scholarly journals Quercetin Ameliorates Insulin Resistance and Restores Gut Microbiome in Mice on High-Fat Diets

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1251
Author(s):  
Yuqing Tan ◽  
Christina C. Tam ◽  
Matt Rolston ◽  
Priscila Alves ◽  
Ling Chen ◽  
...  

Quercetin is a flavonoid that has been shown to have health-promoting capacities due to its potent antioxidant activity. However, the effect of chronic intake of quercetin on the gut microbiome and diabetes-related biomarkers remains unclear. Male C57BL/6J mice were fed HF or HF supplemented with 0.05% quercetin (HFQ) for 6 weeks. Diabetes-related biomarkers in blood were determined in mice fed high-fat (HF) diets supplemented with quercetin. Mice fed the HFQ diet gained less body, liver, and adipose weight, while liver lipid and blood glucose levels were also lowered. Diabetes-related plasma biomarkers insulin, leptin, resistin, and glucagon were significantly reduced by quercetin supplementation. In feces, quercetin supplementation significantly increased the relative abundance of Akkermansia and decreased the Firmicutes/Bacteroidetes ratio. The expression of genes Srebf1, Ppara, Cyp51, Scd1, and Fasn was downregulated by quercetin supplementation. These results indicated that diabetes biomarkers are associated with early metabolic changes accompanying obesity, and quercetin may ameliorate insulin resistance.

1958 ◽  
Vol 193 (3) ◽  
pp. 499-504 ◽  
Author(s):  
K. J. Carpenter ◽  
Jean Mayer

In our colony, yellow obese mice were longer than nonobese littermates and yellow males were heavier than yellow females. Weight gain was greatest on high fat diets. If the yellow mice were given a possibility to exercise (activity cages), they lost weight. Resistance to cold was good. Fasted blood glucose levels were normal, fed levels frequently elevated in males. Yellow male and female mice showed a degree of insulin resistance; yellow males showed a marked hyperglycemic response to growth hormone, ACTH, cortisone, and glucagon. Blood total lipids were elevated in yellow mice, with the females exhibiting hypercholesterolemia. As in other forms of ‘metabolic’ obesity, blood ketones were decreased by an 18 hours fast.


Appetite ◽  
2008 ◽  
Vol 51 (2) ◽  
pp. 389
Author(s):  
P.K. Olszewski ◽  
R. Fredriksson ◽  
O. Stephansson ◽  
H.B. Schioth ◽  
A.S. Levine

2008 ◽  
Vol 19 (8) ◽  
pp. 505-513 ◽  
Author(s):  
Anne M. Flanagan ◽  
Jackie L. Brown ◽  
Consuelo A. Santiago ◽  
Pauline Y. Aad ◽  
Leon J. Spicer ◽  
...  

2020 ◽  
pp. 1-29 ◽  
Author(s):  
Siofra E. Maher ◽  
Eileen C. O’Brien ◽  
Rebecca L. Moore ◽  
David F. Byrne ◽  
Aisling A. Geraghty ◽  
...  

Abstract During pregnancy, changes occur to influence the maternal gut microbiome, and potentially the fetal microbiome. Diet has been shown to impact the gut microbiome. Little research has been conducted examining diet during pregnancy with respect to the gut microbiome. To meet inclusion criteria, dietary analyses must have been conducted as part of the primary aim. The primary outcome was the composition of the gut microbiome (infant or maternal), as assessed using culture-independent sequencing techniques. This review identified seven studies for inclusion, five examining the maternal gut microbiome and two examining the fetal gut microbiome. Microbial data were attained through analysis of stool samples by 16S rRNA gene-based microbiota assessment. Studies found an association between the maternal diet and gut microbiome. High-fat diets (% fat of total energy), fat-soluble vitamins (mg/day) and fibre (g/day) were the most significant nutrients associated with the gut microbiota composition of both neonates and mothers. High-fat diets were significantly associated with a reduction in microbial diversity. High-fat diets may reduce microbial diversity, while fibre intake may be positively associated with microbial diversity. The results of this review must be interpreted with caution. The number of studies was low, and the risk of observational bias and heterogeneity across the studies must be considered. However, these results show promise for dietary intervention and microbial manipulation in order to favour an increase of health-associated taxa in the gut of the mother and her offspring.


2017 ◽  
Vol 6 ◽  
Author(s):  
Thao Duy Nguyen ◽  
Olena Prykhodko ◽  
Frida Fåk Hållenius ◽  
Margareta Nyman

AbstractButyric acid has been shown to have suppressive effects on inflammation and diseases related to the intestinal tract. The aim of the present study was to investigate whether supplementation of two glycerol esters, monobutyrin (MB) and tributyrin (TB), would reach the hindgut of rats, thus having an effect on the caecal profile of SCFA, microbiota composition and some risk markers associated with chronic inflammation. For this purpose, rats were fed high-fat diets after adding MB (1 and 5 g/kg) and TB (5 g/kg) to a diet without any supplementation (high-fat control; HFC). A low-fat (LF) diet was also included. In the liver, total cholesterol concentrations, LDL-cholesterol concentrations, LDL:HDL ratio, and succinic acid concentrations were reduced in rats given the MB and TB (5 g/kg) diets, compared with the group fed the HFC diet. These effects were more pronounced in MB than TB groups as also expressed by down-regulation of the gene Cyp8b1. The composition of the caecal microbiota in rats fed MB and TB was separated from the group fed the HFC diet, and also the LF diet, as evidenced by the absence of the phylum TM7 and reduced abundance of the genera Dorea (similar to LF-fed rats) and rc4-4. Notably, the caecal abundance of Mucispirillum was markedly increased in the MB group compared with the HFC group. The results suggest that dietary supplementation of MB and TB can be used to counteract disturbances associated with a HFC diet, by altering the gut microbiota, and decreasing liver lipids and succinic acid concentrations.


2014 ◽  
Vol 34 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Colette N. Miller ◽  
Heidi P. Morton ◽  
Paula T. Cooney ◽  
Tricia G. Winters ◽  
Keshia R. Ramseur ◽  
...  

2011 ◽  
Vol 22 (4) ◽  
pp. 366-371 ◽  
Author(s):  
Johan De Vogel-van den Bosch ◽  
Sjoerd A.A. van den Berg ◽  
Silvia Bijland ◽  
Peter J. Voshol ◽  
Louis M. Havekes ◽  
...  

2009 ◽  
Vol 297 (5) ◽  
pp. R1302-R1311 ◽  
Author(s):  
Stéphane Boghossian ◽  
Karalee Lemmon ◽  
MieJung Park ◽  
David A. York

Intracerebroventricular insulin decreases food intake (FI) . The central bed nucleus of the amygdala (CeA), as other regions of the brain regulating feeding behavior, expresses insulin receptors. Our objectives were to show an insulin anorectic response in the amygdala, study the effect of high-fat diets on this response, and map the neural network activated by CeA insulin using c-Fos immunohistochemistry. Sprague-Dawley (SD) rats fitted with unilateral CeA cannulas were adapted to a low-fat (LFD) diet before they were fed a high-fat diet (HFD). Their feeding response to CeA saline or insulin (8 mU) was tested after 24 h, 72 h, or 7 days of being on a HFD. In a second experiment, SD rats were fed the HFD for 3, 7, or 49 days and were then refed with the LFD. They were tested for their insulin response before and after an HFD and every 3 days for the following weeks. Insulin tolerance tests were performed in a parallel group of rats. The CeA insulin stimulation c-Fos expression was studied to identify the distribution of activated neuronal populations. Feeding an HFD for 72 h or more induced a CeA, but not peripheral, insulin resistance, which was slowly reversed by LFD refeeding. The duration of HFD feeding determined the time frame for reversal of the insulin resistance. CeA insulin increased c-Fos in multiple brain regions, including the arcuate nucleus/paraventricular nucleus region of the hypothalamus. We conclude that the amygdala may be an important site for insulin regulation of food intake and may have a significant role in determining susceptibility to HFD-induced obesity.


2009 ◽  
Vol 25 (2) ◽  
pp. 185-194 ◽  
Author(s):  
Silvia Wein ◽  
Siegfried Wolffram ◽  
Jürgen Schrezenmeir ◽  
Daniela Gašperiková ◽  
Iwar Klimeš ◽  
...  

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