Summary
- A novel study assessed the relationship between the levels of fasting insulin and IGF-1 and obesity in obese children and adults among European people.
- The researhers used a method called Mendelian randomization (MR) analysis to explore the variables.
- Findings revealed that insulin-increasing alleles were associated with higher insulin resistance, whereas height changes were linked with IGF-1 variants.
- Understanding the genetic background of obesity may help to support preventive and therapeutic efforts among children and adults.
Childhood obesity has increased around the world, and researchers thrive to assess what might be contributing to this condition. Researchers of a recent recent study in a big cohort of Europeans looked at the potential association between levels of IGF-1 and fasting insulin.
Researchers used data from the UK Biobank for 444,480 participants who had measurements of fasting insulin and IGF-1 concentrations. They validated their findings in a subset of participants for whom childhood BMI was objectively measured.
The researchers used a method called Mendelian randomization (MR) to examine if these biomarkers had any causal relationship with obesity. MR uses genetic data to assess the likely causal relationship between an exposure and an outcome, fasting insulin and IGF-1 in this case.
The researchers genotyped all genetic variants associated with circulating fasting insulin and IGF-1 concentrations to genome-wide significance in this report. Subsequently, these variants were aligned; i.e., the allele increasing exposure was considered as effect allele. Highly correlated proxies were used for variants not found in the outcome data.
The results of the study showed that increased fasting insulin was related to insulin resistance, whereas other signals were associated with higher insulin and bioaction secretion. Conversely, genetic variants associated with higher IGF-1 levels were related to taller childhood height and therefore presumably reflected increased secretion of and action by IGF-1. These findings may add some novel evidence about the potential role of these biomarkers in development of childhood and adult obesity.
The authors concluded that knowledge of the genetic determinants of fasting insulin and IGF-1 levels may provide further insight into childhood-onset obesity as well as adult obesity. These discoveries could lead to future studies and treatments on the intensifying issue of obesity, particularly in kids. Understanding the genetic background of obesity helps us to conceive a perspective on targeted strategies for prevention and treatment in due course.
Diabetes & Endocrinology, Pediatrics