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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.
Individuals who, due to genetic mutation, are unable to produce functional leptin or who produce leptin but are insensitive to it are prone to develop obesity. [4] This has been confirmed by experimental "knockdown" of leptin receptors in the lateral hypothalamus in rats, which caused the rats to consume more calories and increase in body ...
Numerous studies aimed to provide insight into genetic, economic, and/or environmental causes of obesity. According to the "thrifty gene hypothesis, [18] a genetic theory explaining rising obesity rates, certain individuals are genetically predisposed to metabolize food more efficiently than others as a result of human evolution. In times of ...
Research into genetic factors and potential treatments is still underway, but Scherer said the current best approach to medical treatment of obesity is GLP-1 medications.
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 ]
Scientists from the University of Exeter Medical School have found that people missing a specific blood group due to a genetic variant may be genetically predisposed to having obesity or overweight.
During the years, the study developed beyond the classical traits of human behaviour and included more genetically associated traits like genetic disorders (such as fragile X syndrome, Alzheimer's disease and obesity). The traditional methods of behavioural-genetic analysis provide a quantitative evaluation of genetic and non-genetic influences ...
The main problem with this idea is the timing at which the transition is presumed to have happened, and how this would then translate into the genetic predisposition to type 2 diabetes and obesity [citation needed]. For example, the decline in reproductive investment in human societies (the so-called r to K shift) has occurred far too recently ...