الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
More than 1.9 billion adults and about 400 million children and adolescents were
overweight or obese, affecting more than one-third of the world’s population. Egypt is home
to greatest percentage of obese adults globally. There are about 19 million Egyptians are
obese, which has the highest prevalence worldwide. Obesity has well-documented harmful
consequences on reproductive outcomes. Due to its complexity and multifaceted nature, the
mechanism by which obesity affects the reproductive system is difficult to explain. The rapid
increase in obesity over the last 30 years is assumed to have been mostly influenced by
epigenetics. Children are more likely to become obese if one or both of their parents are
obese: the likelihood of becoming obese increases from 30% to 90% depending on which
parent is obese. The present study aimed to explore the effect of parental obesity on ovarian
mitochondrial biogenesis of female rat offspring.
The study was conducted on 40 Wistar albino rats (20 males and 20 females) about 2
months old and weighing 115-125 grams. Obesity was induced in young male and female
albino rats by feeding them with an obesogenic diet for 3 months. The animals were classified
into four groups: group I (Control Parents): Which included mating between 5 healthy female
rats and 5 healthy male rats that were maintained under a normal diet, group II (Obese
Fathers): Which included mating between 5 obese father rats and 5 healthy female rats that
were fed on a normal diet, group III (Obese Mothers): Included mating between 5 obese
mother rats and 5 healthy male rats that were fed on a normal diet and group IV (Obese
Parents): Included mating between 5 obese parents. All female rat offspring were fed a normal
diet when they were old enough to eat, and their weights were monitored for eight weeks after
birth. After the experimental period, rats were sacrificed to obtain blood and ovarian tissues
for tissue homogenate preparations, DNA extraction for mtDNA-CN determination, and total
RNA extraction for determination of gene expression of mitochondria biogenesis parameters,
estrogen receptors and miRNA and for histopathological examination, and
histomorphometrical analysis.
The final findings of the present study are that, the two-month-old female offspring of
obese mother (alone or combined with the father obesity) showed early signs of obesity as
indicated by heavier body weights, hyperglycemia, IR, and dyslipidemia. These metabolic
abnormalities were associated with signs of ovarian lesion, impaired folliculogenesis, and
decreased oocyte quality. While, the two-month-old female offspring of obese father showed
normal body weight with no or mild signs of ovarian abnormalities and near-normal
folliculogenesis, but those offspring suffer from hyperglycemia, IR and mild dyslipidemia and
also showed significant alterations in mitochondrial biogenesis, redox status, inflammation,
and microRNA expression which may suggest that those females offspring may develop
ovarian abnormalities like those offspring of maternal obesity but at older age . These
differential impacts of maternal and paternal obesity on the ovarian heath of the female
offspring may be interpreted in the context of the pattern of transmission and the duration of
the impact.
from this study, we concluded that:
1. The maternal obesity operates early during the pre-gestational period on the developing
ova through epigenetic effects of maternal obesity on nuclear genes and impairments of
mitochondrial biogenesis and functions that affect folliculogenesis and the quality of the
ova.
Summary and Conclusions
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2. After fertilization and during the gestation maternal obesity may impact and reprogram
the developing fetus through the obesogenic intrauterine milieu with disturbed
metabolites, adipocytokines, and hormones.
3. Post-gestation the maternal obesity still affecting the newborn baby during lactation
through suckling obesogenic milk with high fat contents.
4. The impact of paternal obesity is limited to the epigenetic effects on the sperm that may
induced during the pregestational period.
5. Maternal obesity has more potential impact on the ovarian tissues of the female
offspring than the paternal obesity.
6. We suggest that altered ovarian expression of microRNAs (miR-149 and miR-494) and
associated impaired mitochondrial biogenesis pathway may be the root causes for the
observed intergeneration transmission of the obesogenic phenotype.
7. The extent and the interplay of these possible mechanisms need further investigation.