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Pregnancy Timeline by SemestersDevelopmental TimelineFertilizationFirst TrimesterSecond TrimesterThird TrimesterFirst Thin Layer of Skin AppearsEnd of Embryonic PeriodEnd of Embryonic PeriodFemale Reproductive SystemBeginning Cerebral HemispheresA Four Chambered HeartFirst Detectable Brain WavesThe Appearance of SomitesBasic Brain Structure in PlaceHeartbeat can be detectedHeartbeat can be detectedFinger and toe prints appearFinger and toe prints appearFetal sexual organs visibleBrown fat surrounds lymphatic systemBone marrow starts making blood cellsBone marrow starts making blood cellsInner Ear Bones HardenSensory brain waves begin to activateSensory brain waves begin to activateFetal liver is producing blood cellsBrain convolutions beginBrain convolutions beginImmune system beginningWhite fat begins to be madeHead may position into pelvisWhite fat begins to be madePeriod of rapid brain growthFull TermHead may position into pelvisImmune system beginningLungs begin to produce surfactant
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
 
Developmental Biology - Premature Epigenome Aging

Our Western Diet Ages Us

Premature aging is triggered by our Western-style diet...

Our epigenome is sometimes referred to as the "software" or "operating system" of our genes. It is made up of small chemical modifications to DNA and the proteins that make up our chromosomes — controlling all the activity of every single gene.

As our organs develop and grow, our genes guide these changes along what are now expected developmental milestones, overseen by our epigenome. However, exposure to endocrine-disrupting chemicals (EDCs) during infancy, childhood as well as adult life, can cause widespread reprogramming of this "software," that will persist through our entire life.
Depending on the organ, the window of vulnerability for reprogramming may be anytime from development in the womb - to childhood - and through adolescence.
"In this study, we found that even brief exposure to certain chemicals while the liver is developing, prematurely aged the liver epigenome [instructions]. Exposure to these EDCs causes the young liver to acquire an adult epigenomic signature. However, this premature aging of the epigenome did not have an effect on health until later in life and after exposure to a high-fat diet," explains Cheryl Walker MD, Professor, Baylor College of Medicine and lead author on the paper.
In a healthy liver, the epigenome goes through a normal aging process. In this study, after exposure to an EDC, researchers saw this process accelerated. So, a 6-day old rat had the same epigenome normally seen in an adult rat.
"The effect of this change on metabolic function wasn't immediate. Instead, it was like a ticking time bomb, igniting when we switched animals to a Western-style diet, high in fat, sugar and cholesterol," explains Walker.

Rats exposed early to EDC and later to a Western-style diet were found to be more susceptible to metabolic dysfunction than those with the same EDC exposure, but kept on a healthy diet.

Rats that remained on a healthy diet, despite their epigenome having been reprogrammed, did not show the same changes in gene activation that controls metabolism, or accumulation of lipids [fats] in their [blood] serum, as seen in rats on a western high fat, sugar and cholesterol diet.
"This study shows us how environmental exposures affect our health and disease susceptibility, both early and later in life.

It also shows us that some people may be more adversely affected by a high-fat diet as adults than others - due to previous environmental exposure earlier in their life."

Cheryl Walker MD, lead author, Professor and Director, Center for Precision Environmental Health; and Alkek Presidential Chair in Environmental Health; Baylor College of Medicine, Houston, Texas, USA.
Read all the details of this work in Nature Communications.

While these findings are only in lab model animals at this time, researchers hope this and similar studies being conducted by the TARGET II Consortium lead the way to identifying biomarkers which more precisely predict those at risk for metabolic dysfunction — described as fatty liver disease, diabetes and/or heart disease, and allow for more precise and early intervention.

This work was featured as the June paper of the month by the National Institute of Environmental Health Sciences (NIEHS).

Abstract
Our early-life environment has a profound influence on developing organs that impacts metabolic function and determines disease susceptibility across the life-course. Using a rat model for exposure to an endocrine disrupting chemical (EDC), we show that early-life chemical exposure causes metabolic dysfunction in adulthood and reprograms histone marks in the developing liver to accelerate acquisition of an adult epigenomic signature. This epigenomic reprogramming persists long after the initial exposure, but many reprogrammed genes remain transcriptionally silent with their impact on metabolism not revealed until a later life exposure to a Western-style diet. Diet-dependent metabolic disruption was largely driven by reprogramming of the Early Growth Response 1 (EGR1) transcriptome and production of metabolites in pathways linked to cholesterol, lipid and one-carbon metabolism. These findings demonstrate the importance of epigenome: environment interactions, which early in life accelerate epigenomic aging, and later in adulthood unlock metabolically restricted epigenetic reprogramming to drive metabolic dysfunction.
Authors
Lindsey S. Treviño, Jianrong Dong, Ahkilesh Kaushal, Tiffany A. Katz, Rahul Kumar Jangid, Matthew J. Robertson, Sandra L. Grimm, Chandra Shekar R. Ambati, Vasanta Putluri, Aaron R. Cox, Kang Ho Kim, Thaddeus D. May, Morgan R. Gallo, David D. Moore, Sean M. Hartig, Charles E. Foulds, Nagireddy Putluri, Cristian Coarfa & Cheryl Lyn Walker.

Acknowledgements
This work was supported in part by NIH grants U01ES026719, 1P30ES030285, and R01ES023206 to CLW, American Diabetes Association grant #1-18-IBS-105 and NIH grant R01DK114356 to S.M.H., and a subaward from NIH grant U24DK097748 to C.E.F. Lipidomics and metabolomics sample processing and analysis were conducted by the Metabolomics Core at Baylor College of Medicine, supported by CPRIT Proteomics and Metabolomics Core Facility funding (RP170005), the NIH (P30 CA125123), and the Dan L. Duncan Cancer Center at Baylor College of Medicine. ChIP-sequencing and RNA-sequencing were conducted by the MD Anderson Cancer Center Science Park Next Generation Sequencing Core, supported by CPRIT Core Facility Support grants (RP120348 and RP170002). Figure 1a was created with Biorender.com.

The work was supported as part of the NIEHS multi-phased Toxicant Exposures and Responses by Genomic and Epigenomic Regulators of Transcription (TaRGET) Program.

The authors declare no competing interests.

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Jun 29 2020   Fetal Timeline   Maternal Timeline   News



Neonatal exposure to several endocrine-disrupting chemicals or EDCs are shown to cause adult metabolic diseases as well as liver dysfunction in pre-natal organ development. CREDIT Pinterest.
Phospholid by Wikipedia