{'fraction_non_alphanumeric': 0.0249728555917481, 'fraction_numerical': 0.004343105320304018, 'mean_word_length': 5.726277372262774, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Early and late effects of maternal obesity on the mother–child dyad

Obesity in pregnancy poses health risks to both the woman herself and the developing fetus, newborn, child, and adult offspring. High maternal body weight in early pregnancy is associated with an increased risk of neonatal mortality. Inflammatory factors secreted by maternal adipose tissue enhance the differentiation of stem cells into adipocytes, thereby accelerating the development of fetal adipose tissue, which is transformed into obesity in offspring. Leptin resistance in offspring at an early age is a direct consequence of maternal obesity. Children born to obese mothers are more likely to develop leukemia in early childhood. High maternal BMI during pregnancy is associated with higher BMI, blood pressure, insulin and triglyceride levels, abdominal obesity, and lower levels of «protective» lipids in offspring. Increased maternal body weight during pregnancy, especially in the early stages, correlates with cardiovascular diseases in offspring in adulthood. Data on the influence of changes in the intestinal microbiome in the form of high concentrations of Bacteroides spp. and Staphylococcus on the development of maternal obesity during pregnancy and on fetal health are presented, which is associated with increased assimilation of energy sources, increased pro-inflammatory processes, and reduced synthesis of several essential factors, particularly folic acid, which may explain the growth of congenital anomalies in offspring. A number of genetic polymorphisms that are relevant to the development of childhood obesity, especially the genes PPAR, MC4R, TMEM18, GNPDA2, NEGR1, KCTD15, ETV5, and among others FTO, are considered. Key words: inflammation, genetic polymorphisms, FTO gene, children, gut microbiome, maternal obesity, pregnancy pathology