A 1H-NMR based metabolomics study of the intervention effect of mangiferin on hyperlipidemia hamsters induced by a high-fat diet

2017 ◽  
Vol 8 (7) ◽  
pp. 2455-2464 ◽  
Author(s):  
Fuchuan Guo ◽  
Tianqi Zi ◽  
Liyan Liu ◽  
Rennan Feng ◽  
Changhao Sun

Mangiferin ameliorated hyperlipidemia by intervening in some major metabolic pathways.

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0120950 ◽  
Author(s):  
Ze-Yun Li ◽  
Li-Li Ding ◽  
Jin-Mei Li ◽  
Bao-Li Xu ◽  
Li Yang ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Najla Gooda Sahib Jambocus ◽  
Nazamid Saari ◽  
Amin Ismail ◽  
Alfi Khatib ◽  
Mohamad Fawzi Mahomoodally ◽  
...  

The prevalence of obesity is increasing worldwide, with high fat diet (HFD) as one of the main contributing factors. Obesity increases the predisposition to other diseases such as diabetes through various metabolic pathways. Limited availability of antiobesity drugs and the popularity of complementary medicine have encouraged research in finding phytochemical strategies to this multifaceted disease. HFD induced obese Sprague-Dawley rats were treated with an extract ofMorinda citrifoliaL. leaves (MLE 60). After 9 weeks of treatment, positive effects were observed on adiposity, fecal fat content, plasma lipids, and insulin and leptin levels. The inducement of obesity and treatment with MLE 60 on metabolic alterations were then further elucidated using a1H NMR based metabolomics approach. Discriminating metabolites involved were products of various metabolic pathways, including glucose metabolism and TCA cycle (lactate, 2-oxoglutarate, citrate, succinate, pyruvate, and acetate), amino acid metabolism (alanine, 2-hydroxybutyrate), choline metabolism (betaine), creatinine metabolism (creatinine), and gut microbiome metabolism (hippurate, phenylacetylglycine, dimethylamine, and trigonelline). Treatment with MLE 60 resulted in significant improvement in the metabolic perturbations caused obesity as demonstrated by the proximity of the treated group to the normal group in the OPLS-DA score plot and the change in trajectory movement of the diseased group towards the healthy group upon treatment.


2020 ◽  
Vol 11 ◽  
Author(s):  
Verónica Hurtado-Carneiro ◽  
Ana Pérez-García ◽  
Elvira Alvarez ◽  
Carmen Sanz

The protein kinase with PAS domains (PASK) is a nutrient and energy sensor located in the cells of multiple organs. Many of the recent findings for understanding PASK functions in mammals have been reported in studies involving PASK-deficient mice. This minireview summarizes the PASK role in the control of fasting and feeding responses, focusing especially on the hypothalamus and liver. In 2013, PASK was identified in the hypothalamic areas involved in feeding behavior, and its expression was regulated under fasting/refeeding conditions. Furthermore, it plays a role in coordinating the activation/inactivation of the hypothalamic energy sensors AMPK and mTOR/S6K1 pathways in response to fasting. On the other hand, PASK deficiency prevents the development of obesity and non-alcoholic fatty liver in mice fed with a high-fat diet. This protection is explained by the re-establishment of several high-fat diet metabolic alterations produced in the expression of hepatic transcription factors and key enzymes that control the main metabolic pathways involved in maintaining metabolic homeostasis in fasting/feeding responses. This minireview covers the effects of PASK inactivation in the expression of certain transcription factors and target enzymes in several metabolic pathways under situations such as fasting and feeding with either a standard or a high-fat diet.


Molecules ◽  
2019 ◽  
Vol 24 (24) ◽  
pp. 4524 ◽  
Author(s):  
Runbin Sun ◽  
Jingqiu Huang ◽  
Na Yang ◽  
Jun He ◽  
Xiaoyi Yu ◽  
...  

High-calorie diet, circadian rhythms and metabolic features are intimately linked. However, the mediator(s) between nutritional status, circadian rhythms and metabolism remain largely unknown. This article aims to clarify the key metabolic pathways bridging nutritional status and circadian rhythms based on a combination of metabolomics and molecular biological techniques. A mouse model of high-fat diet-induced obesity was established and serum samples were collected in obese and normal mice at different zeitgeber times. Gas chromatography/mass spectrometry, multivariate/univariate data analyses and metabolic pathway analysis were used to reveal changes in metabolism. Metabolites involved in the metabolism of purines, carbohydrates, fatty acids and amino acids were markedly perturbed in accordance with circadian related variations, among which purine catabolism showed a typical oscillation. What’s more, the rhythmicity of purine catabolism dampened in the high-fat diet group. The expressions of clock genes and metabolic enzymes in the liver were measured. The mRNA expression of Xanthine oxidase (Xor) was highly correlated with the rhythmicity of Clock, Rev-erbα and Bmal1, as well as the metabolites involved in purine catabolism. These data showed that a high-fat diet altered the circadian rhythm of metabolic pathways, especially purine catabolism. It had an obvious circadian oscillation and a high-fat diet dampened its circadian rhythmicity. It was suggested that circadian rhythmicity of purine catabolism is related to circadian oscillations of expression of Xor, Uox and corresponding clock genes.


2020 ◽  
Vol 11 ◽  
Author(s):  
Huantian Cui ◽  
Yuting Li ◽  
Yuming Wang ◽  
Lulu Jin ◽  
Lu Yang ◽  
...  

The dysbiosis in gut microbiota could affect host metabolism and contribute to the development of nonalcoholic fatty liver disease (NAFLD). Da-Chai-Hu decoction (DCH) has demonstrated protective effects on NAFLD, however, the exact mechanisms remain unclear. In this study, we established a NAFLD rat model using a high fat diet (HFD) and provided treatment with DCH. The changes in gut microbiota post DCH treatment were then investigated using 16S rRNA sequencing. Additionally, serum untargeted metabolomics were performed to examine the metabolic regulations of DCH on NAFLD. Our results showed that DCH treatment improved the dyslipidemia, insulin resistance (IR) and ameliorated pathological changes in NAFLD model rats. 16S rRNA sequencing and untargeted metabolomics showed significant dysfunction in gut microbiota community and serum metabolites in NAFLD model rats. DCH treatment restored the dysbiosis of gut microbiota and improved the dysfunction in serum metabolism. Correlation analysis indicated that the modulatory effects of DCH on the arachidonic acid (AA), glycine/serine/threonine, and glycerophospholipid metabolic pathways were related to alterations in the abundance of Romboutsia, Bacteroides, Lactobacillus, Akkermansia, Lachnoclostridium and Enterobacteriaceae in the gut microflora. In conclusion, our study revealed the ameliorative effects of DCH on NAFLD and indicated that DCH’s function on NAFLD may link to the improvement of the dysbiosis of gut microbiota and the modulation of the AA, glycerophospholipid, and glycine/serine/threonine metabolic pathways.


Life Sciences ◽  
2018 ◽  
Vol 215 ◽  
pp. 190-197 ◽  
Author(s):  
Abdelaziz Ghanemi ◽  
Aicha Melouane ◽  
Octave Mucunguzi ◽  
Mayumi Yoshioka ◽  
Jonny St-Amand

Diabetes ◽  
2015 ◽  
Vol 65 (3) ◽  
pp. 574-584 ◽  
Author(s):  
Michael Kruse ◽  
Farnaz Keyhani-Nejad ◽  
Frank Isken ◽  
Barbara Nitz ◽  
Anja Kretschmer ◽  
...  

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S94.3-S94
Author(s):  
I Barba ◽  
E Pladevall ◽  
D Garcia-Dorado

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