Used to evaluate whether a person is at a healthy weight or not, regardless of appearances, Body Mass Index (BMI) is a value derived from the weight and height of a person, designed to classify physically inactive populations. Obesity, defined by high BMI, is a complex condition associated with an increased risk of chronic disease. Consequently, the overall prevalence of childhood obesity remains very high, with the majority of adolescents who are obese remaining so in adulthood.
BMI in adulthood primarily reflects weight independent of height. Conversely, changes in BMI throughout childhood are influenced by adjustments in both height and weight, also known as growth. This aside, there is little knowledge regarding the genetic factors influencing growth and BMI during the first 5 years of human life, however.
New developmental genetics
Now, a study from researchers at the University of Bergen identifies previously unknown genetic signals for the regulation of growth in infancy. The team states a clearer insight into infant growth is important as growth-related diseases such as obesity and malnutrition are major health challenges. The opensource study is published in the journal Nature Communications.
Previous studies show BMI patterns in infancy and childhood follow well-charted trajectories, namely, a rapid increase soon after birth until 9 months, the adiposity peak. Furthermore, this period is followed by a gradual decline until 4–6 years of age, and then the adiposity rebound when BMI starts to increase again until the end of puberty.
Research indicates the most powerful predictor of obesity in adolescence is an increase in BMI between 2 and 6 years of age, however, the underlying cause for this remains unknown. The current study identifies common genetic variation in BMI development using continuous BMI measurements from birth to eight years of age in children.
The current study performs genome-wide association studies of BMI at 12-time points from birth to eight years in 9286 children. The results of which were then replicated in a further 5235 children. Results identify variants in five loci in the leptin signaling pathway, which has an important role in fetal growth. These data include the leptin receptor and leptin gene associating with BMI at distinct developmental stages.
Data findings indicate the presence of a BMI-linked transient effect in the leptin receptor locus with no effect at birth. This transient effect was shown to increase in infancy, peaking at 6–12 months, with little effect after the age of five. A similar BMI-linked transient effect was also identified near the leptin gene, peaking at 1.5 years of age.
The lab explains leptin is a hormone predominantly made by the adipose tissue regulating the energy balance by reducing appetite, which in turn diminishes fat storage in adipocytes.
Implications for childhood obesity
They go on to add increased levels of leptin’s binding partner, the leptin receptor, in infants has a positive effect on weight gain without being linked to overt weight gain in adults. They conclude an improved understanding of infant weight biology is important as childhood obesity, as well as malnutrition and premature births are worldwide challenges.
The team surmises their data uncovers a previously unknown role of common genetic variants in genes involved in the leptin signaling pathway which affects BMI during fetal, newborn, and infant growth.
For the future, the researchers state their study provides knowledge of time-resolved genetic determinants for infant and early childhood growth. Accordingly, this suggests weight management intervention should be tailored to the developmental stage and genetic profile of the patients.
Source: University of Bergen
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