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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. [4] [5]
The extreme endpoint of this distribution are the so-called 'monogenic' obesities where most of the impact on body weight can be tied to a mutation in a single gene that runs in a single family. The classic example of such a genetic effect is the presence of mutations in the leptin gene. [29]
A study presented at the Digestive Disease Week 2024 conference examined 84 people with obesity or other weight management issues in order to investigate how genetics plays a role in weight loss ...
FTO has been demonstrated to efficiently demethylate the related modified ribonucleotide, N6,2'-O-dimethyladenosine, and to an equal or lesser extent, m 6 A, in vitro . [5] [15] FTO knockdown with siRNA led to increased amounts of m 6 A in polyA-RNA, whereas overexpression of FTO resulted in decreased amounts of m 6 A in human cells. [10]
The relationship between stress and weight gain is complicated. A recent review suggests stress may influence weight through cognitive, behavioral, and physiological pathways, including hormone ...
Hormones have much to do with metabolism, food cravings, hunger-fullness cues and even how weight is distributed around the body. Several female hormone types matter for weight loss.
[184] [185] Fat: Fighting the Obesity Epidemic and Rethinking Thin: The New Science of Weight Loss and the Myths and Realities of Dieting review the work in the Friedman laboratory that led to the cloning of the ob gene, while The Hungry Gene draws attention to the contributions of Leibel. [citation needed]
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