By Margarita Snegireva. Obesity may be caused not only by eating habits but also by genetic roots in the brain.
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| Is obesity predetermined by our brain? |
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New research on obesity shows brain differences between rats that are genetically prone to becoming obese and rats without that obesity tendency.
The differences are in part of the hypothalamus, which is a brain region that's involved in appetite and hunger.
In rats that are genetically prone to obesity, certain brain cells in the hypothalamus don't grow as much and are less sensitive to the fullness hormone leptin, compared with other rats.
Flier summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity. This field of research had been almost unapproached until leptin was discovered in 1994. Since this discovery, many other hormonal mechanisms have been elucidated that participate in the regulation of appetite and food intake, storage patterns of adipose tissue, and development of insulin resistance. Since leptin's discovery, ghrelin, orexin, PYY 3-36, cholecystokinin, adiponectin, and many other mediators have been studied. The adipokines are mediators produced by adipose tissue; their action is thought to modify many obesity-related diseases.
Leptin and ghrelin are considered to be complementary in their influence on appetite, with ghrelin produced by the stomach modulating short-term appetitive control (i.e. to eat when the stomach is empty and to stop when the stomach is stretched). Leptin is produced by adipose tissue to signal fat storage reserves in the body, and mediates long-term appetitive controls (i.e. to eat more when fat storages are low and less when fat storages are high). Although administration of leptin may be effective in a small subset of obese individuals who are leptin deficient, many more obese individuals are thought to be leptin resistant. This resistance is thought to explain in part why administration of leptin has not been shown to be effective in suppressing appetite in most obese subjects.
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