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Sellayah and colleagues have postulated an 'Out of Africa' theory to explain the evolutionary origins of obesity. The theory cites diverse ethnic based differences in obesity susceptibility in western civilizations to contend that, neither the thrifty or drifty gene hypotheses can explain the demographics of the modern obesity crisis.
However, the proposed connection between a single gene and a single protein enzyme outlived the protein theory of gene structure. In a 1948 paper, Norman Horowitz named the concept the "one gene–one enzyme hypothesis". [2] Although influential, the one gene–one enzyme hypothesis was not unchallenged.
Pathophysiology of obesity is the study of disordered physiological processes that cause, result from, or are otherwise associated with obesity. A number of possible pathophysiological mechanisms have been identified which may contribute in the development and maintenance of obesity.
Osteoarthritis and obesity are closely linked. Obesity is one of the most important preventable factors for the development of osteoarthritis. Originally, the relationship between osteoarthritis and obesity was considered to be exclusively biomechanically based, according to which the excess weight caused the joint to become worn down more quickly.
The science behind weight management is complex, but one of the key concepts that governs weight management is Energy Balance. [9] Energy Balance is the phrase used to describe the difference between the number of calories a person consumes and the number of calories that same person expends (a.k.a. burns) in a given time period. [9]
In one study, researchers told 10- to 12-year-olds all the genetic and medical factors that contribute to obesity. Afterward, the kids could recite back the message they received—fat kids didn’t get that way by choice—but they still had the same negative attitudes about the bigger kids sitting next to them.
The malfunction of just one type of enzyme out of the thousands of types present in the human body can be fatal. An example of a fatal genetic disease due to enzyme insufficiency is Tay–Sachs disease, in which patients lack the enzyme hexosaminidase. [101] [102] One example of enzyme deficiency is the most common type of phenylketonuria.
When lipase enzymes are phosphorylated, they can access lipid droplets and through multiple steps of hydrolysis, breakdown triglycerides into fatty acids and glycerol. Each step of hydrolysis leads to the removal of one fatty acid. The first step and the rate-limiting step of lipolysis is carried out by adipose triglyceride lipase (ATGL).