Maternal Manganese Restriction Increases Susceptibility to High-Fat Diet-Induced Dyslipidemia and Altered Adipose Function in WNIN Male Rat Offspring

Growthin uterois largely a reflection of nutrient and oxygen supply to the foetus. We studied the effects of Mn restrictionper se, maternal Mn restriction, and postnatal high-fat feeding in modulating body composition, lipid metabolism and adipocyte function in Wistar/NIN (WNIN) rat offspring. Female weanling, WNIN rats receivedad libitumfor 4 months, a control or Mn-restricted diet and were mated with control males. Some restricted mothers were rehabilitated with control diet from conception (MnRC) or parturition (MnRP), and their offspring were raised on control diet. Some restricted offspring were weaned onto control diet (MnRW), while others continued on restricted diet throughout (MnR). A set of offspring from each group was fed high-fat diet from 9 months onwards. Body composition, adipocytes function, and lipid metabolism were monitored in male rat offspring at regular intervals. Maternal manganese restriction increased the susceptibility of the offspring to high-fat-induced adiposity, dyslipidaemia, and a proinflammatory state but did not affect their glycemic or insulin status.

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Perinatal maternal high-fat diet promotes alterations in hepatic lipid metabolism and resistance to the hypolipidemic effect of fish oil in adolescent rat offspring

Molecular Nutrition & Food Research ◽

10.1002/mnfr.201600171 ◽

2016 ◽

Vol 60 (11) ◽

pp. 2493-2504 ◽

Cited By ~ 13

Author(s):

Lorraine S. Oliveira ◽

Luana L. Souza ◽

Aline F. P. Souza ◽

Aline Cordeiro ◽

George E. G. Kluck ◽

...

Keyword(s):

Lipid Metabolism ◽

Fish Oil ◽

High Fat Diet ◽

Hypolipidemic Effect ◽

High Fat ◽

Hepatic Lipid Metabolism ◽

Hepatic Lipid ◽

Rat Offspring

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Perinatal High-Fat Diet Influences Ozone-Induced Responses on Pulmonary Oxidant Status and the Molecular Control of Mito-Phagy in Female Rat Offspring

International Journal of Molecular Sciences ◽

10.3390/ijms22147551 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7551

Author(s):

Sven H. Rouschop ◽

Samantha J. Snow ◽

Urmila P. Kodavanti ◽

Marie-José Drittij ◽

Lou M. Maas ◽

...

Keyword(s):

Oxidative Phosphorylation ◽

High Fat Diet ◽

Control Diet ◽

Ozone Exposure ◽

Female Rat ◽

Induced Responses ◽

High Fat ◽

Molecular Control ◽

Rat Offspring ◽

Oxidant Status

Previous research has shown that a perinatal obesogenic, high-fat diet (HFD) is able to exacerbate ozone-induced adverse effects on lung function, injury, and inflammation in offspring, and it has been suggested that mitochondrial dysfunction is implicated herein. The aim of this study was to investigate whether a perinatal obesogenic HFD affects ozone-induced changes in offspring pulmonary oxidant status and the molecular control of mitochondrial function. For this purpose, female Long-Evans rats were fed a control diet or HFD before and during gestation, and during lactation, after which the offspring were acutely exposed to filtered air or ozone at a young-adult age (forty days). Directly following this exposure, the offspring lungs were examined for markers related to oxidative stress; oxidative phosphorylation; and mitochondrial fusion, fission, biogenesis, and mitophagy. Acute ozone exposure significantly increased pulmonary oxidant status and upregulated the molecular machinery that controls receptor-mediated mitophagy. In female offspring, a perinatal HFD exacerbated these responses, whereas in male offspring, responses were similar for both diet groups. The expression of the genes and proteins involved in oxidative phosphorylation and mitochondrial biogenesis, fusion, and fission was not affected by ozone exposure or perinatal HFD. These findings suggest that a perinatal HFD influences ozone-induced responses on pulmonary oxidant status and the molecular control of mitophagy in female rat offspring.

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Flavonoids from Mulberry Leaves Alleviate Lipid Dysmetabolism in High Fat Diet-Fed Mice: Involvement of Gut Microbiota

Microorganisms ◽

10.3390/microorganisms8060860 ◽

2020 ◽

Vol 8 (6) ◽

pp. 860 ◽

Cited By ~ 1

Author(s):

Yinzhao Zhong ◽

Bo Song ◽

Changbing Zheng ◽

Shiyu Zhang ◽

Zhaoming Yan ◽

...

Keyword(s):

Acetic Acid ◽

Lipid Metabolism ◽

Gut Microbiota ◽

High Fat Diet ◽

Control Diet ◽

Liver Steatosis ◽

High Fat ◽

Acetic Acid Production ◽

Mulberry Leaves ◽

Brown Adipose

Here, we investigated the roles and mechanisms of flavonoids from mulberry leaves (FML) on lipid metabolism in high fat diet (HFD)-fed mice. ICR mice were fed either a control diet (Con) or HFD with or without FML (240 mg/kg/day) by oral gavage for six weeks. FML administration improved lipid accumulation, alleviated liver steatosis and the whitening of brown adipose tissue, and improved gut microbiota composition in HFD-fed mice. Microbiota transplantation from FML-treated mice alleviated HFD-induced lipid metabolic disorders. Moreover, FML administration restored the production of acetic acid in HFD-fed mice. Correlation analysis identified a significant correlation between the relative abundances of Bacteroidetes and the production of acetic acid, and between the production of acetic acid and the weight of selected adipose tissues. Overall, our results demonstrated that in HFD-fed mice, the lipid metabolism improvement induced by FML administration might be mediated by gut microbiota, especially Bacteroidetes-triggered acetic acid production.

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Abstract 58: Angiotensin-(1-7) Mas Receptors In The Arcuate Nucleus Of The Hypothalamus Protect Against High Fat Diet-induced Insulin Resistance In Female Mice

Hypertension ◽

10.1161/hyp.78.suppl_1.58 ◽

2021 ◽

Vol 78 (Suppl_1) ◽

Author(s):

Darren Mehay ◽

Sarah Bingaman ◽

Yuval Silberman ◽

Amy Arnold

Keyword(s):

Body Composition ◽

Insulin Sensitivity ◽

Energy Balance ◽

Glucose Tolerance ◽

High Fat Diet ◽

Metabolic Regulation ◽

Arcuate Nucleus ◽

Control Diet ◽

High Fat ◽

Metabolic Outcomes

Angiotensin (Ang)-(1-7) is a protective hormone of the renin-angiotensin system that improves insulin sensitivity, glucose tolerance, and energy balance in obese rodents. Our recent findings suggest that Ang-(1-7) activates mas receptors (MasR) in the arcuate nucleus of the hypothalamus (ARC), a brain region critical to control of energy balance and glucose homeostasis, to induce these positive metabolic effects. The distribution of MasR in the ARC and their role in metabolic regulation, however, is unknown. We hypothesized: (1) MasR are expressed in the ARC; and (2) deletion of ARC MasR leads to worsened metabolic outcomes following high fat diet (HFD). To test this, male and female C57Bl/6J mice were fed a 60% HFD or matched control diet ad libitum for 12 weeks. RNAscope in situ hybridization was performed on coronal ARC sections in rostral-middle-caudal regions to determine percentage of MasR positive neurons (n=5/group). In a second experiment, we assessed body composition and insulin and glucose tolerance in transgenic mice with deletion of MasR in ARC neurons (MasR-flox with AAV5-hsyn-GFP-Cre). RNAscope revealed a wide distribution on MasR-positive cells throughout the rostral to caudal extent of the ARC. The average percentage of MasR positive neurons was increased in females versus males, with HFD tending to increase MasR expression in both sexes (control diet male: 11±2; control diet female: 17±3; HFD male: 15±5; HFD female: 24±2; p sex : 0.030; p diet : 0.066; p int : 0.615; two-way ANOVA). Deletion of MasR in ARC neurons worsened insulin sensitivity in HFD but not control diet females (area under the curve for change in glucose from baseline: -1989±1359 HFD control virus vs. 2530±1762 HFD Cre virus; p=0.016), while fasting glucose, glucose tolerance, and body composition did not change. There was no effect of ARC MasR deletion on metabolic outcomes in control diet or HFD male mice. These findings suggest females have more MasR positive neurons in the ARC compared to males, which may be a sex-specific protective mechanism for glucose homeostasis. While further studies are needed to explore the role of ARC MasR in metabolic regulation, these findings support targeting Ang-(1-7) as an innovative strategy in obesity.

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SP065DIMETHYL FUMARATE TREATMENT PREVENTS PRENATAL DEXAMETHASONE AND POSTNATAL HIGH FAT DIET INDUCED PROGRAMMED HYPERTENSION IN MALE RAT OFFSPRING

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfy104.sp065 ◽

2018 ◽

Vol 33 (suppl_1) ◽

pp. i367-i367

Author(s):

You-Lin Tain ◽

Chien-Ning Hsu

Keyword(s):

High Fat Diet ◽

Male Rat ◽

High Fat ◽

Rat Offspring

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Effect of a high-fat diet on the incorporation of stored triacylglycerol into hepatic VLDL

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1992.263.4.e615 ◽

1992 ◽

Vol 263 (4) ◽

pp. E615-E623 ◽

Cited By ~ 3

Author(s):

O. L. Francone ◽

G. Griffaton ◽

A. D. Kalopissis

Keyword(s):

Endoplasmic Reticulum ◽

High Fat Diet ◽

Lipid Droplets ◽

Control Diet ◽

Oxidation Products ◽

High Fat ◽

Very Low Density Lipoproteins ◽

Total Utilization ◽

Fat Feeding

Triacylglycerol (TG) stored in cytoplasmic lipid droplets of hepatocytes was labeled by in vivo [1-(14)C]oleic acid injection to study the effect of a high-fat diet on its incorporation into very-low-density lipoproteins (VLDL). Compared with the control diet, hepatocytes of fat-fed rats 1) contained 7.6 times more cytoplasmic (floating fat) TG and 1.9 times more endoplasmic reticulum (microsomal) TG; 2) had 8 and 6 times lower TG specific activities in cytoplasm and endoplasmic reticulum, respectively; 3) incorporated 22% less 14C label into hepatocyte esterified lipids (TG, cholesterol, phospholipid); 4) secreted 48 and 33% less radioactive and total VLDL-TG, respectively; 5) oxidized more cytoplasmic TG-fatty acid (FA); and 6) showed a 50% decreased total utilization of stored TG-FA. With both diets, the lysosomal inhibitor chloroquine concomitantly decreased productions of labeled VLDL-TG, CO2, and acid-soluble oxidation products. The decreased incorporation of stored TG into VLDL-TG appreciably contributes to the overall inhibition of hepatic VLDL secretion by fat feeding. It appears to be related to the decreased mobilization rate of stored TG and its increased channelling toward oxidation.

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