Isoquercetin and inulin synergistically modulate the gut microbiome to prevent development of the metabolic syndrome in mice fed a high fat diet

Abstract7-Hydroxymatairesinol (7-HMR) is a plant lignan abundant in various concentrations in plant foods. The objective of this study was to test HMRLignan™, a purified form of 7-HMR, and the correspondingPicea abiesextract (total extractP. abies; TEP) as dietary supplements on a background of a high-fat diet (HFD)-induced metabolic syndrome in mice and in the 3T3-L1 adipogenesis model. Mice, 3 weeks old, were fed a HFD for 60 d. Subgroups were treated with 3 mg/kg body weight 7-HMR (HMRLignan™) or 10 mg/kg body weight TEP by oral administration. 7-HMR and TEP limited the increase in body weight (−11 and −13 %) and fat mass (−11 and −18 %) in the HFD-fed mice. Epididymal adipocytes were 19 and −12 % smaller and the liver was less steatotic (−62 and −65 %). Serum lipids decreased in TEP-treated mice (−11 % cholesterol, −23 % LDL and −15 % TAG) and sugar metabolism was ameliorated by both lignan preparations, as shown by a more than 70 % decrease in insulin secretion and insulin resistance. The expression of several metabolic genes was modulated by the HFD with an effect that was reversed by lignan. In 3T3-L1 cells, the 7-HMR metabolites enterolactone (ENL) and enterodiol (END) showed a 40 % inhibition of cell differentiation accompanied by the inhibited expression of the adipogenic genesPPARγ,C/EBPαandaP2. Furthermore, END and ENL caused a 10 % reduction in TAG uptake in HEPA 1–6 hepatoma cells. In conclusion, 7-HMR and TEP reduce metabolic imbalances typical of the metabolic syndrome and obesity in male mice, whereas their metabolites inhibit adipogenesis and lipid uptakein vitro.

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Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Molecular Nutrition & Food Research ◽

10.1002/mnfr.201900425 ◽

2019 ◽

Vol 63 (19) ◽

pp. 1900425 ◽

Cited By ~ 3

Author(s):

Sergio Montserrat‐de la Paz ◽

Maria C. Naranjo ◽

Maria C. Millan‐Linares ◽

Sergio Lopez ◽

Rocio Abia ◽

...

Keyword(s):

Metabolic Syndrome ◽

Fatty Acids ◽

High Fat Diet ◽

Monounsaturated Fatty Acids ◽

High Fat ◽

The Metabolic Syndrome ◽

White Fat

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Maternal supplementation with n-3 long chain polyunsaturated fatty acids during perinatal period alleviates the metabolic syndrome disturbances in adult hamster pups fed a high-fat diet after weaning

The Journal of Nutritional Biochemistry ◽

10.1016/j.jnutbio.2014.03.003 ◽

2014 ◽

Vol 25 (7) ◽

pp. 726-733 ◽

Cited By ~ 12

Author(s):

Fatima Kasbi-Chadli ◽

Clair-Yves Boquien ◽

Gilles Simard ◽

Lionel Ulmann ◽

Virginie Mimouni ◽

...

Keyword(s):

Metabolic Syndrome ◽

Fatty Acids ◽

Polyunsaturated Fatty Acids ◽

High Fat Diet ◽

Perinatal Period ◽

High Fat ◽

The Metabolic Syndrome ◽

Maternal Supplementation ◽

Adult Hamster ◽

Long Chain

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Fetal origins of insulin resistance and obesity

Proceedings of The Nutrition Society ◽

10.1079/pns2005417 ◽

2005 ◽

Vol 64 (2) ◽

pp. 143-151 ◽

Cited By ~ 116

Author(s):

Claire J. Stocker ◽

Jonathan R. S. Arch ◽

Michael A. Cawthorne

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

G Protein ◽

High Fat Diet ◽

High Fat ◽

Fetal Origins ◽

Thrifty Phenotype ◽

The Metabolic Syndrome ◽

Increased Susceptibility

A number of epidemiological studies worldwide have demonstrated a relationship between poor early growth and an increased susceptibility to insulin resistance, visceral obesity, type 2 diabetes and other features of the metabolic syndrome in adulthood. However, the mechanistic basis of this relationship and the relative roles of genes and the environment remain a subject of debate. The ‘thrifty phenotype’ hypothesis proposes that poor fetal nutrition leads to programming of metabolism and an adult phenotype that is adapted to poor but not plentiful nutrition. The maternal reduced-protein rat model has been used to examine the importance of the maternal environment in determining susceptibility to adult disease. Pregnant and lactating rat dams are fed a diet containing 80 g protein/kg as compared with 200 g protein/kg, which leads to growth restriction in utero. Offspring of low-protein dams have increased susceptibility to diabetes, insulin resistance and hypertension when fed a palatable high-fat diet that promotes obesity. Administration of leptin during pregnancy and lactation to these protein-restricted dams produces offspring that have increased metabolic rate and do not become obese or insulin resistant when fed on a high-fat diet. Increased glucocorticoid exposure, particularly during late gestation, has been linked with insulin resistance in adulthood. High levels of fetal glucocorticoids may result from a decreased activity of placental 11β-hydroxysteroid dehydrogenase (11β-HSD) type 2, which normally protects the fetus from high maternal glucocorticoid levels. Leptin administration to protein-restricted dams inhibits the suppression of 11β-HSD-2 and may be one mechanism by which the metabolic syndrome is prevented.

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Metabolic and hormonal indices in rats with a prolonged model of the metabolic syndrome induced by a high-carbohydrate and high-fat diet

Advances in Gerontology ◽

10.1134/s2079057017020035 ◽

2017 ◽

Vol 7 (2) ◽

pp. 130-136

Author(s):

K. V. Derkach ◽

V. M. Bondareva ◽

A. P. Trashkov ◽

O. V. Chistyakova ◽

N. A. Verlov ◽

...

Keyword(s):

Metabolic Syndrome ◽

High Fat Diet ◽

High Fat ◽

High Carbohydrate ◽

The Metabolic Syndrome

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Effects of a High-Fat Diet Exposure in Utero on the Metabolic Syndrome-Like Phenomenon in Mouse Offspring through Epigenetic Changes in Adipocytokine Gene Expression

Endocrinology ◽

10.1210/en.2011-2161 ◽

2012 ◽

Vol 153 (6) ◽

pp. 2823-2830 ◽

Cited By ~ 124

Author(s):

Hisashi Masuyama ◽

Yuji Hiramatsu

Keyword(s):

Gene Expression ◽

Metabolic Syndrome ◽

High Fat Diet ◽

Control Diet ◽

Caloric Intake ◽

In Utero ◽

Shared Environment ◽

Epigenetic Changes ◽

High Fat ◽

The Metabolic Syndrome

The links between obesity in parents and their offspring and the role of genes and a shared environment are not completely understood. Adipocytokines such as leptin and adiponectin play important roles in glucose and lipid metabolism. Therefore, we examined whether the offspring from dams exposed to a high-fat diet during pregnancy (OH mice) exhibited hypertension, insulin resistance, and hyperlipidemia along with epigenetic changes in the expression of adipocytokine genes. OH mice were significantly heavier than the offspring of dams exposed to a control diet during pregnancy (OC mice) from 14 wk of age after an increased caloric intake from 8 wk. OH mice exhibited higher blood pressure and worse glucose tolerance than the OC mice at 24 wk. Total triglyceride and leptin levels were significantly higher and the adiponectin level was significantly lower in OH compared with OC mice at 12 wk of age. This was associated with changes in leptin and adiponectin expression in white adipose tissue. There were lower acetylation and higher methylation levels of histone H3 at lysine 9 of the promoter of adiponectin in adipose tissues of OH mice at 2 wk of age as well as at 12 and 24 wk of age compared with OC mice. In contrast, methylation of histone 4 at lysine 20 in the leptin promoter was significantly higher in OH compared with OC mice. Thus, exposure to a high-fat diet in utero might cause a metabolic syndrome-like phenomenon through epigenetic modifications of adipocytokine, adiponectin, and leptin gene expression.

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Effects of yam dioscorin interventions on improvements of the metabolic syndrome in high-fat diet-induced obese rats

Botanical Studies ◽

10.1186/s40529-015-0084-8 ◽

2015 ◽

Vol 56 (1) ◽

Cited By ~ 9

Author(s):

Shen-Liang Shih ◽

Yin-Shiou Lin ◽

Shyr-Yi Lin ◽

Wen-Chi Hou

Keyword(s):

Metabolic Syndrome ◽

High Fat Diet ◽

High Fat ◽

The Metabolic Syndrome ◽

Obese Rats

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Brown adipose tissue-derived exosomes mitigate the metabolic syndrome in high fat diet mice

Theranostics ◽

10.7150/thno.43968 ◽

2020 ◽

Vol 10 (18) ◽

pp. 8197-8210 ◽

Cited By ~ 3

Author(s):

Xueying Zhou ◽

Zhelong Li ◽

Meihao Qi ◽

Ping Zhao ◽

Yunyou Duan ◽

...

Keyword(s):

Metabolic Syndrome ◽

Adipose Tissue ◽

Brown Adipose Tissue ◽

High Fat Diet ◽

High Fat ◽

The Metabolic Syndrome ◽

Brown Adipose

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High-fat diet-induced met-hemoglobin formation in rats prone (WOKW) or resistant (DA) to the metabolic syndrome: Effect of CoQ10supplementation

BioFactors ◽

10.1002/biof.1190 ◽

2014 ◽

Vol 40 (6) ◽

pp. 603-609 ◽

Cited By ~ 8

Author(s):

Patrick Orlando ◽

Sonia Silvestri ◽

Francesca Brugè ◽

Luca Tiano ◽

Ingrid Kloting ◽

...

Keyword(s):

Metabolic Syndrome ◽

High Fat Diet ◽

High Fat ◽

The Metabolic Syndrome

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Long-Term Dietary Nitrate Supplementation Does Not Prevent Development of the Metabolic Syndrome in Mice Fed a High-Fat Diet

International Journal of Endocrinology ◽

10.1155/2018/7969750 ◽

2018 ◽

Vol 2018 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

V. B. Matthews ◽

R. Hollingshead ◽

H. Koch ◽

K. D. Croft ◽

N. C. Ward

Keyword(s):

Metabolic Syndrome ◽

Glucose Tolerance ◽

High Fat Diet ◽

High Fat ◽

Running Wheel ◽

Dietary Nitrate ◽

The Metabolic Syndrome ◽

Normal Chow ◽

Nitrate Supplementation

Background. Nitric oxide (NO) is an important vascular signaling molecule that plays a role in vascular homeostasis. A reduction in NO bioavailability is thought to contribute to endothelial dysfunction, an early risk factor for both cardiovascular disease and type 2 diabetes. Dietary nitrate, through the nitrate-nitrite-NO pathway, may provide an alternate source of NO when the endogenous eNOS system is compromised. In addition to a role in the vascular system, NO may also play a role in the metabolic syndrome including obesity and glucose tolerance. Aim. To investigate the effect of long-term dietary nitrate supplementation on development of the metabolic syndrome in mice fed a high-fat diet. Methods. Following 1 week of acclimatisation, male (6–8 weeks) C57BL6 mice were randomly assigned to the following groups (10/group) for 12 weeks: (i) normal chow + NaCl (1 mmol/kg/day), (ii) normal chow + NaNO3 (1 mmol/kg/day), (iii) high-fat diet + NaCl (1 mmol/kg/day), and (iv) high-fat diet + NaNO3 (1 mmol/kg/day). Body weight and food consumption were monitored weekly. A subset of mice (5/group) underwent running wheel assessment. At the end of the treatment period, all mice underwent fasting glucose tolerance testing. Caecum contents, serum, and tissues (liver, skeletal muscle, white and brown adipose, and kidney) were collected, frozen, and stored at −80°C until analysis. Results. Consumption of the high-fat diet resulted in significantly greater weight gain that was not affected by dietary nitrate. Mice on the high-fat diet also had impaired glucose tolerance that was not affected by dietary nitrate. There was no difference in adipose tissue expression of thermogenic proteins or energy expenditure as assessed by the running wheel activity. Mice on the high-fat diet and those receiving dietary nitrate had reduced caecum concentrations of both butyrate and propionate. Conclusions. Dietary nitrate does not prevent development of the metabolic syndrome in mice fed a high-fat diet. This may be due, in part due, to reductions in the concentration of important short-chain fatty acids.

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