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Precision nutrition for children with early puberty: leveraging nutrigenomics and lipidomics analysis

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Background: Precocious puberty (PP) is puberty occurring at an unusually early age that brings in adverse health outcomes during adolescence and adulthood. Pubertal development is a complex biological process of sexual development and is affected by genetic, nutritional, environmental, and socio-ec

onomic factors. However, the relationship between pre-pubertal intakes of energy, fat, fiber, protein levels and pubertal timing has been debated. In the genomic era, it is necessary to examine the individual response to a specific diet and how diet influences metabolic regulation in children with P

P personally. Limited evidence investigated the timing of pubertal onset by examining the interaction of nutrient intake and PP-related genetic loci. Importantly, endocrine disorders can alter lipid metabolism. The fact that puberty onset requires critical weight and body fat based on the “critical

weight hypothesis” and many lipid species have been noticed in many human obesity and metabolic syndrome studies. However, a lack of evidence works on lipidomes to propose the based-lipid biomarker and lipid metabolism in predicting PP in children.Methods: By performing a systematic review and meta-

analysis of prospective studies, we aimed to disclose the role of pre-pubertal and pubertal nutrient intake in PP development. Thereafter, we conducted a Taiwan Puberty Longitudinal Study (TPLS) in recruiting adolescents from pubertal and pediatric endocrine clinics in the Northern/Southern part of

Taiwan. The buccal samples for deoxyribonucleic acid (DNA) extraction and genotyping were collected from a total of 1404 children. We will examine the nutrient intake on the interaction with PP-related SNPs on pubertal timing using the “interaction term” of logistic regression. Also, lipidomic analy

sis deriving from 178 subjects’ plasma samples was used to identify the critical lipid biomarkers in diagnosing PP and central precocious puberty (CPP).Results: A high intake of protein, particularly animal protein, monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs) among prepu

bertal girls were significantly associated with PP risk. We also found that SNP rs12617311, rs2090409, and rs12148769 were significantly associated with PP in children. Specifically, different genotypes interacted with such food groups and micronutrient intake. A significant interaction was observed

between intake of vegetables, fruits, fructose and menarcheal loci rs12617311 (PCL1). The rs2090409 (TMEM38B) was more likely to interact with vitamin intake. Importantly, rs12148769 (MKRN3) appeared a significant interaction with saturated FA and MUFA intake. Whist, SNP rs10980921 (ZNF483) showed

a significant interaction with total PUFAs intake. The intake of sucrose, MUFAs, and PUFAs was associated with the potential lipid-based biomarkers, such as Cer(d16:1/22:0), PI(18:2/22:1), and PI(18:2/22:2) of girls and Cer(t20:0/18:0), Cer(d18:1/16:0) and Cer(d18:1/18:1) of boys that could predict

PP and CPP onset. In addition, the lipidomic analysis proposed several candidate lipids metabolism pathways, such as sphingolipid metabolism, steroid biosynthesis, and bile acid biosynthesis for an in-depth lipid mechanism that can be linked to PP and CPP pathophysiology.Conclusion: There was an int

eraction between genetic variant, lipid metabolism, and nutrient intake that was convinced to be associated with PP and CPP development in girls and boys. Nutrient intake may be an important factor in modulating early puberty, especially the consumption of sugar, fructose, and specific saturated fat

ty acids, monounsaturated fatty acids, polyunsaturated fatty acids. Additional research is needed to determine the biological causes of individual variability in response to dietary intake. Likewise, understanding the influence of nutrigenetic interactions on dyslipidemia can aid in the development

and implementation of personalized dietary strategies to improve the PP and CPP treatment.