Hello, everyone.
My name is Anusha Mahtani and my poster presentation is titled,
The Impact of a High Fat Diet on MeCP2 Expression.
My research evaluated the relationship between epigenetic and obesity.
Which is one that has recently been brought to the attention
of the scientific community.
Obesity is rapidly becoming more prevalent in our global population every day.
In 2016, the World Health Organization estimated that 39%
of all adults globally, obese.
With these rising numbers,
more research is being conducted on epigenetic factors such as MeCP2.
Epigenetic differences can be caused due to a change in diet, lifestyle, behavior,
environment and other factors.
A mouse model was utilized to evaluate changes.
Then MeCP2 protein expression,
as a function of high fat diet exposure during gestation or adulthood.
The experiment analyzed the differences on the effect of gestational and postnatal
exposure to a high fat diet on MeCP2 expression in both male and female mice.
Gestational exposure to a high fat diet significantly decreased.
And the MeCP2 expression in the arcuate nucleus region of the hypothalamus in
both male and female mice.
No significant impact was seen when exposure was given postnatally.
The data suggests that exposure to a high fat diet during developmentally
sensitive time periods, can impact MeCP2 expression in the hypothalamus,
in a sexually dimorphic way.
In order to execute this experiment, mice were bred and either given access to
a high fat or normal child diet, based on random selection.
For gestational exposure, the mice were exposed to maternal diets during gestation
for 21 days, and for six to seven weeks after weaning.
Offspring were singly house at 21 days of age, and provided access to food and
water according to the corresponding maternal diet.
For adulthood exposure, mice age six to eight weeks old were randomly assigned to
a high fat, or normal child diet, and were maintained on assigned diets.
Both mice, the gestational and adulthood group or sacrifice in the hypothalamus and
ventral striatum,
were collected to assess MeCP2 protein levels using immunohistochemistry.
The figure on the left illustrates MeCP2 expression during gestation.
It can be seen that MeCP2 expression in rostral regions of the hypothalamus,
decrease in females when given a high fat diet in utero as
opposed to our normal child diet, seen by 1-way ANOVA.
The figure also depicts MeCP2 expression in caudal regions of the hypothalamus,
to have decreased in males when given a high fat diet in utero,
as compared to a normal diet.
Although 1-way ANOVA did not show significant differences,
a t-test revealed significant differences in protein expression between groups.
The second figure illustrates MeCP2 expression during adulthood.
The data revealed no significant changes in MeCP2 protein expression in mice
during adulthood exposure, for both rostral and caudal regions.
The illustration on the left is a reference image from the island brain
outlets depicting the arcuate nucleus subregion of the hypothalamus.
The illustration on the right are images collected from this experiment at 20X
magnification.
The result of this experiment found a significant decrease in MeCP2 protein
expression to be seen in the arcuate nuclear subregion,
during gestational exposure for both male and female mice.
No significant differences were seen between groups who are exposed to a high
fat diet type during adulthood.
In conclusion, MeCP2 expression levels are altered in a sex-specific manner,
in particular regions of the arcuate nucleus,
during gestational exposure to a high fat diet.
Exposure to a high fat diet during adulthood,
does not significantly alter MeCP2 expression, indicating that protein
levels are more subject to modifications during early developmental period.
Thank you for your time and the opportunity to present my research.