Question 1

You are performing laser ablation experiments on laboratory animals to ascertain the effects, on feeding behaviors, of damage to certain regions of the brain. In one series of experiments it is found that loss of the targeted brain region causes the animals eat nearly continuously, no matter the time of day, nor the composition of the chow. The ablation was centered on the hypothalamus and these results strongly indicate the damage affected which of the following regions of this structure?
A) lateral hypothalamic area (LHA)
B) nucleus of the solitary tract (NTS, NST)
C) paraventricular nucleus of the hypothalamus (PVN, PVH)
D) suprachiasmatic nucleus (SCN)
E) ventromedial hypothalamus (VMH, VMN)

Accepted Answer

The ventromedial hypothalamus (VMH) is associated with satiety and the regulation of feeding behavior. Damage to this area can lead to hyperphagia, causing animals to eat excessively.  The hypothalamus is involved in control of feeding behavior as well as the secretion of various pituitary releasing hormones. Specific nuclei within the hypothalamus exert different effects on appetite and the desire for food. The ventromedial hypothalamic nucleus (VMH), and to a lesser extent the dorsomedial hypothalamic nucleus (DMH) is involved in the sensation of satiety and lesions in these regions of the hypothalamus result in hyperphagia (excessive hunger) and obesity.

Question 2

You are assessing the effects of injecting synthetic peptides into laboratory mice. You discover that injecting one of the peptides induces hyperphagia. Which of the following hormones is most likely being mimicked by the actions of the synthetic peptide?
A) cholecystokinin, CCK
B) cocaine- and amphetamine-regulated transcript, CART
C) ghrelin
D) α-melanocyte stimulating hormone, α-MSH
E) peptide tyrosine tyrosine, PYY

Accepted Answer

Ghrelin is known as the "hunger hormone" and stimulates appetite, leading to increased food intake or hyperphagia.  Ghrelin is produced and secreted by the X/A-like enteroendocrine cells of the stomach oxyntic (acid-secreting) glands. The major effect of ghrelin is exerted within the central nervous system at the level of the arcuate nucleus where it stimulates the release of neuropeptide Y (NPY) and agouti-related protein (AgRP). The actions of NPY and AgRP enhance appetite and thus, food intake.

Question 3

Fatty acid metabolism within the brain is not a significant pathway for the generation of ATP. However, this does not mean that fatty acid metabolism is not a useful pathway in brain. Which of the following would be expected to be found at elevated levels in brain tissues following the metabolism of free fatty acids?
A) acetate
B) alanine
C) ceramide
D) citrate
E) sphingosine

Accepted Answer

Ceramide is a lipid molecule that can be synthesized from fatty acids and is involved in various cellular processes in the brain, including signaling pathways. Although β-oxidation of fatty acids represents a minor, if at all, source of the ATP pool in neurons, it is an important metabolic pathway determining the ultimate fate of fatty acids that enter the brain. As a result of fatty acid oxidation, a number of aqueous byproducts are detected in the brain such as fatty acyl-CoAs, fatty acyl-carnitines, ketone bodies, and various amino acids. Central metabolism of palmitate diverts its carbon atoms into the amino acids glutamate, glutamine, aspartate, asparagine, and GABA. In addition, numerous organic acids including citrate, malate, β-hydroxybutyrate, and acetyl-CoA result from palmitate oxidation. By far, citrate represents the largest by-product of fatty acid oxidation in the brain.

Question 4

You are examining feeding behavior in laboratory animals in response to the addition of a test organic molecule to their chow. Following consumption of the compound you discover that the animals loose interest in food. Additional experiments demonstrate that central metabolism of palmitic acid is reduced in these animals. Given these observations you believe that the test compound is most likely inhibiting which of the following hypothalamic enzymes?
A) acetyl-CoA carboxylase
B) carnitine palmitoyltransferase I
C) fatty acid synthase
D) malonyl-CoA decarboxylase
E) medium-chain acyl-CoA dehydrogenase

Accepted Answer

Carnitine palmitoyltransferase I is involved in the transport of fatty acids into the mitochondria for β-oxidation. Inhibition of this enzyme would reduce the metabolism of palmitic acid, leading to decreased energy production and reduced interest in food. Fatty acids, specifically long-chain fatty acids via the formation of long-chain fatty acylCoAs, exert anorexigenic effects via the hypothalamus. Mitochondrial CPT-1 activity is involved in the central effects of fatty acids. Inhibition of hypothalamic CPT-1 leads to an increase in cytosolic long-chain acyl-CoA content and results in anorexigenic effects.

Question 5

You are testing the effects of central administration of inhibitors of fatty acid oxidation on hypothalamic activity. Which of the following neuropeptides would you expect to see expressed at elevated levels in response to the actions of the inhibitor?
A) agouti-related peptide, AgRP
B) cocaine- and amphetamine-regulated transcript, CART
C) galanin
D) melanin-concentrating hormone, MCH
E) neuropeptide Y, NPY

Accepted Answer

Melanin-concentrating hormone (MCH) expression is responsive to differences in fuel source availability in the brain. Pharmacological inhibition or activation of glucose metabolism exerts no effect on the expression of MCH, however, inhibition of fatty acid oxidation results in increased expression and release of the hormone

Question 6

The pancreatic polypeptide (PP) family of proteins binds to a family of receptors that were originally characterized as NPY receptors. There are 4 NPY receptors in humans and they are designated as Y1, Y2, Y4, and Y5. Which of the following hormone-receptor combinations is involved in exerting anorexigenic responses?
A) NPY + Y1
B) NPY + Y4
C) PP + Y4
D) PYY + Y2
E) PYY + Y4

Accepted Answer

Peptide YY (PYY) binding to the Y2 receptor is known to exert anorexigenic effects, reducing appetite and food intake.  Receptors Y1, Y2, and Y5 preferentially bind NPY and PYY, whereas, Y4 exhibits highest affinity for PP. The Y2 receptor is involved in anorexigenic responses, whereas the Y1 and Y5 receptors have been shown to induce orexigenic responses. The Y2 receptors are thus, referred to as inhibitory receptors with respect to the activity of NPY and they are abundantly expressed on NPY neurons in the ARC of the hypothalamus.

Question 7

Which of the following gut hormones is known to bind to one of the cholecystokinin receptors resulting in activation of the oxyntic glands of the
Stomach?
A) cholecystokinin, CCK
B) gastrin
C) ghrelin
D) GLP-I
E) protein tyrosine tyrosine, PYY

Accepted Answer

Gastrin is produced in enteroendocrine G cells of the gastric antrum and duodenum and exists in 2 forms, little gastrin (17 amino acids) and big gastrin (34 amino acids). Gastrin is responsible for inducing gastric acid production and pepsin secretion. Both forms of gastrin bind to the CCK2 (CCKB) receptor on stomach and gut parietal cells with an affinity equal to that of CCK. Activation of the CCK_B receptor by gastrin triggers the production of gastric acid.

Question 8

Laser ablation experiments are being performed in laboratory animals to ascertain the effects, on feeding behaviors, of damage to certain regions of the brain. In one series of experiments it is found that loss of the targeted brain region causes the animals to avoid food, no matter the time of day, nor how long they have gone without eating. The ablation was centered on the hypothalamus and these results strongly indicate the damage affected in which of the following regions of this structure?
A) lateral hypothalamic area (LHA)
B) nucleus of the solitary tract (NTS, NST)
C) paraventricular nucleus of the hypothalamus (PVN, PVH)
D) suprachiasmatic nucleus (SCN)
E) ventromedial hypothalamus (VMH, VMN)

Accepted Answer

The lateral hypothalamic area (LHA) is known to be involved in promoting feeding behavior. Damage to this area can lead to a lack of interest in food, which aligns with the observed behavior in the experiments.  The hypothalamus is involved in control of feeding behavior as well as the secretion of various pituitary releasing hormones. Specific nuclei within the hypothalamus exert different effects on appetite and the desire for food. The lateral hypothalamic area (LHA) is responsible for transmitting orexigenic signals (desire for food intake) and loss of this region results in starvation.

Question 9

A patient is diagnosed with problems in emptying the gallbladder. On a blood checkup, one hormone/peptide that is known to stimulate gallbladder contraction is inappropriately low. Which of the following hormones is most likely deficient leading to the observed symptoms?
A) cholecystokinin, CCK
B) gastrin
C) GLP-1
D) pancreatic polypeptide
E) peptide tyrosine tyrosine, PYY

Accepted Answer

Cholecystokinin (CCK) is the hormone responsible for stimulating gallbladder contraction and bile release. A deficiency in CCK would lead to problems in emptying the gallbladder.  Cholecystokinin (CCK) is secreted from intestinal enteroendocrine I cells predominantly in the duodenum and jejunum. The level of CCK in the blood rises within 15 minutes of food ingestion and reaches a peak by 25 minutes. Upon binding its receptors in the gut, CCK induces contractions of the gallbladder and release of pancreatic enzymes and also inhibits gastric emptying.

Question 10

Blocking the actions of which of the following hormones would be expected to lead to the greatest level of appetite suppression?
A) adiponectin
B) ghrelin
C) GLP-1
D) obestatin
E) peptide tyrosine tyrosine, PYY

Accepted Answer

Ghrelin is known as the "hunger hormone" because it stimulates appetite. Blocking ghrelin would likely lead to significant appetite suppression. Ghrelin is produced and secreted by the X/A-like enteroendocrine cells of the stomach oxyntic (acid-secreting) glands. The major effect of ghrelin is exerted within the central nervous system at the level of the arcuate nucleus where it stimulates the release of neuropeptide Y (NPY) and agouti-related protein (AgRP). The actions of NPY and AgRP enhance appetite and thus, food intake.

Question 11

Several gut-derived factors control feeding behaviors elicited by the brain. Most of these factors exert their effects by reducing the desire for food intake. The synthesis of one of these factors is stimulated by fat intake and inhibited by leptin release from adipose tissue. In addition, vagal efferents are not required for release but the activity of another gut factor is involved in its release. Which one of the following factors fits each of these statements?
A) apolipoprotein A-IV, apoA-IV
B) cholecystokinin, CCK
C) ghrelin
D) GLP-1
E) peptide tyrosine tyrosine, PYY

Accepted Answer

Apolipoprotein A-IV (apoA-IV) synthesis is stimulated by fat intake and inhibited by leptin. It does not require vagal efferents for release, but its release is influenced by other gut factors. Apolipoprotein A-IV (apoA-IV) is synthesized exclusively in the small intestine and the hypothalamus. Intestinal synthesis of apoA-IV increases in response to ingestion and absorption of fat and it is subsequently incorporated into chylomicrons and delivered to the circulation via the lymphatic system. Systemic apoA-IV exerts effects in the CNS involving the sensation of satiety.

Question 12

The gut peptide ghrelin is posttranslationally modified before it is fully active. Which of the following represents the type of modification that is necessary for its biological action?
A) acetylation
B) acylation
C) methylation
D) phosphorylation
E) prenylation

Accepted Answer

Ghrelin requires acylation, specifically octanoylation, for its biological activity, which allows it to bind to its receptor and exert its effects. Bioactive ghrelin is acylated on the serine at position 3 with n-octanoic acid. The attachment of octanoic acid to Ser3 of ghrelin is accomplished by the acyltransferase identified as ghrelin O-acyltransferase (GOAT; also referred to as membrane-bound O-acyltransferase domain-containing 4, MBOAT4).

Question 13

You are investigating the potential of a new drug to be useful in treating obesity. Specifically you are hoping that the drug either stimulates anorexigenic peptide release or inhibits orexigenic peptide release. You discover that addition of the drug to water consumed by your test animals results in inhibition of glucose oxidation within the hypothalamus. Based upon your findings what peptide would you most likely expect to see increased in these test animals?
A) agouti-related peptide, AgRP
B) cocaine- and amphetamine-regulated transcript, CART
C) galanin
D) melanin-concentrating hormone, MCH
E) neuropeptide Y, NPY

Accepted Answer

The activation of NPY neurons in the hypothalamus exhibits fuel source specificity in that oxidation of glucose and fatty acids exert differing effects. Glucose oxidation signals ample energy supply and thus results in reduced NPY expression. On the other hand, fatty acid oxidation has limited, if any, effect on NPY release. Inhibition of glucose oxidation results in dramatically increased NPY release even in the presence of fatty acid metabolism. Thus, a compound that blocks glucose oxidation in the hypothalamus would be expected to result in a significant increase in the level of NPY expression.

Question 14

A defect in activity of which of the following hormones has been associated with the sleep disorder known as narcolepsy?
A) agouti-related peptide, AgRP
B) cocaine- and amphetamine-regulated transcript, CART
C) galanin-like peptide, GALP
D) melanin-concentrating hormone, MCH
E) orexin A

Accepted Answer

Orexin A is a hormone that plays a crucial role in regulating wakefulness and arousal. A deficiency in orexin (also known as hypocretin) is associated with narcolepsy, a sleep disorder characterized by excessive daytime sleepiness and sudden loss of muscle tone (cataplexy).  The orexin peptides function to increase food consumption. However, in addition to increased feeding behavior central orexin action increases wakefulness and suppresses REM sleep. These latter observations demonstrate that orexins play a causative role in the regulation of sleep-wake cycles. Indeed, loss of orexin function results in a condition in animals that mimics the sleep disorder in humans known as narcolepsy.

Question 15

Vagal afferents are involved in the responses of the CNS to certain gastrointestinal hormones. Which of the following gut hormones exerts some of its orexigenic responses via these vagal pathways?
A) cholecystokinin, CCK
B) ghrelin
C) glucose-dependent insulinotropic peptide, GIP
D) GLP-1
E) protein tyrosine tyrosine, PYY

Accepted Answer

Ghrelin is known as the "hunger hormone" and stimulates appetite. It exerts some of its orexigenic (appetite-stimulating) effects via vagal afferent pathways, signaling the central nervous system to increase food intake.  Ghrelin is produced and secreted by the X/A-like enteroendocrine cells of the stomach oxyntic (acid-secreting) glands. The major effect of ghrelin is exerted within the central nervous system at the level of the arcuate nucleus where it stimulates the release of neuropeptide Y (NPY) and agouti-related protein (AgRP). The actions of NPY and AgRP enhance appetite and thus, food intake.

Question 16

Which of the following gut hormones is responsible for the feeding phenomenon referred to as the ileal brake?
A) CCK
B) ghrelin
C) GIP
D) oxyntomodulin, OXM
E) protein tyrosine tyrosine, PYY

Accepted Answer

The ileal brake is a feedback mechanism that slows gastric emptying and intestinal transit when nutrients are present in the ileum. Protein tyrosine tyrosine (PYY) is a gut hormone released from the ileum and colon in response to food intake, and it plays a significant role in this process.  PYY produced by and secreted from intestinal enteroendocrine L cells of the ileum and colon. The release of PYY results in reduced gut motility, a delay in gastric emptying, and an inhibition of gallbladder contraction. All of these actions are associated with the ileal brake.

Question 17

Although the level of leptin secretion is proportional to the amount of fat in adipose tissue, obese individuals are resistant to the anorexigenic effects of the increased hormone levels. Which of the following hypothalamic hormones would be expected to have the greatest increase in expression as a consequence of obesity-induced leptin resistance?
A) cocaine- and amphetamine-regulated transcript, CART
B) galanin-like peptide, GALP
C) α-melanocyte stimulating hormone, α-MSH
D) neuropeptide Y, NPY

Accepted Answer

In obesity-induced leptin resistance, the anorexigenic effects of leptin are diminished, leading to increased expression of orexigenic hormones like neuropeptide Y (NPY), which stimulates appetite.  Peripheral hormones that act on the ARC and thereby affect the actions of NPY (and AgRP) are leptin and ghrelin. Leptin binds to its receptor present on NPY neurons and inhibits their firing resulting in reduced GABA release onto POMC neurons. This leptin-induced reduction in GABA action at POMC neurons is a disinhibition and allows for increased release of the anorexigenic peptide, α-MSH. This is, in part, the mechanism by which leptin decreases feeding behaviors. Loss of leptin effects on NPY and POMC neurons would lead to increased orexigenic responses contributing to obesity.

Question 18

You are studying a strain of laboratory mice that get obese even on a low-fat lab chow. In examination of the brains of these mice you find an abnormal poorly developed area of the hypothalamus. A defect in which of the following regions would most likely account for the observed obesity? 
A) lateral hypothalamic area (LHA)
B) nucleus of the solitary tract (NTS, NST)
C) paraventricular nucleus of the hypothalamus (PVN, PVH)
D) suprachiasmatic nucleus (SCN)
E) ventromedial hypothalamus (VMH, VMN)

Accepted Answer

The ventromedial hypothalamus (VMH) is involved in satiety and energy balance. A defect in this area can lead to hyperphagia and obesity. The hypothalamus is involved in control of feeding behavior as well as the secretion of various pituitary releasing hormones. Specific nuclei within the hypothalamus exert different effects on appetite and the desire for food. The ventromedial hypothalamic nucleus (VMH), and to a lesser extent the dorsomedial hypothalamic nucleus (DMH) is involved in the sensation of satiety and lesions in these regions of the hypothalamus result in hyperphagia (excessive hunger) and obesity.

Question 19

Which of the following brain regions sends and receives information to the visceral organs via the vagal nerve?
A) arcuate nucleus (ARC)
B) area postrema
C) nucleus of the solitary tract (NTS, NST)
D) perifornical lateral hypothalamus (PFLH)
E) ventromedial hypothalamus (VMH)

Accepted Answer

The nucleus of the solitary tract (NTS) is a critical brain region that receives sensory information from visceral organs via the vagus nerve and sends motor information back to these organs.  Satiety signals from the liver and gastrointestinal tract signal through the vagus nerve to the nucleus of the solitary tract (NTS) to cause meal termination, and in combination with the hypothalamus, integrate the various signals to determine the feeding responses of the organism.

Question 20

Which of the following hormones is expressed and released from the stomach and is involved in the stimulation of food intake?
A) cholecystokinin, CCK
B) ghrelin
C) GLP-1
D) neuropeptide Y, NPY
E) protein tyrosine tyrosine, PYY

Accepted Answer

Ghrelin is a hormone produced and released from the stomach that stimulates appetite and food intake.  Ghrelin is produced and secreted by the X/A-like enteroendocrine cells of the stomach oxyntic (acid-secreting) glands. The major effect of ghrelin is exerted within the central nervous system at the level of the arcuate nucleus where it stimulates the release of neuropeptide Y (NPY) and agouti-related protein (AgRP). The actions of NPY and AgRP enhance appetite and thus, food intake.

Quiz 44: Gut-Brain Interactions and Feeding Behaviors

You are assessing the effects of injecting synthetic peptides into laboratory mice. You discover that injecting one of the peptides induces hyperphagia. Which of the following hormones is most likely being mimicked by the actions of the synthetic peptide?

You are testing the effects of central administration of inhibitors of fatty acid oxidation on hypothalamic activity. Which of the following neuropeptides would you expect to see expressed at elevated levels in response to the actions of the inhibitor?

Which of the following gut hormones is known to bind to one of the cholecystokinin receptors resulting in activation of the oxyntic glands of the Stomach?

A patient is diagnosed with problems in emptying the gallbladder. On a blood checkup, one hormone/peptide that is known to stimulate gallbladder contraction is inappropriately low. Which of the following hormones is most likely deficient leading to the observed symptoms?

Blocking the actions of which of the following hormones would be expected to lead to the greatest level of appetite suppression?

The gut peptide ghrelin is posttranslationally modified before it is fully active. Which of the following represents the type of modification that is necessary for its biological action?

A defect in activity of which of the following hormones has been associated with the sleep disorder known as narcolepsy?

Vagal afferents are involved in the responses of the CNS to certain gastrointestinal hormones. Which of the following gut hormones exerts some of its orexigenic responses via these vagal pathways?

Which of the following gut hormones is responsible for the feeding phenomenon referred to as the ileal brake?

You are studying a strain of laboratory mice that get obese even on a low-fat lab chow. In examination of the brains of these mice you find an abnormal poorly developed area of the hypothalamus. A defect in which of the following regions would most likely account for the observed obesity?

Which of the following brain regions sends and receives information to the visceral organs via the vagal nerve?

Which of the following hormones is expressed and released from the stomach and is involved in the stimulation of food intake?