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Like many other medical conditions, obesity is the result of an interplay between environmental and genetic factors. [2] [3] Studies have identified variants in several genes that may contribute to weight gain and body fat distribution; although, only in a few cases are genes the primary cause of obesity.
16p11.2 deletion syndrome is a rare genetic condition caused by microdeletion on the short arm of chromosome 16. Most affected individuals experience global developmental delay and intellectual disability, as well as childhood-onset obesity. [1] 16p11.2 deletion is estimated to account for approximately 1% of autism spectrum disorder cases. [3] [4]
In 1993, a genetic polymorphism within lipomas was localized to chromosome 12q15, where the HMGIC gene encodes the high-mobility-group protein isoform I-C. [2] This is one of the most commonly found mutations in solitary lipomatous tumors but lipomas often have multiple mutations. Reciprocal translocations involving chromosomes 12q13 and 12q14 ...
Fat mass and obesity-associated protein also known as alpha-ketoglutarate-dependent dioxygenase FTO is an enzyme that in humans is encoded by the FTO gene located on chromosome 16. As one homolog in the AlkB family proteins, it is the first messenger RNA (mRNA) demethylase that has been identified. [ 5 ]
Obesity is a disease characterized by having excessive body fat, increasing a person’s risk for many serious health problems, such as heart disease, diabetes, and even some cancers.
Chromosome 16 is one of the 23 pairs of chromosomes in humans. People normally have two copies of this chromosome. People normally have two copies of this chromosome. Chromosome 16 spans about 90 million base pairs (the building material of DNA) and represents just under 3% of the total DNA in cells .
A new study published Friday in the journal, JAMA Health Forum, found that obesity numbers ticked down slightly from 46% in 2022 to 45.6% in 2023. While only a slight decline, this is the first ...
The mechanism is due to maternal meiotic non-disjunction followed by mitotic loss of the paternal chromosome 15 after fertilization. The third cause for PWS is the disruption of the imprinting process on the paternally inherited chromosome 15 (epigenetic phenomena). This disruption is present in approximately 2–5% of affected individuals.