Amazing stuff! Maternal obesity during pregnancy has consequences.
"... They conducted a pre-clinical trial and found that cellular processes within the egg at the time of fertilisation determine the telomere length in the offspring. ...
The team conducted the trials using mouse models and found that when mitochondrial activity is disrupted, whether by high oxygen levels, or conditions such as maternal obesity and metabolic syndrome, the embryo fails to properly “reset” its telomere length. This leads to babies being born with shorter telomeres. ..."
"... “Some babies are born with shorter telomeres than others, increasing their lifetime risk of chronic diseases associated with ageing.
“As just one example, shorter telomeres are observed in children of women with obesity or metabolic syndrome. As adults, these individuals are at increased risk of premature mortality from cardiovascular events, like a heart attack or stroke, even when they are not obese themselves. ...
“There are specific types of cellular damage during the very first days of embryo development which cause the defect in the telomeres of the embryo, which causes them to be shorter at the time of birth,”...
“The process is highly responsive to signals from the mother’s body. Our findings show maternal health and environmental conditions at the time of conception can have long-term consequences and can even influence the offspring’s susceptibility versus resilience to ageing-associated diseases in later life. ..."
From the abstract:
"The initial setting of telomere length during early life in each individual has a major influence on lifetime risk of aging-associated diseases; however there is limited knowledge of biological signals that regulate inheritance of telomere length, and whether it is modifiable is not known.
We now show that when mitochondrial activity is disrupted in mouse zygotes, via exposure to 20% O2 or rotenone, telomere elongation between the 8-cell and blastocyst stage is impaired, with shorter telomeres apparent in the pluripotent Inner Cell Mass (ICM) and persisting after organogenesis.
Identical defects of elevated mtROS in zygotes followed by impaired telomere elongation, occurred with maternal obesity or advanced age. We further demonstrate that telomere elongation during ICM formation is controlled by mitochondrial-nuclear communication at fertilization.
Using mitochondrially-targeted therapeutics (BGP-15, MitoQ, SS-31, metformin) we demonstrate that it is possible to modulate the preimplantation telomere resetting process and restore deficiencies in neonatal telomere length."
Embryo development holds key to healthy lifestyles (original new release)
Telomere length in offspring is determined by mitochondrial-nuclear communication at fertilization (open access) "Researchers from the University of Adelaide have discovered that the earliest days of embryo development have a measurable impact on a person’s future health and ageing."
Fig. 1: Telomere elongation during pre-implantation embryogenesis is impaired by oxidative stress.
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