scholarly journals Maternal High-Fat Feeding Affects the Liver and Thymus Metabolic Axis in the Offspring and Some Effects Are Attenuated by Maternal Diet Normalization in a Minipig Model

Metabolites ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 800
Author(s):  
Federica La Rosa ◽  
Letizia Guiducci ◽  
Maria Angela Guzzardi ◽  
Andrea Cacciato Insilla ◽  
Silvia Burchielli ◽  
...  
Keyword(s):  
Weight Gain ◽  
Maternal Diet ◽  
Liver Steatosis ◽  
Normal Diet ◽  
Liver Fat ◽  
High Fat ◽  
Immune Development ◽  
Severe Insulin Resistance ◽  
Positron Emission ◽  
Fat Feeding

Maternal high-fat diet (HFD) affects metabolic and immune development. We aimed to characterize the effects of maternal HFD, and the subsequent diet-normalization of the mothers during a second pregnancy, on the liver and thymus metabolism in their offspring, in minipigs. Offspring born to high-fat (HFD) and normal diet (ND) fed mothers were studied at week 1 and months 1, 6, 12 of life. Liver and thymus glucose uptake (GU) was measured with positron emission tomography during hyperinsulinemic-isoglycemia. Histological analyses were performed to quantify liver steatosis, inflammation, and hepatic hematopoietic niches (HHN), and thymocyte size and density in a subset. The protocol was repeated after maternal-diet-normalization in the HFD group. At one week, HFDoff were characterized by hyperglycemia, hyperinsulinemia, severe insulin resistance (IR), and high liver and thymus GU, associating with thymocyte size and density, with elevated weight-gain, liver IR, and steatosis in the first 6 months of life. Maternal diet normalization reversed thymus and liver hypermetabolism, and increased HHN at one week. It also normalized systemic insulin-sensitivity and liver fat content at all ages. Instead, weight-gain excess, hyperglycemia, and hepatic IR were still observed at 1 month, i.e., end-lactation. We conclude that intra-uterine HFD exposure leads to time-changing metabolic and immune-correlated abnormalities. Maternal diet-normalization reversed most of the effects in the offspring.

scholarly journals Alterations in hepatic one-carbon metabolism and related pathways following a high-fat dietary intervention

2011 ◽  
Vol 43 (8) ◽  
pp. 408-416 ◽  
Author(s):  
Isabel Rubio-Aliaga ◽  
Baukje de Roos ◽  
Manuela Sailer ◽  
Gerard A. McLoughlin ◽  
Mark V. Boekschoten ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Carbon Metabolism ◽  
Dietary Intervention ◽  
Liver Steatosis ◽  
Oxidative Capacity ◽  
Blood Cholesterol ◽  
High Fat ◽  
One Carbon Metabolism ◽  
Fat Feeding

Obesity frequently leads to insulin resistance and the development of hepatic steatosis. To characterize the molecular changes that promote hepatic steatosis, transcriptomics, proteomics, and metabolomics technologies were applied to liver samples from C57BL/6J mice obtained from two independent intervention trials. After 12 wk of high-fat feeding the animals became obese, hyperglycemic, and insulin resistant, had elevated levels of blood cholesterol and VLDL, and developed hepatic steatosis. Nutrigenomic analysis revealed alterations of key metabolites and enzyme transcript levels of hepatic one-carbon metabolism and related pathways. The hepatic oxidative capacity and the lipid milieu were significantly altered, which may play a key role in the development of insulin resistance. Additionally, high choline levels were observed after the high-fat diet. Previous studies have linked choline levels with insulin resistance and hepatic steatosis in conjunction with changes of certain metabolites and enzyme levels of one-carbon metabolism. The present results suggest that the coupling of high levels of choline and low levels of methionine plays an important role in the development of insulin resistance and liver steatosis. In conclusion, the complexities of the alterations induced by high-fat feeding are multifactorial, indicating that the interplay between several metabolic pathways is responsible for the pathological consequences.

scholarly journals Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring

2007 ◽  
Vol 293 (3) ◽  
pp. R1056-R1062 ◽  
Author(s):  
Jacqueline Férézou-Viala ◽  
Anne-France Roy ◽  
Colette Sérougne ◽  
Daniel Gripois ◽  
Michel Parquet ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Maternal Diet ◽  
The Body ◽  
Female Rats ◽  
Leptin Resistance ◽  
High Fat ◽  
Leptin Sensitivity ◽  
The Impact

Epidemiological and animal studies suggest that the alteration of hormonal and metabolic environment during fetal and neonatal development can contribute to development of metabolic syndrome in adulthood. In this paper, we investigated the impact of maternal high-fat (HF) diet on hypothalamic leptin sensitivity and body weight gain of offspring. Adult Wistar female rats received a HF or a control normal-fat (C) diet for 6 wk before gestation until the end of the suckling period. After weaning, pups received either C or HF diet during 6 wk. Body weight gain and metabolic and endocrine parameters were measured in the eight groups of rats formed according to a postweaning diet, maternal diet, and gender. To evaluate hypothalamic leptin sensitivity in each group, STAT-3 phosphorylation was measured in response to leptin or saline intraperitoneal bolus. Pups exhibited similar body weights at birth, but at weaning, those born to HF dams weighed significantly less (−12%) than those born to C dams. When given the HF diet, males and females born to HF dams exhibited smaller body weight and feed efficiency than those born to C dams, suggesting increased energy expenditure programmed by the maternal HF diet. Thus, maternal HF feeding could be protective against adverse effects of the HF diet as observed in male offspring of control dams: overweight (+17%) with hyperleptinemia and hyperinsulinemia. Furthermore, offspring of HF dams fed either C or HF diet exhibited an alteration in hypothalamic leptin-dependent STAT-3 phosphorylation. We conclude that maternal high-fat diet programs a hypothalamic leptin resistance in offspring, which, however, fails to increase the body weight gain until adulthood.

scholarly journals Body composition and behaviour in adult rats are influenced by maternal diet, maternal age and high-fat feeding

2015 ◽  
Vol 4 ◽  
Author(s):  
S. Ware ◽  
J.-P. Voigt ◽  
S. C. Langley-Evans
Keyword(s):  
Body Composition ◽  
Weight Gain ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Maternal Age ◽  
Maternal Diet ◽  
High Fat ◽  
Older Mothers ◽  
Maternal Undernutrition ◽  
Low Protein

AbstractFetal exposure to maternal undernutrition has lifelong consequences for physiological and metabolic function. Maternal low-protein diet is associated with an age-related phenotype in rats, characterised by a period of resistance to development of obesity in early adulthood, giving way to an obesity-prone, insulin-resistant state in later adulthood. Offspring of rats fed a control (18 % casein) or low-protein (9 % casein; LP) diet in pregnancy were challenged with a high-fat diet at 9 months of age. To assess whether other maternal factors modulated the programming effects of nutrition, offspring were studied from young (2–4 months old) and older (6–9 months old) mothers. Weight gain with a high-fat diet was attenuated in male offspring of older mothers fed LP (interaction of maternal age and diet; P = 0·011) and adipose tissue deposition was lower with LP feeding in both males and females (P < 0·05). Although the resistance to weight gain and adiposity was partially explained by lower energy intake in offspring of LP mothers (P < 0·001 males only), it was apparent that energy expenditure must be influenced by maternal diet and age. Assessment of locomotor activity indicated that energy expenditure associated with physical activity was unlikely to explain resistance to weight gain, but showed that offspring of older mothers were more anxious than those of younger mothers, with more rearing observed in a novel environment and on the elevated plus-maze. The data showed that in addition to maternal undernutrition, greater maternal age may influence development and long-term body composition in the rat.

scholarly journals Protein and folic acid content in the maternal diet determine lipid metabolism and response to high-fat feeding in rat progeny in an age-dependent manner

2011 ◽  
Vol 7 (2) ◽  
pp. 223-234 ◽  
Author(s):  
Agata Chmurzynska ◽  
Monika Stachowiak ◽  
Jan Gawecki ◽  
Ewa Pruszynska-Oszmalek ◽  
Małgorzata Tubacka
Keyword(s):  
Folic Acid ◽  
Lipid Metabolism ◽  
Acid Content ◽  
Maternal Diet ◽  
Dependent Manner ◽  
High Fat ◽  
Age Dependent ◽  
Fat Feeding

scholarly journals Regulating AMPKα and insulin level by Vinegar, Swimming and Refeeding on High-Fat Diet Rats to Rebuild Lipid Homeostasis

2020 ◽  
Author(s):  
Yuan Yang ◽  
Feng Zhang ◽  
Xiao Xiao ◽  
Chunlian Ma ◽  
Hua Liu ◽  
...  
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Insulin Level ◽  
Diet Group ◽  
Normal Diet ◽  
Lipid Homeostasis ◽  
Control Group ◽  
High Fat ◽  
Better Regulation ◽  
Rice Vinegar

AbstractOur aims were to explore the effects of dietary and behavior interventions on lipometabolism caused by unhealthy high-fat diet and the best method to rebuild lipid homeostasis of this lifestyle. Apart from normal diet rats, 34 rats were fed with high-fat emulsion for 4 weeks before being divided into 4 groups and intervened for another 4 weeks. 8 of them were classified into high-fat control group and 9 were sorted into high-fat diet with rice vinegar group. Meanwhile, 10 were put into high-fat diet with swimming group and 7 were just for refeeding normal diet group. Then the data of body weight was recorded and analyzed. Serum, pancreas, liver, cardiac tissues and epididymis adipose were sampled as required. Indexes of serum were tested by kits. AMPKα, HNF1α, CTRP6 from tissues were detected by western blot. According to our experiments, Swimming and refeeding groups reflected a better regulation on lipid homeostasis mainly by up-regulating the expression of pancreas AMPKα. To be more specific, the refeeding rats showed lower T-CHO (P<0.001) and LDL-C (P<0.05), but higher weight gain (P<0.001),insulin level (P<0.01)and pancreas AMPKα (P<0.01)than high-fat control rats. Compared with rats experimented by swimming or rice vinegar, they showed higher weight gain (P<0.001),insulin level (P<0.01)and HNF1α, but lower of CTRP6. In summary, refeeding diet functioned better in regulating the lipometabolic level after high-fat diet. Whatever approach mentioned above we adopted to intervene, the best policy to keep the balance of lipid homeostasis is to maintain a healthy diet.

scholarly journals A Combination of Apple Vinegar Drink with Bacillus coagulans Ameliorates High Fat Diet-Induced Body Weight Gain, Insulin Resistance and Hepatic Steatosis

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2504
Author(s):  
Raquel Urtasun ◽  
Joana Díaz-Gómez ◽  
Miriam Araña ◽  
María José Pajares ◽  
María Oneca ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Bacillus Coagulans ◽  
Normal Diet ◽  
High Fat ◽  
Blood Biochemical ◽  
Traditional Remedy

Obesity is a worldwide epidemic characterized by excessive fat accumulation, associated with multiple comorbidities and complications. Emerging evidence points to gut microbiome as a driving force in the pathogenesis of obesity. Vinegar intake, a traditional remedy source of exogenous acetate, has been shown to improve glycemic control and to have anti-obesity effects. New functional foods may be developed by supplementing traditional food with probiotics. B. coagulans is a suitable choice because of its resistance to high temperatures. To analyze the possible synergic effect of Vinegar and B. coagulans against the metabolic alterations induced by a high fat diet (HFD), we fed twelve-week-old C57BL/6 mice with HFD for 5 weeks after 2 weeks of acclimation on a normal diet. Then, food intake, body weight, blood biochemical parameters, histology and liver inflammatory markers were analyzed. Although vinegar drink, either alone or supplemented with B. coagulans, reduced food intake, attenuated body weight gain and enhanced glucose tolerance, only the supplemented drink improved the lipid serum profile and prevented hepatic HFD-induced overexpression of CD36, IL-1β, IL-6, LXR and SREBP, thus reducing lipid deposition in the liver. The beneficial properties of the B. coagulans-supplemented vinegar appear to be mediated by a reduction in insulin and leptin circulating levels.

scholarly journals Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain

2011 ◽  
Vol 52 (9) ◽  
pp. 1723-1732 ◽  
Author(s):  
David W. Nelson ◽  
Yu Gao ◽  
Nicole M. Spencer ◽  
Taylor Banh ◽  
Chi-Liang Eric Yen
Keyword(s):  
Weight Gain ◽  
Energy Expenditure ◽  
Obese Mice ◽  
High Fat ◽  
Excessive Weight Gain ◽  
Excessive Weight ◽  
Fat Feeding

scholarly journals Oleuropein Induces AMPK-Dependent Autophagy in NAFLD Mice, Regardless of the Gender

2018 ◽  
Vol 19 (12) ◽  
pp. 3948 ◽  
Author(s):  
Cristiana Porcu ◽  
Silvia Sideri ◽  
Maurizio Martini ◽  
Alessandra Cocomazzi ◽  
Andrea Galli ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Liver Steatosis ◽  
Normal Diet ◽  
Male Mice ◽  
High Fat ◽  
Unhealthy Diet ◽  
Autophagic Process ◽  
Related Proteins ◽  
Gender Specific ◽  
Novel Therapeutic

Oleuropein (Ole) is one of the most plentiful phenolic compounds with antioxidant, anti-inflammatory, anti-atherogenic, hypoglycemic and hypolipidemic effects. The aim of our study was to establish whether the positive Ole-related effects on liver steatosis could be associated with autophagy. Female and male C57BL/6J mice were fed normal diet (ND) or high-fat diet (HFD) for eight weeks, and Ole was added or not for the following eight weeks. The autophagy-related proteins Akt, mTOR, AMPK, ULK1, Beclin-1, LC3B and p62/Sqstm1 were analyzed. Interestingly, Ole induced a different regulation of the Akt/mTOR pathway in female compared to male mice, but was able to activate the autophagic process in ND and HFD mice through AMPK-dependent phosphorylation of ULK1 at Ser555, regardless of the gender. Our work reveals the ability of Ole to induce, in liver of ND and HFD mice, autophagy independently by gender-specific mTOR activation. We highlight Ole as a novel therapeutic approach to counteract unhealthy diet-related liver steatosis by targeting autophagy.

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