scholarly journals Maternal diet disrupts the placenta-brain axis in a sex-specific manner

2021 ◽  
Author(s):  
Alexis M Ceasrine ◽  
Benjamin A Devlin ◽  
Jessica L Bolton ◽  
Young Chan Jo ◽  
Carolyn Huynh ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Age Of Onset ◽  
Maternal Diet ◽  
Fetal Brain ◽  
First Trimester ◽  
Autism Spectrum ◽  
Adult Brain ◽  
Maternal Weight ◽  
High Fat ◽  
Triglyceride Accumulation

High maternal weight is associated with a number of detrimental outcomes in offspring, including increased susceptibility to neurological disorders such as anxiety, depression, and communicative disorders (e.g. autism spectrum disorders). Despite widespread acknowledgement of sex-biases in the prevalence, incidence, and age of onset of these disorders, few studies have investigated potential sex-biased mechanisms underlying disorder susceptibility. Here, we use a mouse model to demonstrate how maternal high-fat diet causes perinatal inflammation that influences sex-specific behavioral outcomes in offspring. In male high-fat diet offspring, increased macrophage toll like receptor 4 signaling results in excess phagocytosis of serotonin neurons in the developing dorsal raphe nucleus, decreasing serotonin bioavailability in the fetal and adult brain. Bulk sequencing from a large cohort of matched first trimester human fetal brain, placenta, and maternal decidua samples reveals sex-specific transcriptome-wide changes in placenta and brain tissue. Further, we find that fetal brain serotonin is significantly negatively correlated with maternal triglyceride accumulation (a proxy for dietary fat content) in male pregnancies only. These findings uncover a fundamental mechanism through which maternal diet may increase offspring susceptibility for neuropsychiatric disorder development.

scholarly journals Alteration of the Early Development Environment by Maternal Diet and the Occurrence of Autistic-like Phenotypes in Rat Offspring

2021 ◽  
Vol 22 (18) ◽  
pp. 9662
Author(s):  
Kinga Gawlińska ◽  
Dawid Gawliński ◽  
Ewelina Kowal-Wiśniewska ◽  
Małgorzata Jarmuż-Szymczak ◽  
Małgorzata Filip
Keyword(s):  
High Fat Diet ◽  
Maternal Obesity ◽  
Maternal Diet ◽  
Repetitive Behavior ◽  
Autism Spectrum ◽  
High Fat ◽  
Development Environment ◽  
Rat Offspring ◽  
Adolescent Offspring ◽  
Pregnancy And Lactation

Epidemiological and preclinical studies suggest that maternal obesity increases the risk of autism spectrum disorder (ASD) in offspring. Here, we assessed the effects of exposure to modified maternal diets limited to pregnancy and lactation on brain development and behavior in rat offspring of both sexes. Among the studied diets, a maternal high-fat diet (HFD) disturbed the expression of ASD-related genes (Cacna1d, Nlgn3, and Shank1) and proteins (SHANK1 and TAOK2) in the prefrontal cortex of male offspring during adolescence. In addition, a maternal high-fat diet induced epigenetic changes by increasing cortical global DNA methylation and the expression of miR-423 and miR-494. As well as the molecular changes, behavioral studies have shown male-specific disturbances in social interaction and an increase in repetitive behavior during adolescence. Most of the observed changes disappeared in adulthood. In conclusion, we demonstrated the contribution of a maternal HFD to the predisposition to an ASD-like phenotype in male adolescent offspring, while a protective effect occurred in females.

Cholate inhibits high-fat diet-induced hyperglycemia and obesity with acyl-CoA synthetase mRNA decrease

1997 ◽  
Vol 273 (1) ◽  
pp. E37-E45 ◽  
Author(s):  
S. Ikemoto ◽  
M. Takahashi ◽  
N. Tsunoda ◽  
K. Maruyama ◽  
H. Itakura ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Skeletal Muscles ◽  
Unsaturation Index ◽  
Sodium Cholate ◽  
Fat Absorption ◽  
High Fat ◽  
Cholesterol Accumulation ◽  
Triglyceride Accumulation ◽  
Responsive Element

The effects of sodium cholate on high-fat diet-induced hyperglycemia and obesity were investigated. Insulin resistance was estimated by measuring 2-deoxyglucose uptake in epitrochlearis muscles incubated in vitro. Addition of 0.5% cholate to high-safflower oil diet completely prevented high fat-induced hyperglycemia and obesity in C57BL/6J mice with a slight decrease of energy intake but with no inhibition of fat absorption. Furthermore, the addition of cholate decreased blood insulin levels and prevented high-fat diet-induced decrease of glucose uptake in epitrochlearis. However, there was no change in the unsaturation index of fatty acids in skeletal muscles and in GLUT-4 levels by cholate. In liver, cholate addition resulted in cholesterol accumulation and completely prevented high-fat diet-induced triglyceride accumulation. The changes of triglyceride level in the liver were paralleled to the changes of acyl-CoA synthetase (ACS) mRNA. ACS catalyzes the formation of acyl-CoA from fatty acid, and acyl-CoA is utilized for triglyceride formation in liver. ACS has a sterol-responsive element 1 in its promoter region. These data indicate that the favorable effects of cholate could be partly the result of downregulation of ACS mRNA.

scholarly journals K27Q/K29Q mutations in sphingosine kinase 1 attenuate high-fat diet induced obesity and altered glucose homeostasis in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jing Xie ◽  
Yong Shao ◽  
Jin Liu ◽  
Meilan Cui ◽  
Xiuxiao Xiao ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Diseases ◽  
Sphingosine Kinase ◽  
Protective Role ◽  
Sphingolipid Metabolism ◽  
Acid Oxidation ◽  
Sphingosine Kinase 1 ◽  
High Fat ◽  
Triglyceride Accumulation ◽  
Altered Glucose

AbstractObesity and its associated metabolic disorders are increasingly impacting public health worldwide. Sphingosine kinase 1 (Sphk1) is a critical enzyme in sphingolipid metabolism that has been implicated in various metabolic syndromes. In this study, we developed a mouse model constitutively expressing pseudoacetylated mouse Sphk1 (QSPHK1) to study its role in regulating glucose and lipid metabolism. The results showed that QSPHK1 mice gained less body weight than wide type (WT) mice on a high-fat diet, and QSPHK1 mice had improved glucolipid metabolism and insulin. Moreover, QSPHK1 mice had alleviated hepatic triglyceride accumulation and had high-fat-diet-induced hepatic steatosis that occurred as a result of reduced lipogenesis and enhanced fatty acid oxidation, which were mediated by the AMPK/ACC axis and the FGF21/adiponectin axis. Collectively, this study provided evidence that the K27Q/K29Q mutations of Sphk1 could have a protective role in preventing obesity and the related metabolic diseases. Hence, our results contribute to further understanding of the biological functions of Sphk1, which has great pharmaceutical implications.

Relationship of maternal high-fat diet during pregnancy and lactation to offspring health

2020 ◽  
Author(s):  
Kinga Gawlińska ◽  
Dawid Gawliński ◽  
Małgorzata Filip ◽  
Edmund Przegaliński
Keyword(s):  
High Fat Diet ◽  
Maternal Nutrition ◽  
System Development ◽  
Maternal Diet ◽  
Nervous System Development ◽  
High Fat ◽  
Preclinical Research ◽  
Intrauterine Development ◽  
Increased Risk ◽  
Pregnancy And Lactation

Abstract A balanced maternal diet is essential for proper fetal development, and the consumption of a nutritionally inadequate diet during intrauterine development and early childhood is associated with a significantly increased risk of metabolic and brain disorders in offspring. The current literature indicates that maternal exposure to a high-fat diet exerts an irreversible influence on the general health of the offspring. This review of preclinical research examines the relationship between a maternal high-fat diet during pregnancy or lactation and metabolic changes, molecular alterations in the brain, and behavioral disorders in offspring. Animal models indicate that offspring exposed to a maternal high-fat diet during pregnancy and lactation manifest increased depressive-like and aggressive behaviors, reduced cognitive development, and symptoms of metabolic syndrome. Recently, epigenetic and molecular studies have shown that maternal nutrition during pregnancy and the suckling period modifies the development of neurotransmitter circuits and many other factors important to central nervous system development. This finding confirms the importance of a balanced maternal diet for the health of offspring.

scholarly journals Maternal high-fat diet during pregnancy and lactation reduces the appetitive behavioral component in female offspring tested in a brief-access taste procedure

2014 ◽  
Vol 306 (7) ◽  
pp. R499-R509 ◽  
Author(s):  
Yada Treesukosol ◽  
Bo Sun ◽  
Alexander A. Moghadam ◽  
Nu-Chu Liang ◽  
Kellie L. Tamashiro ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
High Fat Diet ◽  
Corn Oil ◽  
Sucrose Concentration ◽  
Maternal Diet ◽  
Female Offspring ◽  
Chow Diet ◽  
High Fat ◽  
Endogenous Opioid ◽  
Pregnancy And Lactation

Maternal high-fat diet appears to disrupt several energy balance mechanisms in offspring. Here, female offspring from dams fed a high-fat diet (HF) did not significantly differ in body weight compared with those fed chow (CHOW), when weaned onto chow diet. Yet when presented with both a chow and a high-fat diet, high-fat intake was significantly higher in HF compared with CHOW offspring. To assess taste-based responsiveness, offspring (12 wk old) were tested in 30-min sessions (10-s trials) to a sucrose concentration series in a brief-access taste test. Compared with CHOW, the HF offspring initiated significantly fewer trials but did not significantly differ in the amount of concentration-dependent licking. Thus, rather than affect lick response (consummatory), maternal diet affects spout approach (appetitive), which may be attributed to motivation-related mechanisms. Consistent with this possibility, naltrexone, an opioid receptor antagonist, further reduced trial initiation, but not licking in both groups. With naltrexone administration, the group difference in trial initiation was no longer evident, suggesting differences in endogenous opioid activity between the two groups. Relative expression of μ-opioid receptor in the ventral tegmental area was significantly lower in HF rats. When trial initiation was not required in one-bottle intake tests, no main effect of maternal diet on the intake of sucrose and corn oil emulsions was observed. Thus, the maternal high-fat diet-induced difference in diet preference is not likely due to changes in the sensory orosensory component of the taste stimulus but may depend on alterations in satiety signals or absorptive mechanisms.

scholarly journals A long-term maternal diet intervention is necessary to avoid the obesogenic effect of maternal high-fat diet in the offspring

2018 ◽  
Vol 62 ◽  
pp. 210-220 ◽  
Author(s):  
Huiting Xu ◽  
Qiang Fu ◽  
Yi Zhou ◽  
Chengbin Xue ◽  
Patrick Olson ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Maternal Diet ◽  
High Fat ◽  
Diet Intervention

scholarly journals Effects of Maternal Resveratrol on Maternal High-Fat Diet/Obesity with or without Postnatal High-Fat Diet

2020 ◽  
Vol 21 (10) ◽  
pp. 3428 ◽  
Author(s):  
Mei-Hsin Hsu ◽  
Jiunn-Ming Sheen ◽  
I-Chun Lin ◽  
Hong-Ren Yu ◽  
Mao-Meng Tiao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Cognitive Impairment ◽  
Adult Male ◽  
High Fat Diet ◽  
Dorsal Hippocampus ◽  
Fetal Brain ◽  
Male Offspring ◽  
High Fat ◽  
Peripheral Insulin Resistance

To examine the effects of maternal resveratrol in rats borne to dams with gestational high-fat diet (HFD)/obesity with or without postnatal high-fat diet. We first tested the effects of maternal resveratrol intake on placenta and male fetus brain in rats borne to dams with gestational HFD/obesity. Then, we assessed the possible priming effect of a subsequent insult, male offspring were weaned onto either a rat chow or a HFD. Spatial learning and memory were assessed by Morris water maze test. Blood pressure and peripheral insulin resistance were examined. Maternal HFD/obesity decreased adiponectin, phosphorylation alpha serine/threonine-protein kinase (pAKT), sirtuin 1 (SIRT1), and brain-derived neurotrophic factor (BDNF) in rat placenta, male fetal brain, and adult male offspring dorsal hippocampus. Maternal resveratrol treatment restored adiponectin, pAKT, and BDNF in fetal brain. It also reduced body weight, peripheral insulin resistance, increased blood pressure, and alleviated cognitive impairment in adult male offspring with combined maternal HFD and postnatal HFD. Maternal resveratrol treatment restored hippocampal pAKT and BDNF in rats with combined maternal HFD and postnatal HFD in adult male offspring dorsal hippocampus. Maternal resveratrol intake protects the fetal brain in the context of maternal HFD/obesity. It effectively reduced the synergistic effects of maternal HFD/obesity and postnatal HFD on metabolic disturbances and cognitive impairment in adult male offspring. Our data suggest that maternal resveratrol intake may serve as an effective therapeutic strategy in the context of maternal HFD/obesity.

scholarly journals Anti-adipogenic and anti-obesity activities of purpurin in 3T3-L1 preadipocyte cells and in mice fed a high-fat diet

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Woo Nam ◽  
Seok Hyun Nam ◽  
Sung Phil Kim ◽  
Carol Levin ◽  
Mendel Friedman
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Biological Activities ◽  
The Body ◽  
High Fat ◽  
In Vivo Models ◽  
Triglyceride Accumulation ◽  
In Cells

Abstract Background The body responds to overnutrition by converting stem cells to adipocytes. In vitro and in vivo studies have shown polyphenols and other natural compounds to be anti-adipogenic, presumably due in part to their antioxidant properties. Purpurin is a highly antioxidative anthraquinone and previous studies on anthraquinones have reported numerous biological activities in cells and animals. Anthraquinones have also been used to stimulate osteoblast differentiation, an inversely-related process to that of adipocyte differentiation. We propose that due to its high antioxidative properties, purpurin administration might attenuate adipogenesis in cells and in mice. Methods Our study will test the effect purpurin has on adipogenesis using both in vitro and in vivo models. The in vitro model consists of tracking with various biomarkers, the differentiation of pre-adipocyte to adipocytes in cell culture. The compound will then be tested in mice fed a high-fat diet. Murine 3T3-L1 preadipocyte cells were stimulated to differentiate in the presence or absence of purpurin. The following cellular parameters were measured: intracellular reactive oxygen species (ROS), membrane potential of the mitochondria, ATP production, activation of AMPK (adenosine 5′-monophosphate-activated protein kinase), insulin-induced lipid accumulation, triglyceride accumulation, and expression of PPARγ (peroxisome proliferator activated receptor-γ) and C/EBPα (CCAAT enhancer binding protein α). In vivo, mice were fed high fat diets supplemented with various levels of purpurin. Data collected from the animals included anthropometric data, glucose tolerance test results, and postmortem plasma glucose, lipid levels, and organ examinations. Results The administration of purpurin at 50 and 100 μM in 3T3-L1 cells, and at 40 and 80 mg/kg in mice proved to be a sensitive range: the lower concentrations affected several measured parameters, whereas at the higher doses purpurin consistently mitigated biomarkers associated with adipogenesis, and weight gain in mice. Purpurin appears to be an effective antiadipogenic compound. Conclusion The anthraquinone purpurin has potent in vitro anti-adipogenic effects in cells and in vivo anti-obesity effects in mice consuming a high-fat diet. Differentiation of 3T3-L1 cells was dose-dependently inhibited by purpurin, apparently by AMPK activation. Mice on a high-fat diet experienced a dose-dependent reduction in induced weight gain of up to 55%.

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 Maternal High-Fat Diet Exposure During Gestation and Lactation Affects Intestinal Development in Suckling Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Monika Słupecka-Ziemilska ◽  
Paulina Grzesiak ◽  
Paweł Kowalczyk ◽  
Piotr Wychowański ◽  
Jarosław Woliński
Keyword(s):  
High Fat Diet ◽  
Metabolic Diseases ◽  
Maternal Diet ◽  
Dependent Manner ◽  
Intestinal Development ◽  
High Fat ◽  
Rat Pups ◽  
Diet Induced Obesity ◽  
Cholinergic Signaling ◽  
And Function

Maternal health and diet influence metabolic status and play a crucial role in the development of metabolic function in offspring and their susceptibility to metabolic diseases in adulthood. The pathogenesis of various metabolic disorders is often associated with impairment in intestinal structure and function. Thus, the aim of the current study was to determine the effects of maternal exposure to a high fat diet (HFD), during gestation and lactation, on small intestinal growth and maturation in rat pups at 21 days old. Female, Wistar Han rats were fed either a breeding diet (BD) or high fat diet (HFD), from mating until the 21st day of lactation. Maternal HFD exposure increased body weight, BMI and adiposity. Compared to the maternal BD, HFD exposure influenced small intestine histomorphometry in a segment-dependent manner, changed the activity of brush border enzymes and had an impact on intestinal contractility via changes in cholinergic signaling. Moreover, offspring from the maternal HFD group had upregulated mRNA expression of cyclooxygenase (COX)-2, which plays a role in the inflammatory process. These results suggest that maternal HFD exposure, during gestation and lactation, programs the intestinal development of the offspring in a direction toward obesity as observed changes are also commonly reported in models of diet-induced obesity. The results also highlight the importance of maternal diet preferences in the process of developmental programming of metabolic diseases.

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