The effects of breastfeeding and formula feeding on the metabolic factors and the expression level of obesity and diabetes-predisposing genes in healthy infants

Background: Diabetes mellitus (DM) and obesity are common illnesses characterized by glucose metabolism issues and excessive weight gain. Breastfeeding is the best way to feed a newborn up to six months old and it has been shown to reduce the risk of diabetes and obesity later in life due to its nutritional properties. The aim of this study was to investigate the effects of breastfeeding, formula feeding, and formula-plus breastfeeding (mix-feeding) on the anthropometric indices, metabolic variables, and the expression level of obesity and diabetes-predisposing genes of healthy infants. Methods A total of 150 healthy infants were enrolled in this cross-sectional study. All infants (aged 24 months) were divided into three groups based on the type of feeding, breastfeeding, formula feeding, and mix-feeding. The anthropometric indices, glycemic indexes, lipid profile, and the expression levels of acetyl-coenzyme A carboxylase beta ( ACACB ), brain-derived neurotrophic factor ( BDNF ), liver X receptor α ( LXR-α ), peroxisome proliferator-activated receptor γ ( PPAR-γ ), and phosphatase and tensin homolog ( PTEN ) genes were measured in all infants using reverse transcription-polymerase chain reaction (RT-PCR) method. Results The anthropometric indices including weight, height, head circumference, insulin, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were lower in the breastfeeding infants in comparison to other groups. As well, the expression level of the ACACB gene was significantly downregulated in breastfeeding infants, while the PPAR-γ gene was significantly upregulated, but the expression levels of LXR- α , PTEN and BDNF didn’t change significantly across groups. Conclusions Breastfeeding compared to formula feeding had positive effects on anthropometric indices, metabolic variables, and diabetes-predisposing genes.