Neurobiology Of Appetite Regulation

Hyperphagia refers to a condition characterized by excessive food intake and hunger. It is a medical term used to describe an abnormal increase in appetite, leading to overeating and a constant feeling of hunger. This can be caused by various factors such as hormonal imbalances, certain medications, or psychological disorders. Individuals with hyperphagia may have difficulty controlling their food intake, which can result in weight gain and other health issues.

Leptin is a hormone that plays a crucial role in regulating energy balance and appetite. It is primarily produced and released by adipose tissue, which is the body's main source of stored fat. Adipose tissue releases leptin into the bloodstream in proportion to the amount of fat it stores. This hormone then acts on the brain, particularly the hypothalamus, to suppress appetite and increase energy expenditure. Therefore, adipose tissue is considered the major source of leptin in the body.

Stimulation of the vagus nerve causes satiety. The vagus nerve is a cranial nerve that plays a crucial role in regulating various bodily functions, including digestion and appetite. When the vagus nerve is stimulated, it sends signals to the brain to promote feelings of fullness and satisfaction, leading to satiety. This can help regulate food intake and prevent overeating.

Leptin is a hormone produced by fat cells that helps regulate energy balance and appetite. In normal healthy individuals, the amount of circulating leptin is directly proportional to body fat. This means that as body fat increases, the amount of leptin in the bloodstream also increases. Leptin acts on the brain to suppress appetite and increase energy expenditure, thus helping to maintain a healthy body weight. Therefore, the correct answer is body fat.

The arcuate nucleus is located in the hypothalamus. The hypothalamus is a small region in the brain that plays a crucial role in regulating various bodily functions, including hormone secretion, body temperature, hunger, thirst, and sleep. The arcuate nucleus, specifically, is involved in the regulation of appetite and energy balance. It contains neurons that produce and release important appetite-regulating hormones, such as neuropeptide Y and alpha-melanocyte-stimulating hormone. Dysfunction of the arcuate nucleus can lead to disruptions in appetite control and contribute to conditions like obesity.

Ghrelin signals hunger, therefore the levels rise before a meal. However, like leptin, ghrelin levels appear to be "doing what they are supposed to" in obese persons (low ghrelin levels should reduce hunger and therefore weight) but obesity appears to be associated with "ghrelin insensitivity"

A rare homozygous frame-shift mutation is associated with very low leptin levels and early-onset obesity. THis is treatable with exogenous leptin

Peptides which stimulate feeding are orexigenic

Agouti related peptide (AgRP) and Neuropeptide Y (NPY) are examples of orexigenic peptides. These peptides stimulate appetite and increase food intake. AgRP is produced in the hypothalamus and acts on the melanocortin receptors to increase food consumption. Neuropeptide Y is also produced in the hypothalamus and stimulates feeding behavior by acting on various receptors in the brain. Both AgRP and NPY play important roles in regulating energy balance and promoting feeding behavior.

Leptin is produced by the Ob gene on human chromosome 7. Leptin is a hormone that plays a crucial role in regulating appetite and metabolism. It is primarily produced by adipose tissue (fat cells) and acts on the hypothalamus in the brain to suppress appetite and increase energy expenditure. Leptin levels are closely related to body fat percentage, and deficiencies in leptin production or receptor function can lead to obesity and other metabolic disorders.

AgRP, or Agouti-related protein, is a neuropeptide that acts as an antagonist to the melanocortin receptor 4 (MCR4). When AgRP binds to MCR4, it blocks the receptor's activation by other ligands, such as alpha-MSH, ghrelin, leptin, and serotonin. This inhibition of MCR4 activity by AgRP ultimately leads to increased appetite and food intake. Therefore, AgRP is the correct answer as it directly blocks the function of MCR4.

Lesioning the lateral region of the hypothalamus produces a reduction in the "setpoint." The lateral region of the hypothalamus is involved in regulating hunger and feeding behavior. When this region is damaged, it can lead to a decrease in appetite and a lower setpoint for hunger, resulting in reduced food intake.

The correct answer is alpha-MSH. Melanocortin receptor 4 (MCR4) is a G-protein coupled receptor that plays a crucial role in regulating energy homeostasis and body weight. It is primarily activated by alpha-MSH (melanocyte-stimulating hormone), which is produced by the cleavage of proopiomelanocortin (POMC). Alpha-MSH binding to MCR4 leads to the activation of intracellular signaling pathways that regulate appetite and energy expenditure. AgRP, ghrelin, leptin, and serotonin are also involved in the regulation of appetite and body weight, but they do not directly activate MCR4.

When the ventromedial region of the hypothalamus is lesioned, it leads to hyperphagia, which is an excessive and uncontrollable increase in appetite and food intake. This region of the hypothalamus is responsible for regulating satiety and controlling the feeling of fullness after a meal. Lesions in the ventromedial region disrupt this regulation, causing a loss of appetite control and leading to overeating.

Anorexigenic peptides are substances that suppress appetite and promote satiety, leading to a decrease in food intake. Alpha-melanocyte stimulating hormone (alpha-MSH) is an anorexigenic peptide that is released by the brain to regulate food intake and body weight. It acts on melanocortin receptors in the hypothalamus to decrease appetite and increase energy expenditure. Cocaine and amphetamine related transcript (CART) is another anorexigenic peptide that is involved in regulating appetite and energy balance. It is released in response to fasting and acts in the brain to decrease food intake and increase energy expenditure. Both alpha-MSH and CART play important roles in the regulation of food intake and body weight.

Most obese people have high leptin levels, but they also have high levels of body fat, meaning their leptin levels are approximately what they should be. The point bring, most cases of obesity are not associated with altered leptin levels, rather, obesity appears to be "leptin-insensitive".

The vagus nerve is activated by choleocystokinin and stomach distension. Choleocystokinin is a hormone released by the small intestine in response to the presence of food. It stimulates the release of bile from the gallbladder and pancreatic enzymes. Stomach distension refers to the stretching of the stomach wall due to the presence of food. Both choleocystokinin and stomach distension activate the vagus nerve, which plays a role in regulating various bodily functions such as digestion, heart rate, and breathing.

Insulin and leptin are both considered adipostats because they play a role in regulating body weight and fat storage. Insulin is a hormone released by the pancreas in response to elevated blood glucose levels. It helps to regulate glucose metabolism and promotes the storage of excess glucose as fat. Leptin is a hormone produced by fat cells that signals to the brain to reduce appetite and increase energy expenditure. It acts as a feedback mechanism to maintain body weight and fat stores. Ghrelin, cholecystokinin, and serotonin are also involved in appetite regulation, but they are not specifically classified as adipostats.