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Leptin and Obesity

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Although the nervous system does not have a direct chemical pathway to signal the caloric content of food, research with rodents has shown there is a signal for energy reserve levels. In 1953, Gordon Kennedy proposed the lipostatic hypothesis. This hypothesis provided an explanation that claimed that the brain is able to monitor the amount of stored body fat.

In the 1960s, Jackson Laboratories found mice that lacked copies of the ob gene were obese. The protein leptin encoded by the ob gene was found by scientists at Rockefeller University in 1994. Mice without the ob gene had a complete reversal of obesity when injected with leptin. If leptin signals fat stores and causes the brain to reduce eating, then leptin injections should be a beneficial treatment to reduce obesity.

However, contrary to predictions, injections of leptin have reduced obesity in only the small number of patients that lack the ob gene. Most obesity patients do not benefit from leptin injections.

Review the following statements, and select the statements that would be a correct reason why all obesity patients do NOT benefit from leptin treatments. ​​

Select ALL that apply.

A

Many obesity patients already have high levels of circulating leptin.

B

Leptin does not block the activation of MCH4 receptors.

C

Many obesity patients have neurons that have a decreased sensitivity to circulating levels of leptin.

D

Obesity patients may have a ​lower transfer of leptin across the blood-brain barrier.