Dietary Switch from High Fat Diet to Normal Diet During Early Adulthood Does Not Restore Sperm Quality But Prevents Onset of the Metabolic Syndrome

2019 ◽  
Author(s):  
Luís Crisóstomo ◽  
Luís Rato ◽  
Ivana Jarak ◽  
Branca M. Silva ◽  
João F. Raposo ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Sperm Quality ◽  
Early Adulthood ◽  
Normal Diet ◽  
High Fat ◽  
The Metabolic Syndrome ◽  
Dietary Switch

scholarly journals A switch from high-fat to normal diet does not restore sperm quality but prevents metabolic syndrome

Reproduction ◽  
2019 ◽  
Vol 158 (4) ◽  
pp. 377-387 ◽  
Author(s):  
Luís Crisóstomo ◽  
Luís Rato ◽  
Ivana Jarak ◽  
Branca M Silva ◽  
João F Raposo ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Molecular Mechanisms ◽  
Sperm Quality ◽  
Early Adulthood ◽  
Disease Onset ◽  
Normal Diet ◽  
Whole Body ◽  
Control Group ◽  
High Fat ◽  
Diet Switch

In recent decades, the prevalence of metabolic diseases has concomitantly increased with a decline on fertility rates and sperm quality. High-fat diets (HFD) are seldom considered part of the problem, but the molecular mechanisms underlying its effects on male fertility remain poorly understood. Herein we postulated that HFD alter sperm quality. We evaluated the effects of switching from a HFD to a normal diet in early adulthood on metabolic disease onset, testicular metabolism and sperm quality. Thirty-six male C57BL6/J mice were divided in: a control group fed with standard chow; a group fed with HFD for 200 days; and a group fed with HFD for 60 days and then with standard chow (HFDt). Biometric data and whole-body metabolism were assessed. Epididymal sperm was studied for concentration, motility, viability and morphology. 1H-NMR metabolomics approach was performed on testicular extracts to trace the metabolic changes. Diet switch reduced body weight and fat mass, preventing metabolic syndrome onset. However, sperm viability, motility and morphology were deteriorated by HFD consumption and not restored by diet switch. HFD induced irreversible changes in pyruvate and glutamate metabolism, ethanol degradation and ammonia recycling in testis. Furthermore, HFDt changed purine and cysteine metabolism, urea cycle, and glutathione content. Overall, HFD caused irreversible changes in testicular metabolism even after switching to normal diet. HFD feeding until early adulthood decreases sperm quality, which cannot be restored by diet switch or weight loss, even when development of metabolic syndrome is avoided.

scholarly journals 7-Hydroxymatairesinol improves body weight, fat and sugar metabolism in C57BJ/6 mice on a high-fat diet

2018 ◽  
Vol 120 (7) ◽  
pp. 751-762 ◽  
Author(s):  
Giorgio Biasiotto ◽  
Isabella Zanella ◽  
Federica Predolini ◽  
Ivonne Archetti ◽  
Moris Cadei ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
High Fat Diet ◽  
Sugar Metabolism ◽  
Lipid Uptake ◽  
High Fat ◽  
Total Extract ◽  
The Metabolic Syndrome ◽  
Metabolic Genes

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.

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

2019 ◽  
Vol 63 (19) ◽  
pp. 1900425 ◽  
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

scholarly journals Impairment of spermatogenesis and sperm motility by the high-fat diet-induced dysbiosis of gut microbes

Gut ◽  
2020 ◽  
Vol 69 (9) ◽  
pp. 1608-1619 ◽  
Author(s):  
Ning Ding ◽  
Xin Zhang ◽  
Xue Di Zhang ◽  
Jun Jing ◽  
Shan Shan Liu ◽  
...  
Keyword(s):  
Sperm Motility ◽  
High Fat Diet ◽  
Sperm Quality ◽  
Sperm Count ◽  
Normal Diet ◽  
High Fat ◽  
Strong Negative Correlation ◽  
Gut Microbes ◽  
Mitochondrial Functions ◽  
Registration Number

ObjectiveHigh-fat diet (HFD)-induced metabolic disorders can lead to impaired sperm production. We aim to investigate if HFD-induced gut microbiota dysbiosis can functionally influence spermatogenesis and sperm motility.DesignFaecal microbes derived from the HFD-fed or normal diet (ND)-fed male mice were transplanted to the mice maintained on ND. The gut microbes, sperm count and motility were analysed. Human faecal/semen/blood samples were collected to assess microbiota, sperm quality and endotoxin.ResultsTransplantation of the HFD gut microbes into the ND-maintained (HFD-FMT) mice resulted in a significant decrease in spermatogenesis and sperm motility, whereas similar transplantation with the microbes from the ND-fed mice failed to do so. Analysis of the microbiota showed a profound increase in genus Bacteroides and Prevotella, both of which likely contributed to the metabolic endotoxaemia in the HFD-FMT mice. Interestingly, the gut microbes from clinical subjects revealed a strong negative correlation between the abundance of Bacteroides-Prevotella and sperm motility, and a positive correlation between blood endotoxin and Bacteroides abundance. Transplantation with HFD microbes also led to intestinal infiltration of T cells and macrophages as well as a significant increase of pro-inflammatory cytokines in the epididymis, suggesting that epididymal inflammation have likely contributed to the impairment of sperm motility. RNA-sequencing revealed significant reduction in the expression of those genes involved in gamete meiosis and testicular mitochondrial functions in the HFD-FMT mice.ConclusionWe revealed an intimate linkage between HFD-induced microbiota dysbiosis and defect in spermatogenesis with elevated endotoxin, dysregulation of testicular gene expression and localised epididymal inflammation as the potential causes.Trial registration numberNCT03634644.

scholarly journals Fetal origins of insulin resistance and obesity

2005 ◽  
Vol 64 (2) ◽  
pp. 143-151 ◽  
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.

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

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Si Tan ◽  
Jose A. Caparros-Martin ◽  
Vance B. Matthews ◽  
Henrietta Koch ◽  
Fergal O’Gara ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
High Fat ◽  
The Metabolic Syndrome

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

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

scholarly journals The Effects of High-Fat Diet Exposure In Utero on the Obesogenic and Diabetogenic Traits Through Epigenetic Changes in Adiponectin and Leptin Gene Expression for Multiple Generations in Female Mice

Endocrinology ◽  
2015 ◽  
Vol 156 (7) ◽  
pp. 2482-2491 ◽  
Author(s):  
Hisashi Masuyama ◽  
Takashi Mitsui ◽  
Etsuko Nobumoto ◽  
Yuji Hiramatsu
Keyword(s):  
Metabolic Syndrome ◽  
Fat Mass ◽  
High Fat Diet ◽  
Mass Gain ◽  
Female Offspring ◽  
In Utero ◽  
Normal Diet ◽  
Epigenetic Changes ◽  
High Fat ◽  
Multiple Generations

Recent studies demonstrate that epigenetic changes under malnutrition in utero might play important roles in transgenerational links with metabolic diseases. We have previously shown that exposure to a high-fat diet (HFD) in utero may cause a metabolic syndrome-like phenomenon through epigenetic modifications of Adiponectin and Leptin genes. Because an association of obesity between mother and offspring endured in multiple generations, we examined whether HFD exposure in utero might affect the metabolic status of female offspring through multigenerational epigenetic changes of Adiponectin and Leptin genes and whether a normal diet in utero for multiple generations might abolish such epigenetic changes after exposure to a HFD in utero using ICR mice. We observed that the effect of maternal HFD on offspring over multiple generations in metabolic syndrome-like phenomenon such as weight and fat mass gain, glucose intolerance, hypertriglyceridemia, abnormal adiponectin and leptin levels, and hypertension, were accumulated with expression and epigenetic changes in Adiponectin and Leptin genes. A normal diet in utero in the subsequent generations after HFD exposure in utero diminished, and a normal diet in utero for 3 generations completely abolished, the effect of HFD in utero on weight and fat mass gain, insulin resistance, serum triglyceride, adiponectin, and leptin levels, with epigenetic changes of Adiponectin and Leptin genes. Exposure to a HFD in utero might affect glucose and lipid metabolism of female offspring through epigenetic modifications to Adiponectin and Leptin genes for multiple generations. Obesogenic and diabetogenic traits were abolished after a maternal normal diet for 3 generations.

scholarly journals 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 ◽  
2012 ◽  
Vol 153 (6) ◽  
pp. 2823-2830 ◽  
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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