The absence of lactation after pregnancy induces long-term lipid accumulation in maternal liver of mice

Life Sciences ◽  
2019 ◽  
Vol 217 ◽  
pp. 261-270
Author(s):  
Julia Modesto Vicente ◽  
Caio Jordão Teixeira ◽  
Junia Carolina Santos-Silva ◽  
Dailson Nogueira de Souza ◽  
Natália Tobar ◽  
...  
2016 ◽  
Vol 36 (4) ◽  
pp. 349-358 ◽  
Author(s):  
Xiaoyu Zhang ◽  
Juliang Qin ◽  
Yihan Zhao ◽  
Jueping Shi ◽  
Rong Lan ◽  
...  

Author(s):  
Xinhui Guo ◽  
Wei Xue ◽  
Yujiao Wang ◽  
Jiangang Zhang ◽  
Qinghong Meng ◽  
...  

Resveratrol (RSV) as a naturally occurring small molecule has been reported to benefit the cardiovascular system through a dietary supplementation. However, the relevant genetic regulation by RSV has been uncovered. This work is solely to investigate how RSV increases a fecal excretion of total sterols of HF fed C57BL/6J mice to block lipid accumulation in vivo through regulation of PPRAa, HMG-CoA-R, CYP7A1, LDL-R and ABCG5 genes. The results showed that RSV significantly improved the excretion of total sterols through up regulation of mRNA expressions of PPARa, CYP7A1, LDL-R, ABCG5 and down regulation of HMG-CoA-R. These data indicate that beneficial effects from RSV were associated with the favorably altered expression of hepatic and large intestine genes in HF fed mice.


2018 ◽  
Vol 121 (2) ◽  
pp. 121-129 ◽  
Author(s):  
Sarah C. Cottin ◽  
Guenievre Roussel ◽  
Lorraine Gambling ◽  
Helen E. Hayes ◽  
Valerie J. Currie ◽  
...  

AbstractFe deficiency is relatively common in pregnancy and has both short- and long-term consequences. However, little is known about the effect on the metabolism of other micronutrients. A total of fifty-four female rats were fed control (50 mg Fe/kg) or Fe-deficient diets (7·5 mg/kg) before and during pregnancy. Maternal liver, placenta and fetal liver were collected at day 21 of pregnancy for Cu and Zn analysis and to measure expression of the major genes of Cu and Zn metabolism. Cu levels increased in the maternal liver (P=0·002) and placenta (P=0·018) of Fe-deficient rats. Zn increased (P<0·0001) and Cu decreased (P=0·006) in the fetal liver. Hepatic expression of the Cu chaperones antioxidant 1 Cu chaperone (P=0·042) and cytochrome c oxidase Cu chaperone (COX17, P=0·020) decreased in the Fe-deficient dams, while the expression of the genes of Zn metabolism was unaltered. In the placenta, Fe deficiency reduced the expression of the chaperone for superoxide dismutase 1, Cu chaperone for superoxide dismutase (P=0·030), ceruloplasmin (P=0·042) and Zn transport genes, ZRT/IRT-like protein 4 (ZIP4, P=0·047) and Zn transporter 1 (ZnT1, P=0·012). In fetal liver, Fe deficiency increased COX17 (P=0·020), ZRT/IRT-like protein 14 (P=0·036) and ZnT1 (P=0·0003) and decreased ZIP4 (P=0·004). The results demonstrate that Fe deficiency during pregnancy has opposite effects on Cu and Zn levels in the fetal liver. This may, in turn, alter metabolism of these nutrients, with consequences for development in the fetus and the neonate.


2019 ◽  
Author(s):  
Anna Tsara ◽  
Narjes Nasiri-Ansari ◽  
Georgios K Dimitriadis ◽  
Stamatis Theocharis ◽  
Angeliki Karapanagiotil ◽  
...  

2016 ◽  
Vol 38 (6) ◽  
pp. 458-468 ◽  
Author(s):  
Francesca M. Notarangelo ◽  
Robert Schwarcz

Stressful events during pregnancy adversely affect brain development and may increase the risk of psychiatric disorders later in life. Early changes in the kynurenine (KYN) pathway (KP) of tryptophan (TRP) degradation, which contains several neuroactive metabolites, including kynurenic acid (KYNA), 3-hydroxykynurenine (3-HK), and quinolinic acid (QUIN), may constitute a molecular link between prenatal stress and delayed pathological consequences. To begin testing this hypothesis experimentally, we examined the effects of a 2-h restraint stress on KP metabolism in pregnant FVB/N mice on gestational day 17. TRP, KYN, KYNA, 3-HK, and QUIN levels were measured in maternal and fetal plasma and brain, as well as in the placenta, immediately after stress termination and 2 h later. In the same animals, we determined the activity of TRP 2,3-dioxygenase (TDO) in the maternal liver and in the placenta. Compared to unstressed controls, mostly transient changes in KP metabolism were observed in all of the tissues examined. Specifically, stress caused significant elevations of KYNA levels in the maternal plasma, placenta, and fetal brain, and also resulted in increased levels of TRP and KYN in the placenta, fetal plasma, and fetal brain. In contrast, 3-HK and QUIN levels remained unchanged from control values in all tissues at any time point. In the maternal liver, TDO activity was increased 2 h after stress cessation. Taken together, these findings indicate that an acute stress during the late gestational period preferentially affects the KYNA branch of KP metabolism in the fetal brain. Possible long-term consequences for postnatal brain development and pathology remain to be examined.


2021 ◽  
Vol 22 (20) ◽  
pp. 10937
Author(s):  
Anna F. Bekebrede ◽  
Thirza van Deuren ◽  
Walter J. J. Gerrits ◽  
Jaap Keijer ◽  
Vincent C. J. de Boer

Butyrate is considered the primary energy source of colonocytes and has received wide attention due to its unique health benefits. Insight into the mechanistic effects of butyrate on cellular and metabolic function relies mainly on research in in-vitro-cultured cells. However, cells in culture differ from those in vivo in terms of metabolic phenotype and nutrient availability. For translation, it is therefore important to understand the impact of different nutrients on the effects of butyrate. We investigated the metabolic consequences of butyrate exposure under various culturing conditions, with a focus on the interaction between butyrate and glucose. To investigate whether the effects of butyrate were different between cell­­s with high and low mitochondrial capacity, we cultured HT29 cells under either low- (0.5 mM) or high- (25 mM) glucose conditions. Low-glucose culturing increased the mitochondrial capacity of HT29 cells compared to high-glucose (25 mM) cultured HT29 cells. Long-term exposure to butyrate did not alter mitochondrial bioenergetics, but it decreased glycolytic function, regardless of glucose availability. In addition, both high- and low-glucose-grown HT29 cells showed increased lipid droplet accumulation following long-term butyrate exposure. Acute exposure of cultured cells (HT29 and Caco-2) to butyrate increased their oxygen consumption rate (OCR). A simultaneous decrease in extracellular acidification rate (ECAR) was observed. Furthermore, in the absence of glucose, OCR did not increase in response to butyrate. These results lead us to believe that butyrate itself was not responsible for the observed increase in OCR, but, instead, butyrate stimulated pyruvate flux into mitochondria. Indeed, blocking of the mitochondrial pyruvate carrier prevented a butyrate-induced increase in oxygen consumption. Taken together, our results indicate that butyrate itself is not oxidized in cultured cells but instead alters pyruvate flux and induces lipid accumulation.


2011 ◽  
Vol 64 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Akane Noguchi ◽  
Akiho Moriyama ◽  
Shigeru Mineo ◽  
Yoko Fujisawa ◽  
Marika Sugiyama ◽  
...  
Keyword(s):  

Author(s):  
Hopper Wade ◽  
Veria Spiro ◽  
Glosser Logan ◽  
Garg Anu ◽  
Awad Mohammed T ◽  
...  

Xanthomas are benign cutaneous manifestations of extracellular lipid accumulation. Eruptive xanthoma is characterized by the acute, widespread presentation of a papular rash and usually involves the back, buttocks, and extremities. Eruptive xanthoma is associated with hyperlipidemia, hypertriglyceridemia, and an increased long-term risk of atherosclerotic cardiovascular disease. We present a case of eruptive xanthoma accompanied by severe hypertriglyceridemia (10,164 mg/dL) in which the course of the disease was reversed following implementation of lipid-lowering pharmacotherapy.


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