scholarly journals Maternal obesity alters placental lysophosphatidylcholines, lipid storage, and the expression of genes associated with lipid metabolism‡

2020 ◽  
Author(s):  
Katie L Bidne ◽  
Alana L Rister ◽  
Andrea R McCain ◽  
Brianna D Hitt ◽  
Eric D Dodds ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Maternal Obesity ◽  
Nutrient Transport ◽  
Digital Pcr ◽  
Lipid Profiles ◽  
Lipid Storage ◽  
Acid Oxidation ◽  
Expression Of Genes

Abstract Dyslipidemia is a characteristic of maternal obesity and previous studies have demonstrated abnormalities in fatty acid oxidation and storage in term placentas. However, there is little information about the effect of pre-pregnancy obesity on placental lipid metabolism during early pregnancy. The objective of this study was to determine the relationship between lipid profiles and markers of metabolism in placentas from obese and lean dams at midgestation. Mice were fed a western diet (WD) or normal diet (ND) and lysophosphatidylcholines (LPCs) and/or phosphatidylcholines (PCs) were measured in dam circulation and placenta sections using liquid chromatography–tandem mass spectrometry and mass spectrometry imaging, respectively. In WD dam, circulating LPCs containing 16:1, 18:1, 20:0, and 20:3 fatty acids were increased and 18:2 and 20:4 were decreased. In WD placenta from both sexes, LPC 18:1 and PC 36:1 and 38:3 were increased. Furthermore, there were moderate to strong correlations between LPC 18:1, PC 36:1, and PC 38:3. Treatment-, spatial-, and sex-dependent differences in LPC 20:1 and 20:3 were also detected. To identify genes that may regulate diet-dependent differences in placenta lipid profiles, the expression of genes associated with lipid metabolism and nutrient transport was measured in whole placenta and isolated labyrinth using droplet digital PCR and Nanostring nCounter assays. Several apolipoproteins were increased in WD placentas. However, no differences in nutrient transport or fatty acid metabolism were detected. Together, these data indicate that lipid storage is increased in midgestation WD placentas, which may lead to lipotoxicity, altered lipid metabolism and transport to the fetus later in gestation.

scholarly journals Leptin Regulates Peripheral Lipid Metabolism Primarily through Central Effects on Food Intake

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5432-5439 ◽  
Author(s):  
Xavier Prieur ◽  
Y. C. Loraine Tung ◽  
Julian L. Griffin ◽  
I. Sadaf Farooqi ◽  
Stephen O'Rahilly ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Liver Weight ◽  
Metabolic Effects ◽  
Acid Oxidation ◽  
Mediated Effects ◽  
Expression Of Genes ◽  
Acyl Coenzyme A

The metabolic effects of leptin may involve both centrally and peripherally mediated actions with a component of the central actions potentially independent of alterations in food intake. Ob/ob mice have significant abnormalities in lipid metabolism, correctable by leptin administration. We used ob/ob mice to study the relative importance of the subtypes of actions of leptin (central vs. peripheral; food intake dependent vs. independent) on lipid metabolism. Mice were treated for 3 d with leptin, either centrally [intracerebroventricular (icv)] or peripherally (ip), and compared with mice pair-fed to the leptin-treated mice (PF) and with ad libitum-fed controls (C). All treatment groups (icv, ip, PF) showed indistinguishable changes in liver weight; hepatic steatosis; hepatic lipidemic profile; and circulating free fatty acids, triglycerides, and cholesterol lipoprotein profile. Changes in the expression of genes involved in lipogenesis and fatty acid oxidation in liver, muscle, and white fat were broadly similar in ip, icv, and PF groups. Leptin (both icv and ip) stimulated expression of both mitochondrial and peroxisomal acyl-coenzyme A oxidase (liver) and peroxisomal proliferator-activated receptor-α (skeletal muscle) to an extent not replicated by pair feeding. Leptin had profound effects on peripheral lipid metabolism, but the majority were explained by its effects on food intake. Leptin had additional centrally mediated effects to increase the expression of a limited number of genes concerned with fatty acid oxidation. Whereas we cannot exclude direct peripheral effects of leptin on certain aspects of lipid metabolism, we were unable to detect any such effects on the parameters measured in this study.

scholarly journals Effects of dietary lipid level on growth, fatty acid profiles, antioxidant capacity and expression of genes involved in lipid metabolism in juvenile swimming crab, Portunus trituberculatus

2019 ◽  
Vol 123 (2) ◽  
pp. 149-160 ◽  
Author(s):  
Peng Sun ◽  
Min Jin ◽  
Lefei Jiao ◽  
Óscar Monroig ◽  
Juan Carlos Navarro ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Lipid Level ◽  
Dietary Lipid ◽  
The Other ◽  
Acid Oxidation ◽  
Swimming Crab ◽  
Lipid Levels ◽  
Expression Of Genes ◽  
Dietary Lipid Level

AbstractThe regulation of lipogenesis and lipolysis mechanisms related to consumption of lipid has not been studied in swimming crab. The aims of the present study were to evaluate the effects of dietary lipid levels on growth, enzymes activities and expression of genes of lipid metabolism in hepatopancreas of juvenile swimming crab. Three isonitrogenous diets were formulated to contain crude lipid levels at 5·8, 9·9 and 15·1 %. Crabs fed the diet containing 15·1 % lipid had significantly lower growth performance and feed utilisation than those fed the 5·8 and 9·9 % lipid diets. Crabs fed 5·8 % lipid had lower malondialdehyde concentrations in the haemolymph and hepatopancreas than those fed the other diets. Highest glutathione peroxidase in haemolymph and superoxide dismutase in hepatopancreas were observed in crabs fed 5·8 % lipid. The lowest fatty acid synthase and glucose 6-phosphate dehydrogenase activities in hepatopancreas were observed in crabs fed 15·1 % lipid, whereas crabs fed 5·8 % lipid had lower carnitine palmitoyltransferase-1 activity than those fed the other diets. Crabs fed 15·1 % lipid showed lower hepatopancreas expression of genes involved in long-chain-PUFA biosynthesis, lipoprotein clearance, fatty acid uptake, fatty acid oxidation, lipid anabolism and lipid catabolism than those fed the other diets, whereas expression of some genes of lipoprotein assembly and fatty acid oxidation was up-regulated compared with crabs fed 5·8 % lipid. Overall, high dietary lipid level can inhibit growth, reduce antioxidant enzyme activities and influence lipid metabolic pathways to regulate lipid deposition in crab.

scholarly journals Interplay between Thyroid Hormones and Stearoyl-CoA Desaturase 1 in the Regulation of Lipid Metabolism in the Heart

2020 ◽  
Vol 22 (1) ◽  
pp. 109
Author(s):  
Adam Olichwier ◽  
Volodymyr V. Balatskyi ◽  
Marcin Wolosiewicz ◽  
James M. Ntambi ◽  
Pawel Dobrzyn
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Thyroid Hormones ◽  
Fatty Acid Oxidation ◽  
Monounsaturated Fatty Acids ◽  
Thyroid Stimulating Hormone ◽  
Acid Oxidation ◽  
Expression Of Genes ◽  
Triglyceride Content ◽  
Stearoyl Coa Desaturase

Stearoyl-CoA desaturase 1 (SCD1), an enzyme that is involved in the biosynthesis of monounsaturated fatty acids, induces the reprogramming of cardiomyocyte metabolism. Thyroid hormones (THs) activate both lipolysis and lipogenesis. Many genes that are involved in lipid metabolism, including Scd1, are regulated by THs. The present study used SCD1 knockout (SCD1−/−) mice to test the hypothesis that THs are important factors that mediate the anti-steatotic effect of SCD1 downregulation in the heart. SCD1 deficiency decreased plasma levels of thyroid-stimulating hormone and thyroxine and the expression of genes that regulate intracellular TH levels (i.e., Slc16a2 and Dio1-3) in cardiomyocytes. Both hypothyroidism and SCD1 deficiency affected genomic and non-genomic TH pathways in the heart. SCD1 deficiency is known to protect mice from genetic- or diet-induced obesity and decrease lipid content in the heart. Interestingly, hypothyroidism increased body adiposity and triglyceride and diacylglycerol levels in the heart in SCD1−/− mice. The accumulation of triglycerides in cardiomyocytes in SCD1−/− hypothyroid mice was caused by the activation of lipogenesis, which likely exceeded the upregulation of lipolysis and fatty acid oxidation. Lipid accumulation was also observed in the heart in wildtype hypothyroid mice compared with wildtype control mice, but this process was related to a reduction of triglyceride lipolysis and fatty acid oxidation. We also found that simultaneous SCD1 and deiodinase inhibition increased triglyceride content in HL-1 cardiomyocytes, and this process was related to the downregulation of lipolysis. Altogether, the present results suggest that THs are an important part of the mechanism of SCD1 in cardiac lipid utilization and may be involved in the upregulation of energetic metabolism that is associated with SCD1 deficiency.

Placental Accumulation of Triacylglycerols in Gestational Diabetes Mellitus and Its Association with Altered Fetal Growth are Related to the Differential Expressions of Proteins of Lipid Metabolism

2020 ◽  
Author(s):  
Manoharan Balachandiran ◽  
Zachariah Bobby ◽  
Gowri Dorairajan ◽  
Sajini Elizabeth Jacob ◽  
Victorraj Gladwin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Fetal Growth ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Acid Oxidation ◽  
Placental Proteins

Abstract Introduction Gestational diabetes mellitus (GDM) exhibit altered placental lipid metabolism. The molecular basis of this altered metabolism is not clear. Altered placental expression of proteins of lipogenesis and fatty acid oxidation may be involved in the placental accumulation of triacylglycerols (TG). The present study was aimed at investigating the differential expressions of placental proteins related to lipid metabolism among GDM women in comparison with control pregnant women (CPW) and to correlate them with maternal and fetal lipid parameters as well as altered fetal growth. Materials and Methods Maternal blood, cord blood, and placental samples were collected from GDM and CPW. The biochemical parameters, glucose, lipid profile and free fatty acids (FFA) were measured. The placental TG content was measured. Differential placental expressions of proteins; phosphatidylinositol-3-kinase (PI3K) p85α, PI3K p110α,liver X receptor alpha (LXRα), sterol regulatory element binding protein1(SREBP1), fatty acid synthase (FAS), stearyl CoA desaturase1 (SCD1), lipoprotein lipase (LPL),Peroxisome proliferator-activated receptor (PPAR)α and PPARγ were analysed by western blotting and immunohistochemistry. Results Placental protein expressions of PI3K p110α, LXRα, FAS, SCD1, and LPL were found to be significantly higher, whereas PPARα and PPARγ were lower in GDM women compared with CPW. The placental TG content and cord plasma FFA were increased in GDM women compared with CPW. The placental TG content positively correlated with Ponderal index of GDM new-borns. Conclusion Differential expressions of placental proteins related to lipid metabolism in GDM might have led to placental TG accumulation. This might have contributed to the fetal overgrowth in GDM.

scholarly journals The role of tandem mass spectrometry in the diagnosis of inherited metabolic diseases

2018 ◽  
Vol 5 (3) ◽  
pp. 96-105 ◽  
Author(s):  
G. V. Baydakova ◽  
T. A. Ivanova ◽  
E. Yu. Zakharova ◽  
O. S. Kokorina
Keyword(s):  
Mass Spectrometry ◽  
Fatty Acid ◽  
Tandem Mass Spectrometry ◽  
Fatty Acid Oxidation ◽  
Metabolic Diseases ◽  
Acid Oxidation ◽  
Tandem Mass ◽  
Organic Acidurias ◽  
Inherited Metabolic Diseases ◽  
Screening Programs

This paper reviews the clinical applications of tandem mass spectrometry in diagnosis and screening for inherited metabolic diseases. The broad-spectrum of diseases covered, specificity, ease of sample preparation, and high throughput provided by the MS/MS technology has led to the development of multi-disorder newborn screening programs in many countries for amino acid disorders, organic acidurias, and fatty acid oxidation defects. The application of MS/MS in selective screening has revolutionized the field and made a major impact on the detection of certain disease classes such as the fatty acid oxidation defects. New specific and rapid tandem mass spectrometry (MS/MS) and high performance liquid chromatography–MS/MS methods are supplementing or replacing some of the classical gas chromatography– MS/MS methods for a multitude of metabolites and disorders. In the near future, we should expect the emergence of new promising methods for diagnosing not only individual nosologic forms, but also entire groups of inherited metabolic diseases.

scholarly journals Kupffer cells facilitate the acute effects of leptin on hepatic lipid metabolism

2017 ◽  
Vol 312 (1) ◽  
pp. E11-E18 ◽  
Author(s):  
Anantha Metlakunta ◽  
Wan Huang ◽  
Maja Stefanovic-Racic ◽  
Nikolaos Dedousis ◽  
Ian Sipula ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Kupffer Cells ◽  
Liver Lipid ◽  
Myeloid Cell ◽  
Metabolic Effects ◽  
Acid Oxidation ◽  
Acute Effects ◽  
Peripheral Tissues ◽  
Liver Lipid Metabolism

Leptin has potent effects on lipid metabolism in a number of peripheral tissues. In liver, an acute leptin infusion (~120 min) stimulates hepatic fatty acid oxidation (~30%) and reduces triglycerides (TG, ~40%), effects that are dependent on phosphoinositol-3-kinase (PI3K) activity. In the current study we addressed the hypothesis that leptin actions on liver-resident immune cells are required for these metabolic effects. Myeloid cell-specific deletion of the leptin receptor (ObR) in mice or depletion of liver Kupffer cells (KC) in rats in vivo prevented the acute effects of leptin on liver lipid metabolism, while the metabolic effects of leptin were maintained in mice lacking ObR in hepatocytes. Notably, liver TG were elevated in both lean and obese myeloid cell ObR, but the degree of obesity and insulin resistance induced by a high-fat diet was similar to control mice. In isolated primary hepatocytes (HEP), leptin had no effects on HEP lipid metabolism and only weakly stimulated PI3K. However, the coculture of KC with HEP restored leptin action on HEP fatty acid metabolism and stimulation of HEP PI3K. Notably, leptin stimulated the release from KC of a number of cytokines. However, the exposure of HEP to these cytokines individually [granulocyte macrophage colony-stimulating factor, IL-1α, IL-1β, IL-6, IL-10, and IL-18] or in combination had no effects on HEP lipid metabolism. Together, these data demonstrate a role for liver mononuclear cells in the regulation of liver lipid metabolism by leptin.

scholarly journals Maternal Diet Transition Before Pregnancy Plays a Transgenerational Effect on Offspring Lipid Homeostasis in Liver (P11-143-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Linglin Xie ◽  
Yi Zhou ◽  
Hui Peng ◽  
Ke K Zhang
Keyword(s):  
Fatty Acid ◽  
Maternal Diet ◽  
De Novo Lipogenesis ◽  
Acid Oxidation ◽  
Childbearing Age ◽  
Alcoholic Fatty Liver ◽  
Diet Intervention ◽  
The Metabolic Syndrome ◽  
Expression Of Genes ◽  
Lipid Panel

Abstract Objectives It is now clear that non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has a developmental origin. Thus, we aims on to evaluate if a maternal diet intervention before pregnancy would be beneficial to reduce the risk for offspring NAFLD. Methods In our study, female mice were either on an NF diet (NF group), or a HF diet (HF group), for 9 weeks and continued on such diet through pregnancy and gestation, or switched from the 9-week HF to an NF diet for 1 week (H1N group) or 9 weeks (H9N group) before pregnancy. After weaning, the male offspring were given the HF diet for 12 weeks to promote NAFLD. Results Comparing to the NF offspring, the H1N and HF but not the H9N offspring, displayed more severe hepatic steatosis and glucose intolerance. More specifically, the H1N and HF offspring had abnormal blood lipid panel and abnormal free fatty acid composition in liver, while the H9N offspring displayed normal. These physiological changes were associated with a desensitized hepatic insulin/AKT signaling, an increased expression of genes and proteins for de novo lipogenesis, a decreased expression of genes and proteins for fatty acid oxidation, increased Pcsk9 expression and the AMPK signaling hypoactivation in the HF and H1N offspring. However, these effects were either completely or partially avoided in the H9N offspring. Conclusions In summary, we showed that an early maternal diet intervention is efficient to reduce the risk for offspring NAFLD caused by the maternal HF diet. These information will provide significant support for setting up guidelines that women at childbearing age could follow to select the ideal diets, prior to and during pregnancy, which not only immediately benefit the pregnant outcome but also give a long-term beneficial effect on offspring health. Funding Sources This project is supported by grants from the National Institutes of Health (NIDDK 1R01DK112368-01 to LX and KZ) and the USDA National Institute of Food and Agriculture, [Hatch] project [1010406] to LX.

scholarly journals Comparison of the Postprandial Metabolic Fate of U- 13 C Stearic Acid and U- 13 C Oleic Acid in Postmenopausal Women

2020 ◽  
Vol 40 (12) ◽  
pp. 2953-2964
Author(s):  
Jose Rodríguez-Morató ◽  
Jean Galluccio ◽  
Gregory G. Dolnikowski ◽  
Alice H. Lichtenstein ◽  
Nirupa R. Matthan
Keyword(s):  
Mass Spectrometry ◽  
Fatty Acid ◽  
Postmenopausal Women ◽  
Oxidation Rate ◽  
Ldl Cholesterol ◽  
Area Under The Curve ◽  
Density Lipoprotein ◽  
Plasma Metabolites ◽  
Acid Oxidation ◽  
Oxidation Rates

Objective: Compare the postprandial fatty acid metabolism of isotopically labeled stearate (U- 13 C18:0) and oleate (U- 13 C18:1). Approach and Results: In conjunction with a randomized-controlled crossover trial, 6 hypercholesterolemic postmenopausal women (≥50 years; body mass index: 25.6±3.0 kg/m 2 ; LDL [low-density lipoprotein]-cholesterol ≥110 mg/dL) consumed isocaloric diets enriched in 18:0 or 18:1 (10%–15% E) for 5 weeks each. On day 1 of week 5, following a 12-hour fast, participants receive their experimental diet divided into 13 hourly meals beginning at 8 am . U- 13 C18:0 or U- 13 C18:1 was incorporated into the 1:00 pm meal (1.0 mg/kg body weight). Serial blood and breath samples were collected over 12 hours and fasting samples at 24 and 48 hours. Plasma and lipid subfraction fatty acid profiles were assessed by gas chromatography-flame ionization detector, isotope-enrichment by liquid chromatography time-of-flight mass spectrometry, and fatty acid oxidation rate (expired 13 CO 2 ) by isotope ratio mass spectrometry. Both diets resulted in similar plasma LDL-cholesterol concentrations. Kinetic curves showed that U- 13 C18:0 had a higher plasma area under the curve (66%), lower plasma clearance rate (−46%), and a lower cumulative oxidation rate (−34%) than U- 13 C18:1. Three labeled plasma metabolites of U- 13 C18:0 were detected: 13 C16:0, 13 C16:1, and 13 C18:1. No plasma metabolites of U- 13 C18:1 were detected within the study time-frame. Higher incorporation of 18:0 in cholesteryl ester and triglyceride fractions was observed on the 18:0 compared with the 18:1 diet. Conclusions: The neutrality of 18:0 on plasma LDL-cholesterol concentrations is not attributable to a single factor. Compared with 18:1, 18:0 had higher plasma area under the curve because of lower clearance and oxidation rates, underwent both a direct and a multistage conversion to 18:1, and was preferentially incorporated into cholesteryl esters and triglycerides.

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