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Book ; Online ; E-Book: Nutrition, epigenetics and health

Burdge, Graham C. / Lillycrop, Karen

2017

Author's details	Graham Burdge ; Karen Lillycrop editors
Keywords	Nutrigenomics ; Epigenomics / methods ; Nutritional Physiological Phenomena / genetics ; Genetic Phenomena ; Risk Factors
Language	English
Size	1 Online-Ressource (viii, 225 Seiten), Illustrationen
Publisher	World Scientific Publishing
Publishing place	New Jersey
Publishing country	United States
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019322308
ISBN	978-9-81314331-9 ; 9789813143302 ; 9-81314331-2 ; 9813143304
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article: Multigenerational diabetes mellitus.

Thornton, Jennifer M / Shah, Nishel M / Lillycrop, Karen A / Cui, Wei / Johnson, Mark R / Singh, Natasha

Frontiers in endocrinology

2024 Volume 14, Page(s) 1245899

Abstract: Gestational diabetes (GDM) changes the maternal metabolic and uterine environment, thus increasing the risk of short- and long-term adverse outcomes for both mother and child. Children of mothers who have GDM during their pregnancy are more likely to ... ...

Abstract	Gestational diabetes (GDM) changes the maternal metabolic and uterine environment, thus increasing the risk of short- and long-term adverse outcomes for both mother and child. Children of mothers who have GDM during their pregnancy are more likely to develop Type 2 Diabetes (T2D), early-onset cardiovascular disease and GDM when they themselves become pregnant, perpetuating a multigenerational increased risk of metabolic disease. The negative effect of GDM is exacerbated by maternal obesity, which induces a greater derangement of fetal adipogenesis and growth. Multiple factors, including genetic, epigenetic and metabolic, which interact with lifestyle factors and the environment, are likely to contribute to the development of GDM. Genetic factors are particularly important, with 30% of women with GDM having at least one parent with T2D. Fetal epigenetic modifications occur in response to maternal GDM, and may mediate both multi- and transgenerational risk. Changes to the maternal metabolome in GDM are primarily related to fatty acid oxidation, inflammation and insulin resistance. These might be effective early biomarkers allowing the identification of women at risk of GDM prior to the development of hyperglycaemia. The impact of the intra-uterine environment on the developing fetus, "developmental programming", has a multisystem effect, but its influence on adipogenesis is particularly important as it will determine baseline insulin sensitivity, and the response to future metabolic challenges. Identifying the critical window of metabolic development and developing effective interventions are key to our ability to improve population metabolic health.
MeSH term(s)	Child ; Female ; Humans ; Pregnancy ; Biomarkers ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/genetics ; Diabetes, Gestational/epidemiology ; Hyperglycemia ; Insulin Resistance/genetics ; Mothers ; Extended Family
Chemical Substances	Biomarkers
Language	English
Publishing date	2024-01-15
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1245899
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book: Nutrition, epigenetics and health

Burdge, Graham / Lillycrop, Karen

2017

Author's details	editors, Graham Burdge, Karen Lillycrop, University of Southampton, UK
Keywords	Epigenetics. ; Nutrition. ; Genetics. ; nutrigenomics ; epigenetics ; methodology ; genetics ; risk factors
Language	English
Size	viii, 225 pages :, illustrations ;, 24 cm
Document type	Book
ISBN	9789813143302 ; 9813143304
Database	NAL-Catalogue (AGRICOLA)

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Book: Nutrition, epigenetics and health

Burdge, Graham / Lillycrop, Karen

2017

Author's details	editors, Graham Burdge & Karen Lillycrop
MeSH term(s)	Nutrigenomics ; Epigenomics/methods ; Nutritional Physiological Phenomena/genetics ; Genetic Phenomena ; Risk Factors
Language	English
Size	viii, 225 pages :, illustrations
Document type	Book
ISBN	9789813143302 ; 9813143304
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: Nutritional modulation of the epigenome and its implication for future health.

Burton, Mark A / Lillycrop, Karen A

The Proceedings of the Nutrition Society

2019 Volume 78, Issue 3, Page(s) 305–312

Abstract: Non-communicable diseases (NCD) such as type-2 diabetes and CVD are now highly prevalent in both developed and developing countries. Evidence from both human and animal studies shows that early-life nutrition is an important determinant of NCD risk in ... ...

Abstract	Non-communicable diseases (NCD) such as type-2 diabetes and CVD are now highly prevalent in both developed and developing countries. Evidence from both human and animal studies shows that early-life nutrition is an important determinant of NCD risk in later life. The mechanism by which the early-life environment influences future disease risk has been suggested to include the altered epigenetic regulation of gene expression. Epigenetic processes regulate the accessibility of genes to the cellular proteins that control gene transcription, determining where and when a gene is switched on and its level of activity. Epigenetic processes not only play a central role in regulating gene expression but also allow an organism to adapt to the environment. In this review, we will focus on how both maternal and paternal nutrition can alter the epigenome and the evidence that these changes are causally involved in determining future disease risk.
MeSH term(s)	Cardiovascular Diseases/genetics ; DNA Methylation/genetics ; DNA Methylation/physiology ; Diabetes Mellitus, Type 2/genetics ; Epigenesis, Genetic/genetics ; Epigenesis, Genetic/physiology ; Epigenome/genetics ; Epigenome/physiology ; Epigenomics ; Genetic Predisposition to Disease/genetics ; Humans ; Nutritional Status/genetics ; Nutritional Status/physiology
Language	English
Publishing date	2019-02-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391142-1
ISSN	1475-2719 ; 0029-6651
ISSN (online)	1475-2719
ISSN	0029-6651
DOI	10.1017/S0029665119000016
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Nutritional modulation of the epigenome and its implication for future health

Burton, Mark A / Lillycrop, Karen A

Proceedings of the Nutrition Society. 2019 Aug., v. 78, no. 3

2019

Abstract	Non-communicable diseases (NCD) such as type-2 diabetes and CVD are now highly prevalent in both developed and developing countries. Evidence from both human and animal studies shows that early-life nutrition is an important determinant of NCD risk in later life. The mechanism by which the early-life environment influences future disease risk has been suggested to include the altered epigenetic regulation of gene expression. Epigenetic processes regulate the accessibility of genes to the cellular proteins that control gene transcription, determining where and when a gene is switched on and its level of activity. Epigenetic processes not only play a central role in regulating gene expression but also allow an organism to adapt to the environment. In this review, we will focus on how both maternal and paternal nutrition can alter the epigenome and the evidence that these changes are causally involved in determining future disease risk.
Keywords	developing countries ; epigenetics ; gene expression ; gene expression regulation ; genes ; noninsulin-dependent diabetes mellitus ; nutrition ; proteins ; risk factors ; transcription (genetics)
Language	English
Dates of publication	2019-08
Size	p. 305-312.
Publishing place	Cambridge University Press
Document type	Article
ZDB-ID	391142-1
ISSN	1475-2719 ; 0029-6651
ISSN (online)	1475-2719
ISSN	0029-6651
DOI	10.1017/S0029665119000016
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Exogenous tetracosahexaenoic acid modifies the fatty acid composition of human primary T lymphocytes and Jurkat T cell leukemia cells contingent on cell type

Irvine, Nicola A. / West, Annette L. / Von Gerichten, Johanna / Miles, Elizabeth A. / Lillycrop, Karen A. / Calder, Philip C. / Fielding, Barbara A. / Burdge, Graham C.

Lipids. 2023 July, v. 58, no. 4 p.185-196

2023

Abstract: Tetracosahexaenoic acid (24:6ω‐3) is an intermediate in the conversion of 18:3ω‐3 to 22:6ω‐3 in mammals. There is limited information about whether cells can assimilate and metabolize exogenous 24:6ω‐3. This study compared the effect of incubation with ... ...

Abstract	Tetracosahexaenoic acid (24:6ω‐3) is an intermediate in the conversion of 18:3ω‐3 to 22:6ω‐3 in mammals. There is limited information about whether cells can assimilate and metabolize exogenous 24:6ω‐3. This study compared the effect of incubation with 24:6ω‐3 on the fatty acid composition of two related cell types, primary CD3⁺ T lymphocytes and Jurkat T cell leukemia, which differ in the integrity of the polyunsaturated fatty acid (PUFA) biosynthesis pathway. 24:6ω‐3 was only detected in either cell type when cells were incubated with 24:6ω‐3. Incubation with 24:6ω‐3 induced similar increments in the amount of 22:6ω‐3 in both cell types and modified the homeoviscous adaptations fatty acid composition induced by activation of T lymphocytes. The effect of incubation with 18:3ω‐3 compared to 24:6ω‐3 on the increment in 22:6ω‐3 was tested in Jurkat cells because primary T cells cannot convert 18:3ω‐3 to 22:6ω‐3. The increment in the 22:6ω‐3 content of Jurkat cells incubated with 24:6ω‐3 was 19.5‐fold greater than that of cells incubated with 18:3ω‐3. Acyl‐coA oxidase siRNA knockdown decreased the amount of 22:6ω‐3 and increased the amount of 24:6ω‐3 in Jurkat cells. These findings show exogenous 24:6ω‐3 can be incorporated into primary human T lymphocytes and Jurkat cells and induces changes in fatty acid composition consistent with its conversion to 22:6ω‐3 via a mechanism involving peroxisomal β‐oxidation that is regulated independently from the integrity of the upstream PUFA synthesis pathway. One further implication is that consuming 24:6ω‐3 may be an effective alternative means of achieving health benefits attributed to 20:5ω‐3 and 22:6ω‐3.
Keywords	T-lymphocytes ; acyl-CoA oxidase ; biosynthesis ; fatty acid composition ; humans ; leukemia ; polyunsaturated fatty acids
Language	English
Dates of publication	2023-07
Size	p. 185-196.
Publishing place	John Wiley & Sons, Inc.
Document type	Article ; Online
Note	JOURNAL ARTICLE
ZDB-ID	241539-2
ISSN	1558-9307 ; 0024-4201
ISSN (online)	1558-9307
ISSN	0024-4201
DOI	10.1002/lipd.12372
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 645: Show issues

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Article ; Online: The serum small non-coding RNA (SncRNA) landscape as a molecular biomarker of age associated muscle dysregulation and insulin resistance in older adults.

Burton, Mark A / Antoun, Elie / Garratt, Emma S / Westbury, Leo / Dennison, Elaine M / Harvey, Nicholas C / Cooper, Cyrus / Patel, Harnish P / Godfrey, Keith M / Lillycrop, Karen A

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2024 Volume 38, Issue 3, Page(s) e23423

Abstract: Small noncoding RNAs (sncRNAs) are implicated in age-associated pathologies, including sarcopenia and insulin resistance (IR). As potential circulating biomarkers, most studies have focussed on microRNAs (miRNAs), one class of sncRNA. This study ... ...

Abstract	Small noncoding RNAs (sncRNAs) are implicated in age-associated pathologies, including sarcopenia and insulin resistance (IR). As potential circulating biomarkers, most studies have focussed on microRNAs (miRNAs), one class of sncRNA. This study characterized the wider circulating sncRNA transcriptome of older individuals and associations with sarcopenia and IR. sncRNA expression including miRNAs, transfer RNAs (tRNAs), tRNA-associated fragments (tRFs), and piwi-interacting RNAs (piRNAs) was measured in serum from 21 healthy and 21 sarcopenic Hertfordshire Sarcopenia Study extension women matched for age (mean 78.9 years) and HOMA2-IR. Associations with age, sarcopenia and HOMA2-IR were examined and predicted gene targets and biological pathways characterized. Of the total sncRNA among healthy controls, piRNAs were most abundant (85.3%), followed by tRNAs (4.1%), miRNAs (2.7%), and tRFs (0.5%). Age was associated (FDR < 0.05) with 2 miRNAs, 58 tRNAs, and 14 tRFs, with chromatin organization, WNT signaling, and response to stress enriched among gene targets. Sarcopenia was nominally associated (p < .05) with 12 tRNAs, 3 tRFs, and 6 piRNAs, with target genes linked to cell proliferation and differentiation such as Notch Receptor 1 (NOTCH1), DISC1 scaffold protein (DISC1), and GLI family zinc finger-2 (GLI2). HOMA2-IR was nominally associated (p<0.05) with 6 miRNAs, 9 tRNAs, 1 tRF, and 19 piRNAs, linked with lysine degradation, circadian rhythm, and fatty acid biosynthesis pathways. These findings identify changes in circulating sncRNA expression in human serum associated with chronological age, sarcopenia, and IR. These may have clinical utility as circulating biomarkers of ageing and age-associated pathologies and provide novel targets for therapeutic intervention.
MeSH term(s)	Humans ; Female ; Aged ; RNA, Small Untranslated/genetics ; Piwi-Interacting RNA ; Sarcopenia/genetics ; Insulin Resistance/genetics ; MicroRNAs/genetics ; RNA, Transfer/genetics ; Muscles/metabolism ; Biomarkers
Chemical Substances	RNA, Small Untranslated ; Piwi-Interacting RNA ; MicroRNAs ; RNA, Transfer (9014-25-9) ; Biomarkers
Language	English
Publishing date	2024-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202301089RR
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Article ; Online: Effect of maternal diet on the epigenome: implications for human metabolic disease.

Lillycrop, Karen A

The Proceedings of the Nutrition Society

2011 Volume 70, Issue 1, Page(s) 64–72

Abstract: The rapid increase in the incidence of chronic non-communicable diseases over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environment also ... ...

Abstract	The rapid increase in the incidence of chronic non-communicable diseases over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environment also strongly influences the risk of developing such diseases in later life. Human studies have shown that low birth weight is associated with an increased risk of CVD, type II diabetes, obesity and hypertension, although recent studies have shown that over-nutrition in early life can also increase susceptibility to future metabolic disease. These findings have been replicated in a variety of animal models, which have shown that both maternal under- and over-nutrition can induce persistent changes in gene expression and metabolism within the offspring. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of chronic diseases raises the possibility that nutritional or pharmaceutical interventions may be used to modify long-term cardio-metabolic disease risk and combat this rapid rise in chronic non-communicable diseases.
MeSH term(s)	Animals ; Diet ; Epigenesis, Genetic ; Epigenomics ; Female ; Humans ; Maternal Nutritional Physiological Phenomena ; Metabolic Syndrome/genetics ; Pregnancy ; Prenatal Exposure Delayed Effects/genetics
Language	English
Publishing date	2011-02
Publishing country	England
Document type	Journal Article
ZDB-ID	391142-1
ISSN	1475-2719 ; 0029-6651
ISSN (online)	1475-2719
ISSN	0029-6651
DOI	10.1017/S0029665110004027
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Folic Acid Induces Intake-Related Changes in the Mammary Tissue Transcriptome of C57BL/6 Mice

Burton, Mark A / Antoun, Elie / Penailillo, Reyna S / Burdge, Graham C / Lillycrop, Karen A

Nutrients. 2020 Sept. 15, v. 12, no. 9

2020

Abstract: Folic acid (FA) intake has been associated with increased breast cancer risk in some studies. Although underlying mechanisms are unknown, epigenetic modifications that persistently alter transcription have been suggested. We tested the hypothesis that ... ...

Abstract	Folic acid (FA) intake has been associated with increased breast cancer risk in some studies. Although underlying mechanisms are unknown, epigenetic modifications that persistently alter transcription have been suggested. We tested the hypothesis that high FA (HFA) intake alters the adult mammary transcriptome in a manner consistent with increased potential for carcinogenesis, detectable beyond the period of intake. C57BL/6 mice were fed control FA (CFA) (1 mg/kg diet) or HFA (5 mg/kg diet) diets for 4 weeks, followed by AIN93M maintenance diet for 4 weeks. Plasma 5-methyltetrahydrofolate, p-aminobenzoylglutamate and unmetabolised FA concentrations were greater (1.62, 1.56, 5.80-fold, respectively) in HFA compared to CFA mice. RNA sequencing of the mammary transcriptome (~20 million reads) showed 222 transcripts (191 upregulated) differentially expressed between groups. Gene Set Enrichment showed upregulated genes significantly enriched in Epithelial Mesenchymal Transition, Myogenesis and Apical Junction and downregulated genes in E2F targets, MYC targets and G2M checkpoint. Cancer was the most altered Disease and Disorder pathway, with Metastasis, Mammary Tumour and Growth of Tumour the most upregulated pathways. ChIP-seq enrichment analysis showed that targets of histone methyltransferase EZH2 were enriched in HFA mice. This study demonstrates HFA intake during adulthood induces mammary transcriptome changes, consistent with greater tumorigenic potential.
Keywords	RNA ; adulthood ; adults ; breast neoplasms ; carcinogenesis ; chromatin immunoprecipitation ; diet ; epigenetics ; epithelium ; folic acid ; genes ; histones ; mammary neoplasms (animal) ; metastasis ; methyltransferases ; muscle development ; risk ; transcriptome
Language	English
Dates of publication	2020-0915
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	NAL-light
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12092821
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