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 The effects of paternal high-fat diet exposure on offspring metabolism with epigenetic changes in the mouse adiponectin and leptin gene promoters

2016 ◽  
Vol 311 (1) ◽  
pp. E236-E245 ◽  
Author(s):  
Hisashi Masuyama ◽  
Takashi Mitsui ◽  
Takeshi Eguchi ◽  
Shoko Tamada ◽  
Yuji Hiramatsu
Keyword(s):  
High Fat Diet ◽  
In Utero ◽  
Epigenetic Modifications ◽  
Normal Diet ◽  
Gene Promoters ◽  
Epigenetic Changes ◽  
High Fat ◽  
Multiple Generations ◽  
Metabolic Traits ◽  
Two Generations

Recent studies have demonstrated that epigenetic changes resulting from malnutrition might play important roles in transgenerational links with metabolic diseases. Previously, we observed that exposure to a high-fat diet (HFD) in utero caused a metabolic syndrome-like phenomenon through epigenetic modifications of the adiponectin and leptin genes that persisted for multiple generations. Recent etiological studies indicated that paternal BMI had effects on offspring BMI that were independent of but additive to maternal BMI effects. Thus, we examined whether paternal HFD-induced obesity affected the metabolic status of offspring through epigenetic changes in the adiponectin and leptin genes. Additionally, we investigated whether a normal diet during subsequent generations abolished the epigenetic changes associated with paternal HFD exposure before conception. We observed the effects of paternal HFD exposure before conception over multiple generations on offspring metabolic traits, including weight and fat gain, glucose intolerance, hypertriglyceridemia, abnormal adipocytokine levels, hypertension, and adiponectin and leptin gene expression and epigenetic changes. Normal diet consumption by male offspring during the subsequent generation following paternal HFD exposure diminished whereas consumption for two generations completely abolished the effect of paternal HFD exposure on metabolic traits and adipocytokine promoter epigenetic changes in the offspring. The effects of paternal HFD exposure on offspring were relatively weaker than those following HFD exposure in utero. However, paternal HFD exposure had an additive metabolic effect for two generations, suggesting that both paternal and maternal nutrition might affect offspring metabolism through epigenetic modifications of adipocytokine genes for multiple 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.

Programmed metabolic syndrome: prenatal undernutrition and postweaning overnutrition

2007 ◽  
Vol 293 (6) ◽  
pp. R2306-R2314 ◽  
Author(s):  
Mina Desai ◽  
Jooby Babu ◽  
Michael G. Ross
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Fat Body ◽  
Female Offspring ◽  
High Fat ◽  
Pregnant Rats ◽  
Glucose Levels ◽  
Thrifty Phenotype ◽  
Calorie Diet ◽  
Plasma Leptin

Maternal nutrient restriction results in intrauterine growth restriction (IUGR) newborns that develop obesity despite normal postweaning diet. The epidemic of metabolic syndrome is attributed to programmed “thrifty phenotype” and exposure to Western diets. We hypothesized that programmed IUGR newborns would demonstrate greater susceptibility to obesity and metabolic abnormalities in response to high-fat diet. From day 10 to term gestation and lactation, control pregnant rats received ad libitum (AdLib) food, whereas study rats were 50% food restricted (FR). Cross-fostering techniques resulted in three offspring groups: control (AdLib/AdLib), FR during pregnancy (FR/AdLib), and FR during lactation (AdLib/FR). At 3 weeks, offspring were weaned to laboratory chow or high-fat calorie diet (9% vs. 17% calorie as fat). Body composition, appetite hormones, and glucose and lipid profiles were determined in 9-mo-old male and female offspring. High-fat diet had no effect on body weight of AdLib/AdLib, but significantly increased weights of FR/AdLib and AdLib/FR offspring. High-fat diet significantly increased body fat, reduced lean body mass, and accentuated plasma leptin but not ghrelin levels in both sexes in all groups. In males, high-fat diet caused a significant increase in glucose levels in all three groups with increased insulin levels in AdLib/AdLib and AdLib/FR, but not in FR/AdLib. In females, high-fat diet had no effect on glucose but significantly increased basal insulin among all three groups. High-fat diet caused hypertriglyceridemia in all three groups although only food-restricted females exhibited hypercholesterolemia. Sex and offspring phenotype-associated effects of high-fat diet indicate differing pathophysiologic mechanisms that require specific therapeutic approaches.

scholarly journals OR-033 Alterations in Inflammatory Markers and Hepatic Lipid Accumulation following Dietary and Exercise Intervention of Obese Rats

2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Yuan Zhang ◽  
Juan Wei ◽  
Xia Huang ◽  
Lei Sheng
Keyword(s):  
Body Weight ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Inflammatory Markers ◽  
Mass Gain ◽  
Normal Diet ◽  
High Fat ◽  
Hepatic Lipid Accumulation ◽  
Obese Rats ◽  
Serum Inflammatory Markers

Objective This study aimed to investigate the effects of diet and different exercise training: High Intensity Interval Training (HIIT) and Continuous Training (CT) on body mass gain, serum inflammatory markers and hepatic lipid accumulation of obese rats. Methods Male Sprague-Dawley rats were fed with a normal standard diet (N) or a high fat diet (H; 45% kcal as fat) for eight weeks without exercise stimuli. Obese rats were defined as increased at least 20% body weight than normal diet rats. After this period, N rats were continue fed with a normal diet (N), and half of obese rats were fed with a normal diet (ON), while the other half were continue fed with a high-fat diet (OH). Each diet type group was then divided into three subgroups, control (NC, ONC, OHC groups), High Intensity Interval training (NHI, ONHI, OHHI groups) and Continuous Training (NCT, ONCT, OHCT groups) (n=10). The interval and continuous straining consisted of a swimming exercise performed over eight weeks. Body weight, serum inflammatory markers, plasma and liver lipid concentrations were measured. Results Obese high fat diet rats showed greater body mass gain, visceral adipose tissue (VAT) mass, serum low density lipoprotein (LDL), triglycerides (TG), total cholesterol (TC), and serum inflammatory markers（MCP-1、IL-1β、TNF-α）in values than normal diet rats (OHC versus NC). In contrast, for the obese normal diet rats, no significantly difference was observed compared with normal diet rats on VAT weight, serum lipids, inflammatory markers except MCP-1 (ONC versus NC). On the other hand, the trained groups of obese high fat diet rats showed lower values of body and VAT weight, serum lipids, inflammatory markers levels compared with the OHC group and CT showed more remarkable effect than HIIT except on VAT weight, serum IL-1β levels (OHHI versus OHC and OHCT versus OHC). However, the significantly positive effect of CT on obese normal diet rats was only observed on serum TG, LDL and MCP-1 levels (ONCT versus ONC). In addition, compared to normal rats, hepatic wet weight (HWW)，liver triglycerides (TG) in the OHC group presented obvious high level (OHC versus NC), no differences were exhibited between ONC and NC groups. Interestingly, HIIT but not CT significantly deceased liver TG content compared with OHC group (OHHI versus OHC and OHCT versus OHC), which consistent with liver oil red O stain images as well as higher hepatic CPT-1 level. Conclusions Both training methodologies were shown to be effective in controlling body mass gain and adiposity levels in high-fat diet fed obese rats, HIIT displayed more positive effect on hepatic lipid accumulation. Additionally, diet and exercise was more effective than exercise alone in reducing body weight, VAT mass, serum inflammatory and liver TG content.

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 In Utero Exposure to a High-Fat Diet Programs Hepatic Hypermethylation and Gene Dysregulation and Development of Metabolic Syndrome in Male Mice

Endocrinology ◽  
2017 ◽  
Vol 158 (9) ◽  
pp. 2860-2872 ◽  
Author(s):  
Yoshinori Seki ◽  
Masako Suzuki ◽  
Xingyi Guo ◽  
Alan Scott Glenn ◽  
Patricia M Vuguin ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
In Utero ◽  
In Utero Exposure ◽  
Male Mice ◽  
High Fat ◽  
Gene Dysregulation

Effects of Maternal Flaxseed Supplementation on Female Offspring of Diabetic Rats in Serum Concentration of Glucose, Insulin, and Thyroid Hormones

2019 ◽  
Vol 89 (1-2) ◽  
pp. 45-54
Author(s):  
Akemi Suzuki ◽  
André Manoel Correia-Santos ◽  
Gabriela Câmara Vicente ◽  
Luiz Guillermo Coca Velarde ◽  
Gilson Teles Boaventura
Keyword(s):  
Thyroid Hormones ◽  
High Fat Diet ◽  
Female Offspring ◽  
Flaxseed Oil ◽  
Diabetic Rats ◽  
High Fat ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Flaxseed Flour ◽  
Maternal Consumption

Abstract. Objective: This study aimed to evaluate the effect of maternal consumption of flaxseed flour and oil on serum concentrations of glucose, insulin, and thyroid hormones of the adult female offspring of diabetic rats. Methods: Wistar rats were induced to diabetes by a high-fat diet (60%) and streptozotocin (35 mg/kg). Rats were mated and once pregnancy was confirmed, were divided into the following groups: Control Group (CG): casein-based diet; High-fat Group (HG): high-fat diet (49%); High-fat Flaxseed Group (HFG): high-fat diet supplemented with 25% flaxseed flour; High-fat Flaxseed Oil group (HOG): high-fat diet, where soya oil was replaced with flaxseed oil. After weaning, female pups (n = 6) from each group were separated, received a commercial rat diet and were sacrificed after 180 days. Serum insulin concentrations were determined by ELISA, the levels of triiodothyronine (T3), thyroxine (T4) and thyroid-stimulating hormone (TSH) were determined by chemiluminescence. Results: There was a significant reduction in body weight at weaning in HG (−31%), HFG (−33%) and HOG (44%) compared to CG (p = 0.002), which became similar by the end of 180 days. Blood glucose levels were reduced in HFG (−10%, p = 0.044) when compared to CG, and there was no significant difference between groups in relation to insulin, T3, T4, and TSH after 180 days. Conclusions: Maternal severe hyperglycemia during pregnancy and lactation resulted in a microsomal offspring. Maternal consumption of flaxseed reduces blood glucose levels in adult offspring without significant effects on insulin levels and thyroid hormones.

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