii ◽  
Metabolic Demand ◽  
High Fat ◽  
Quantitative Microscopy ◽  
Dipeptidyl Peptidase 4 ◽  
Dipeptidyl Peptidase 4 Inhibitor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

AbstractGlucagon-like peptide-1 (GLP-1) is a peripheral incretin and centrally active peptide produced in the intestine and nucleus tractus solitarii (NTS), respectively. GLP-1 not only regulates metabolism but also improves cognition and is neuroprotective. While intestinal GLP-1-producing cells have been well characterized, less is known about GLP-1-producing neurons in NTS. We hypothesized that obesity-induced type 2 diabetes (T2D) impairs the function of NTS GLP-1-producing neurons and glycemia normalization counteracts this effect. We used immunohistochemistry/quantitative microscopy to investigate the number, potential atrophy, and activation (cFos-expression based) of NTS GLP-1-producing neurons, in non-diabetic versus obese/T2D mice (after 12 months of high-fat diet). NTS neuroinflammation was also assessed. The same parameters were quantified in obese/T2D mice treated from month 9 to 12 with two unrelated anti-hyperglycemic drugs: the dipeptidyl peptidase-4 inhibitor linagliptin and the sulfonylurea glimepiride. We show no effect of T2D on the number and volume but increased activation of NTS GLP-1-producing neurons. This effect was partially normalized by both anti-diabetic treatments, concurrent with decreased neuroinflammation. Increased activation of NTS GLP-1-producing neurons could represent an aberrant metabolic demand in T2D/obesity, attenuated by glycemia normalization. Whether this effect represents a pathophysiological process preceding GLP-1 signaling impairment in the CNS, remains to be investigated.

scholarly journals A High-Fat Diet Increases Activation of The Glucagon-Like Peptide-1-Producing Neurons in The Nucleus Tractus Solitarii; An Effect That is Partially Reversed By Drugs Normalizing Glycaemia

2021 ◽  
Author(s):  
Grazyna Lietzau ◽  
Stelia Ntika ◽  
Hiranya Pintana ◽  
Linda Tracy ◽  
Thomas Klein ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Nucleus Tractus Solitarii ◽  
Metabolic Demand ◽  
High Fat ◽  
Quantitative Microscopy ◽  
Dipeptidyl Peptidase 4 ◽  
Dipeptidyl Peptidase 4 Inhibitor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract Glucagon-like peptide-1 (GLP-1) is a peripheral incretin and centrally active peptide produced in the intestine and nucleus tractus solitarii (NTS), respectively. GLP-1 not only regulates metabolism but also improves cognition and is neuroprotective. While intestinal GLP-1-producing cells have been well characterized, less is known about GLP-1-producing neurons in NTS. We hypothesized that obesity-induced type 2 diabetes (T2D) impairs the function of NTS GLP-1-producing neurons and glycaemia normalization counteracts this effect. We used immunohistochemistry/quantitative microscopy to investigate the number, potential atrophy, and activation (c-Fos-expression based) of NTS GLP-1-producing neurons, in non-diabetic versus obese/T2D mice (after 12 months of high-fat diet). NTS neuroinflammation was also assessed. The same parameters were quantified in obese/T2D mice treated from month 9 to 12 with two unrelated anti-hyperglycemic drugs: the dipeptidyl peptidase-4 inhibitor linagliptin and the sulfonylurea glimepiride. We show no effect of T2D on the number and volume but increased activation of NTS GLP-1-producing neurons. This effect was partially normalized by both anti-diabetic treatments, concurrent with decreased neuroinflammation. Increased activation of NTS GLP-1-producing neurons could represent an aberrant metabolic demand in T2D/obesity, attenuated by glycaemia normalization. Whether this effect represents a pathophysiological process preceding GLP-1 signaling impairment in the CNS, remains to be investigated.

scholarly journals MagnoliaExtract (BL153) Ameliorates Kidney Damage in a High Fat Diet-Induced Obesity Mouse Model

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Wenpeng Cui ◽  
Yangwei Wang ◽  
Qiang Chen ◽  
Weixia Sun ◽  
Lu Cai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
High Fat Diet ◽  
Therapeutic Potential ◽  
Kidney Damage ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Plasminogen Activator Inhibitor 1 ◽  
Hexokinase Ii ◽  
Functional Changes

Accumulating evidence demonstrated that obesity is a risk factor for renal structural and functional changes, leading to the end-stage renal disease which imposes a heavy economic burden on the community. However, no effective therapeutic method for obesity-associated kidney disease is available. In the present study, we explored the therapeutic potential of amagnoliaextract (BL153) for treating obesity-associated kidney damage in a high fat diet- (HFD-) induced mouse model. The results showed that inflammation markers (tumor necrosis factor-αand plasminogen activator inhibitor-1) and oxidative stress markers (3-nitrotyrosine and 4-hydroxy-2-nonenal) were all significantly increased in the kidney of HFD-fed mice compared to mice fed with a low fat diet (LFD). Additionally, proteinuria and renal structure changes in HFD-fed mice were much more severe than that in LFD-fed mice. However, all these alterations were attenuated by BL153 treatment, accompanied by upregulation of peroxisome proliferator-activated receptor-γcoactivator-1α(PGC-1α) and hexokinase II (HK II) expression in the kidney. The present study indicates that BL153 administration may be a novel approach for renoprotection in obese individuals by antiinflammation and anti-oxidative stress most likely via upregulation of PGC-1αand HK II signal in the kidney.

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