This is caused by a person or animal having two copies of the ObR gene which causes obesity due to inaccurate reports of leptin.

Grinnell College

Leptin is a satiety hormone produced by fat cells and released into the bloodstream. It signals fullness to the brain, helping to regulate eating behavior by shutting it off. Leptin receptors are found in various brain regions, including the choroid plexus, cortex, and several hypothalamic nuclei. Genetic defects in the gene responsible for leptin production can cause a false underreporting of body fat, leading to overeating and obesity.

Leptin

Weight Regulation Disorders Associated with the Hypothalamus

Breedlove, S. & Watson, N. (2017). Behavioral neuroscience, eighth edition. Oxford University Press.

Behavioral Neuroscience 8th Edition

Inherited Obesity

Leptin is made by fat cells and insulin, which helps convey information about the body's energy reserves. The appetite neurons in the arcuate system have leptin receptors but it affects the receptors in oposite ways depending on which type of appetite neuron it is - NPY or POMC. High levels of leptin activates the appetite-suppressing POMC neurons while inhibiting the appetite-increasing NPY neurons. 

How Leptin Conveys information

Leptin is more of a long term indicator of the body's energy levels. It is possible that it promotes a remodeling of neurons in the arcuate nucleus to change the set point of people.

Leptin in preventing long term weight loss

Based on the principles of appetite regulation, analyze the scenario below and explain the most likely physiological reason for the mice's behavior. What kind of signal is failing, and why does this failure lead to overeating?

Analysis of Appetite Regulation

Based on the case study, explain the physiological reason for the child's constant hunger and subsequent overeating.

Eating to excess. Bilateral lesions to the VMH can cause animals to eat to excess and become obese.

Hyperphagia

Not eating and rapid weight loss. Lesions of the lateral hypothalamus can cause aphagia.

Aphagia

Obese individuals generally have lower levels of ghrelin than skinny participants before meal times, however the levels do not drop after a meal is eaten. This suggests that they experience a constantly elevated level of ghrelin that prompts continual hunger. Levels of leptin also remain high.

Ghrelin levels in obese individuals

Prader-Willi Syndrome (PWS) is a genetic condition linked to hypothalamic abnormalities. These abnormalities are thought to cause the syndrome's characteristic symptoms, including a constant, intense feeling of hunger and a slower metabolism, making PWS the leading genetic cause of severe childhood obesity. Because the hypothalamus also regulates sexual behavior, many individuals with PWS do not achieve sexual maturity during adolescence. Due to the risk of overeating, those with PWS, especially children, often need constant supervision and may face related cognitive and emotional challenges.

Prader-Willi Syndrome (PWS)

A patient presents with a set of distinct symptoms: an uncontrollable, persistent feeling of hunger leading to significant weight gain, a noticeably slow metabolism, and delayed physical maturation. Based on your understanding of how the brain regulates basic drives and physiological processes, which brain structure is most likely malfunctioning, and why does this specific combination of symptoms point to that structure?

Analyzing Symptoms of a Neuroendocrine Disorder

A patient presents with an insatiable appetite and significant, rapid weight gain. They report a constant, intense feeling of hunger and never feel satisfied after eating. Medical tests confirm their metabolic rate is unusually low. A brain scan reveals a lesion in a specific subcortical structure. Based on this information, identify the brain structure most likely affected and explain how its impairment would lead to these specific symptoms.

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