Regulation Of Feeding Behavior

REGULATION OF FEEDING BEHAVIOR

Q. 1

About Neuropeptide Y all are true except:

 A

It is mediated through melanocorticotropin hormone

 B

Decreases thermogenesis

 C

Its level decreases during starvation

 D

Contains 36 aa residues

Q. 1

About Neuropeptide Y all are true except:

 A

It is mediated through melanocorticotropin hormone

 B

Decreases thermogenesis

 C

Its level decreases during starvation

 D

Contains 36 aa residues

Ans. C

Explanation:

its level decreases during starvation [Ref: Guyton 11/e p868-871]

  • As mentioned in the previous question, NPY is an Orexigenic i.e. appetite stimulant. Thus its level increases during starvation to increase food intake and reduce energy expenditure (decrease thermogenesis).
  • NPY is a neurohormone released by hypothalamus.
  • The hypothalamus can sense the body’s state of starvation or welfed through a peptide hormone released by adipocytes –Leptin.
  • When the amount of adipose tissue increases (signalling excess energy storage), the adipocytes produce increased amounts of leptin. Leptin acts on hypothalamic nuclei initiating multiple actions that decrease body’s fat storage. These actions are:

(1)  inactivation of NPY-AGRP neurons decreasing production of appetite stimulators, such as NPY and AGRP;

(2)  activation of POMC neurons, causing release of cc-MSH (melanocorticotropin) and activation of inelanocortin receptors;

(3)     increased production in the hypothalamus of substances, such as corticotropin-releasing hormone, that decrease food intake;

(4)  increased sympathetic nerve activity (through neural projections from the hypothalamus to the vasomotor centers), which increases metabolic rate and energy expenditure; and

(5)  decreased insulin secretion by the pancreatic beta cells, which decreases energy storage.

  • Thus during starvation, leptin production is decreased causing increased levels of NPY.
  • As mentioned in the previous question, there are 2 types of neurons in the hypothalamic nuclei regulating appetite i.e.

1)    NPY-AGRP neurons – which release orixogenic substances NPY and AGRP.

2)    POMC (proopiomelanocortin) neurons – which release a-MSH (a-Melanocyte stimulating hormone or melanocorticotropin) and CART (Cocaine and amphetamine regulated transcript). These are anorexigenic i.e. decrease food intake and increase energy expenditure.

  • Note that some students were of the opinion that one of the option was – `NPY and melanocorticotropin have same effect’. In that case this is a false statement as

NPY is orexigenic, increases food intake.

Melanocorticotropin or MSH is anorexigenic, decreases food intake.

  • “NPY is a polypeptide containing 36 amino acid residues”- Ganong 23/e p145

Q. 2

Appetite is stimulated by all except

 A

Agouti related peptide

 B

Melanocyte concentrating hormone

 C

Melanocyte stimulating hormone

 D

Neuropeptide Y

Q. 2

Appetite is stimulated by all except

 A

Agouti related peptide

 B

Melanocyte concentrating hormone

 C

Melanocyte stimulating hormone

 D

Neuropeptide Y

Ans. C

Explanation:

Melanocyte stimulating hormone [Ref: Ganong 22/e, p 238t; Guyton physiology 11/e, p 869t; Harrison 17/e, p 255, 463, 464; Obesity: Mechanisms & Clinical Management by Robert H. Eckel 2003 – p 129]

a..Melanocyte stimulating hormone (a-MSH) depresses appetite by acting centrally on satiety centre.

Neurotransmitters & Hormones that influence feeding and satiety centres in the hypothalamus

Increase Feeding (Orexigenic)

Decrease Feeding (Anorexigenic)

Neuropeptide Y (NPY)

a-Melanocyte-stimulating hormone (a-MSH)

Agouti-related protein (AGRP)

Leptin

Melanin-concentrating hormone (MCH)

Serotonin

Orexins A and B

Norepinephrine

Endorphins

Corticotropin-releasing hormone (CRH)

Galanin (GAL)

Insulin

Amino acids (glutamate and 7-aminobutyric

Cholecystokinin (CCK)*

acid)

Glucagon-like peptide (GLP)

Cortisol

Cocaine- and amphetamine-regulated transcript (CART)

Ghrelin

Peptide YY (PYY)*

Growth hormone releasing hormone (GHRH)

Bombesin

*CCK & PYY are mentioned as orexigenic in Harrison 17/e, p 464 but in Ganong & Guyton these are mentioned under anorexigenic peptides.

 



Q. 3 Feeding centre is located in:
 A Lateral hypothalamu
 B Ventro medial nucleus
 C Supraoptic nucleus
 D Frontal lobe
Q. 3 Feeding centre is located in:
 A Lateral hypothalamu
 B Ventro medial nucleus
 C Supraoptic nucleus
 D Frontal lobe
Ans. A

Explanation:

Lateral hypothalamus


Q. 4 Ghrelin is responsible for:
 A Stimulation of appetite
 B Suppression of appetite
 C Stimulation of sleep
 D Suppression of sleep
Q. 4 Ghrelin is responsible for:
 A Stimulation of appetite
 B Suppression of appetite
 C Stimulation of sleep
 D Suppression of sleep
Ans. B

Explanation:

Suppression of appetite


Q. 5

Orexins play an important role in people with eating disorders. All of the following are orexins, EXCEPT:

 A

Leptin

 B

Orexin-A

 C

Hypocretin 1

 D

Hypocretin 2

Q. 5

Orexins play an important role in people with eating disorders. All of the following are orexins, EXCEPT:

 A

Leptin

 B

Orexin-A

 C

Hypocretin 1

 D

Hypocretin 2

Ans. A

Explanation:

Orexins (A and B) or Hypocretins (1 and 2):

  • They are produced by neurons in the lateral hypothalamus perifornical area. 
  • Regulated by glucose, leptin, neuropeptide Y, and POMC neurons. 
  • They stimulate food intake.
Leptin:
  • It is produced in adipose tissue. 
  • Acts on neuropeptide Y, AgRP-containing neurons, and -MSH neurons in the arcuate nucleus of the hypothalamus to decrease food intake.
 
Ref: Molina P.E. (2010). Chapter 10. Endocrine Integration of Energy & Electrolyte Balance. In P.E. Molina (Ed), Endocrine Physiology, 3e.

 


Q. 6

The MOST abundant source of ghrelin is:

 A

Gastric fundus

 B

Gastric body

 C

Gastric pylorus

 D

First part of duodenum

Q. 6

The MOST abundant source of ghrelin is:

 A

Gastric fundus

 B

Gastric body

 C

Gastric pylorus

 D

First part of duodenum

Ans. A

Explanation:

Ghrelin is a 28 amino acid peptide mainly secreted from stomach and the most abundant source is gastric fundus.

It also produced from intestine, pancreas, pituitary, kidney, placenta.
ACTION:
  • It increases growth hormone secretion
  • It increases food intake
  • It increases weight gain
 
Ref: Sleisenger and Fordtran’s, Edition-9, Page-8.

Q. 7

The primary action of leptin is:

 A

To increase food intake

 B

To decrease food intake

 C

To increase gastric contraction

 D

To increase intestinal motility

Q. 7

The primary action of leptin is:

 A

To increase food intake

 B

To decrease food intake

 C

To increase gastric contraction

 D

To increase intestinal motility

Ans. B

Explanation:

LEPTIN
 
It is a 167 aa peptide secreted from adipocytes, blood leptin level reflects total body fat.
Its primary action: To decrease food intake. It in CNS decreases NPY and alpha MSH.
Leptin deficiency may lead to obesity.
 
Ref: Sleisenger and Fordtran’s, Edition-9, Page-8.

Q. 8

Appetite is stimulated by all of the following peptides, EXCEPT:

 A

Neuropeptide Y

 B

Agouti – Related Peptide (AGRP)

 C

Melanocyte Stimulating hormone (MSH)

 D

Melanin Concentrating Hormone (MCH)

Q. 8

Appetite is stimulated by all of the following peptides, EXCEPT:

 A

Neuropeptide Y

 B

Agouti – Related Peptide (AGRP)

 C

Melanocyte Stimulating hormone (MSH)

 D

Melanin Concentrating Hormone (MCH)

Ans. C

Explanation:

Pro-opiomelanocortin (POMC) derivatives, particularly alpha MSH decrease food intake. These derivatives have four receptors MC1-R is involved in skin pigmentation, MC2-R is involved in adrenal glucocorticoid production, MC3-R is associated with control of sebaceous gland secretion and MC4-R mediates effects on apetite. Alpha MSH activates the melanocortin 4 receptor and mediates anorexigenic effects.

Ref: Textbook of Medical Physiology By Guyton and Hall, 10th Edition, Page 805 ; Harrison’s Principles of Internal Medicine, 16th Edition, Page 233


Q. 9

Which of the following inhibits appetite by counteracting the effects of neuropeptide Y?

 A

Orexins

 B

Neuropeptide Y

 C

Ghrelin

 D

Leptin

Q. 9

Which of the following inhibits appetite by counteracting the effects of neuropeptide Y?

 A

Orexins

 B

Neuropeptide Y

 C

Ghrelin

 D

Leptin

Ans. D

Explanation:

Leptin acts on receptors in the hypothalamus of the brain where it inhibits appetite by (1) counteracting the effects of neuropeptide Y (a potent feeding stimulant secreted by cells in the gut and in the hypothalamus); (2) counteracting the effects of anandamide (another potent feeding stimulant that binds to the same receptors as THC), and (3) promoting the synthesis of α-MSH, an appetite suppressant.

Ghrelin is a hormone produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas that stimulates hunger.

Neuropeptide Y is a natural substance that acts on the brain to stimulate eating.Leptin reduces the output of NPY from the hypothalamus, a major production center.

Orexins (hypocretins) are neuropeptides primarily localized in the hypothalamus and are implicated in the regulation of a variety of activities, including feeding behavior and energy balance.


Q. 10

Ghrelin is a hormone produced by the enteroendocrine cells of the stomach. It is responsible for:

 A

Stimulation of appetite

 B

Suppression of appetite

 C

Stimulation of sleep

 D

Suppression of sleep

Q. 10

Ghrelin is a hormone produced by the enteroendocrine cells of the stomach. It is responsible for:

 A

Stimulation of appetite

 B

Suppression of appetite

 C

Stimulation of sleep

 D

Suppression of sleep

Ans. A

Explanation:

Ghrelin is a hormone produced by the enteroendocrine cells of the stomach, and to lesser extent by the placenta, pituitary, and hypothalamus. In humans, ghrelin has been shown to be a potent growth hormone secretagogue and appetite stimulant.
 

Good to know:
Increased ghrelin levels seen in,

  • Fasting
  • Individuals consuming low calorie diets
  • Chronic strenuous exercise
  • Cancer anorexia
  • Anorexia nervosa
  • Prader-Willi syndrome

Decreased ghrelin levels seen in,

  • During meals
  • Obesity
Ghrelin levels are decreased in obese individuals.
 
Ref: Molina P.E. (2010). Chapter 10. Endocrine Integration of Energy & Electrolyte Balance. In P.E. Molina (Ed), Endocrine Physiology, 3e.

 


Q. 11

The principal polypeptide that increases food intake are the following, EXCEPT:

 A

Neuropeptide-Y

 B

Leptin

 C

Orexin-A

 D

Endocannabinoid

Q. 11

The principal polypeptide that increases food intake are the following, EXCEPT:

 A

Neuropeptide-Y

 B

Leptin

 C

Orexin-A

 D

Endocannabinoid

Ans. B

Explanation:

The major afferent signal allowing the brain to sense the level of energy stores is the hormone leptin. Circulating leptin levels are proportionate to the amount of body fat. Higher circulating leptin levels generally reduce, while lower levels generally increase, appetite. 
 
Factors that increases the appetite:
  • Neuropeptide Y
  • Melanin-concentrating hormone
  • Agouti-related peptide
  • Orexin
  • Endocannabinoid
Ref: Paulsen D.F. (2010). Chapter 6. Adipose Tissue. In D.F. Paulsen (Ed), Histology & Cell Biology: Examination & Board Review, 5e.

Q. 12

Appetite is stimulated by all of the following peptides, Except:

 A

Agouti – Related Peptide (AGRP)

 B

Melanocyte Stimulating hormone (MSH)

 C

Melanin Concentrating Hormone (MCH)

 D

Neuropeptide Y

Q. 12

Appetite is stimulated by all of the following peptides, Except:

 A

Agouti – Related Peptide (AGRP)

 B

Melanocyte Stimulating hormone (MSH)

 C

Melanin Concentrating Hormone (MCH)

 D

Neuropeptide Y

Ans. B

Explanation:

B i.e. Melanocyte Stimulating hormone (MSH)

MSH (a-melanocyte stimulating hormone) and CART (cocaine & amphetamine regulated transcript) releasing POMC (pro-opio-melano-cortin) neurons are anorexigenic/anti-orexigenic (i.e. produce satiety & decrease appetite). Whereas, AGRP (agouti-related-peptide) and NPY (neuropeptide Y) releasing neurons of arcuate nuclei of hypothalamus are orexigenic (i.e. increase appetite & cause obesity).

Regulation of Food Intake

– Hypothalmus contains hunger (feeding) and satiety centers. The lateral nuclei of hypothalamus serve as a feeding (hunger) center and ventromedial nuclei of hypothalamus serve as the satiety center. Stimulation of feeding center & /or destruction of satiety center cause voracious appetite (hyperphagia) & obesity. Whereas, destruction of feeding center & /or stimulation of satiety center cause anorexia (complete satiety Rack of desire for food) & progressive inanition (weight loss).

– Lesions of paraventricular nuclei of hypothalamus cause excessive eating and lesions of dorsomedial nuclei usually depress eating behaviour.

– Arcuate nuclei of hypothalamus, are the sites where multiple hormones released from gastrointestinal tract and adiose tissue converge to regulate food intake & energy expenditure. It has 2 types of neurons.


Q. 13

Which hormone is secreted from stomach that control intake of food:

 A

Orexin

 B

Insulin like growth hormone

 C

Cholecystokinin

 D

Ghrelin

Q. 13

Which hormone is secreted from stomach that control intake of food:

 A

Orexin

 B

Insulin like growth hormone

 C

Cholecystokinin

 D

Ghrelin

Ans. D

Explanation:

D i.e. Ghrelin

Ghrelin, is released by stomachs, especially during fasting and stimulates appetites (orexigenic).

– CCK, Peptide YY/PYY (secreted from entire gitract but especially from ileum & colon), glucagon like peptide (secreted by intestines d/t presence of food) and insulin (produced in response to GLP) are gastrointestinal hormonal factors, which suppress feeding i.e. cause satiety (anorexigenic). Whereas, ghrelin another gastrointestinal hormone produced mainly by stomach is orexigenic (i.e. increase appetite).

– Growth hormone (GH) also k/a somatotropic hormone or somatotropin exerts much of its effects through intermediate substances called somatomedins secreted by liver (and to a much less extent, other tissues). Because many effects of somatomedins on growth are similar to those of insulin, therefore somatomedins are also called insulin like growth factors (IGFs). Out of 4 somatomedins isolated, the most important is somatomedin C (or IGF-1) and pygmies of Africa & Levi-Lorain dwarf have congenital inability to synthesize significant amount of IGF-1.

– Orexin (hypocretin) producing neurons occur in hypothalamus. Orexins A and B increase feeding (appetite) whereas, brains from humans with narcolepsy have fewer orexin producing neurons in hypothalamus. – Cholecystokinin (CCK) is secreted by I cells of upper small intestine (jejunum) and decreases feeding (antiorexigenic / aorexigenic), inhibits gastric emptying, and stimulates secretion of pancreatic juice rich in enzymes, contraction of gall bladder, secretion of glucagon & insulin and small intestine & colonic motality.

It is a gastrointestinal hormone synthesized & released mainly by oxyntic cells of stomach (Guyton) / P or D1 cells of fundus of stomach. It is also produced by the intestine & epsilon cells of pancreas in small amounts. Ghrelin acts to stimulate hunger (appetite)Q. So blood levels rise during fasting, peak just before eating and then fall rapidly after a meal (orexigenic). In this way, it is counter part of hormone leptin, produced by adipose tissue, which induces satiation (i.e. is anti-orexigenic) when present at higher levels.

– Ghrelin is also produced in arcuate nucleus of hypothalamus and has marked growth hormone stimulating activity i.e. it stimulates GH secretion from anterior pituitary gland by acting directly on receptors in pituitary.

– G protein coupled ghrelin receptor formerly k/a growth hormone secretagogue (GHS) receptor is expressed in arcuate nucleus, lateral hypothalamus, vagal afferent cell bodies & vagal afferent endings through out gastrointestinal tract.

It has an important role in neurotrophy, particularly in hippocampus and is essential for cognitive adaptation to changing environment and process of learning.


Q. 14

All are true about neuropeptide Y except:

 A

Consist of 36 amino acids

 B

Decreases thermogenesis

 C

Decreased in starvation

 D

Same effect like melanocorticotropin

Q. 14

All are true about neuropeptide Y except:

 A

Consist of 36 amino acids

 B

Decreases thermogenesis

 C

Decreased in starvation

 D

Same effect like melanocorticotropin

Ans. C

Explanation:

C i.e. Decreased in starvation

Neuropeptide Y (NPY) is a 36 aminoacidQ polypeptide, which increases during starvation (Martin-52)/ and feeding (Ganong 22/e p 238) to increase the food intake and reduce energy expenditure (i.e. basal /resting metabolic rate, adaptive thermogenesis, thermic effect of exercise and energy cost of metabolizing and storing food). NP-Y decreases during satiety.

NPY & MCH (melanin concentrating hormone) increase appetite whereas, MSH (a-metanocyte stimulating hormone) decrease appetite. NPY decrease the firing of POMC neurons, thereby decreasing the activity of melanocortin (i.e. MSH secreting) pathway. (So the option D has some mistake).

– Neuropeptide Y (found in brain & autonomic nervous system), pancreatic polypeptide (produced by F cells in islets) and polypeptide YY (a gastrointestinal hormone) – are • closely related as they all contain 36 aminoacidsQ, end in tyrosine, are amidated at their carboxy terminals and all act on at least 2 of the 4 known G protein coupled receptors for these peptides : Yl, Y2, Y4 and Y5. However, neuropeptide Y is secreted only by neurons, whereas pancreatic polypeptide & polypeptide YY are secreted by endocrine cells.

NPY is secreted by (adrenergic, noradrenergic & other) neurons of brain (hypothalamus, periaqueductal gray, medulla) and autonomic nervous system.

Neurons that produce orexigenic substances NPY and AGRP, have their cell bodies in arcuate nuclei and project their axons to paraventricular nuclei (of hypothalamus) to antagonize melanocortin receptors (MCR-3 & MCR-4) there by inhibiting the effects of a-MSH produced by POMC neurons. When energy stores of body are low (eg starvation), orexigenic neurons are activated to release NPY, which stimulates appetite and at the same time, firing of POMC neurons is decreased thereby reducing the activity melanocortin pathway, so further stimulating appetite. (Guyton -870) . When injected into hypothalamus, NPY increases food intake, and inhibitors of NPY synthesis decrease food intake. NPY m-RNA in the hypothalamus increases during feeding and decreases during satietyQ. NPY exerts its effects through Y-5 receptor. Knocking out of NPY gene does not produce marked • effects on feeding, pointing that other pathways are also involved, but knockout of NPY gene in leptin deficient cause them to eat less and spend more energy that have normal NPY gene Leptin, a 167 aminoaicd polypeptide, produced primarily in fat cells act on hypothalamus to decreases the activity of NPY neurons and decrease activity of POMC secreting neurons thereby causing anorexia & increased energy consumption. The anorexiant action of leptin is antagonized by blockade of CB1 receptor (marijuana / cannabinoids increase appetite by acting on CB1 receptor) and inhibition of phosphatidylinositol -3-hydroxykinase (an hypothalamic enzyme activated by leptin). Leptin also increases activity of SOCS-3 (suppressor of cytokine signaling-3) in NPY neurons and SOCS-3 supresses further leptin receptor signaling, suggesting a turn off mechanism.

– So NPY (& AGRP) orexigenic neurons increase food intake and reduce energy expenditure (which includes basal /resting metabolic rate , energy cost of metabolizing & storing food, thermic effect of exercise, and adaptive

thermogenesis).

– Cotransmitters in autonomic neurons include, VIP (released with actyl choline) and ATP & NPY (with norepinephrine). The small granulated vesicles in post ganglionic adrenergic neurons contain ATP and norepinephrine (NE) and large granulated vesicles contain NPY. The low frequency stimulation promotes release of ATP, whereas high frequency stimulation causes release of NPY.

– Noradenergic postganglionic sympathetic nerves containing NPY are found on many blood vessels and cause vasoconstriction (whereas cholinergic nerves containing VIP and sensory nerves containing CGRPa & substrance P cause vasoconstriction).

* Large precursor protein (prohormone) propionmelanocortin (POMC) is synthesized in corticotropes of anterior lobe pituitary, intr mediate lobe, hypothalamus, lungs, gastrointestinal tack and placenta. POMC processing by prohormone convertase (PC) 1 & 2 is tissue specific and result in production of different peptides in different tissue. Anterior pituitary corticotropes expresses PC1 resulting in formation of N terminal peptide, joining peptide, ACTH, B-lipotropin (LPH) and a small amount of 3-endorphin. In intermediate lobe &/or hypothalamus, PC-2 expression l/t production of CLIP (corticotropin like intermediate lobe peptide), y-LPH, melanotropins (a-, (3-, and y- MSH) and appreciable quantities (3-endorphins, but not ACTH from POMC.

Neuropeptide (Slowly Acting Transmitters
/Growth Factors)

Neuropeptides (unlike small molecule, rapidly acting transmitters) are not synthesized in the cytosol of presynaptic terminals. Instead, they are produced in neuronal cell body by ribosomes as a part of large protein molecules, which enters ER and then golgi apparatus. In GA, the neuropeptide forming protein is enzymatically split into smaller fragments (some of which are either neuropeptide or its precursor) and packaged into minute transmitter vesicles (TV) which are released into cytoplasm. These TVs are transported by axonal streaming of cytoplasm at a slow rate (few cm/day) to tips of nerve fibers, where they release neurotransmitters in response to action potentials in the same manner as for small molecule, transmitter (SMT). However, these TVs are autolyzed and not recycled & used over & over again (like SMT).

Unlike SMTs, neuropeptides are released in much smaller quantities, are more potent (> thousand times) and have prolonged action. Small molecule rapidly acting transmitters include acetylcholine (Class 1); epinephrine, NE, dopamine, serotonin, histamine (II = amines); GABA, glycine, glutamate, aspartate (III = amino acids) ; and NO

– Hypothalamic releasing hormones (thyrotropin-RH, luteinizing hormone and somtostatin / growth hormone inhibitory factor)

– Pituitary peptides (ACTH, LH, GH, a-MSH, a-MSH, (3-endorphin, prolactin, thyrotrophin vasopressin , oxytocin).

Peptides acting on brain & gut (gastrin, CCK, VIP, insulin, glucagons, substance P, neurotensin, nerve growth factor, brain derived neurotropic factor, leucine & methionine-enkephalin)

Others (angiotensin II, bradykinin, carnosine, calcitonin, sleep peptides)


Q. 15

Satiety center is located in which nucleus of hypothalamus ‑

 A

Posterior

 B

Ventrolateral

 C

Ventromedial

 D

Supraoptic

Q. 15

Satiety center is located in which nucleus of hypothalamus ‑

 A

Posterior

 B

Ventrolateral

 C

Ventromedial

 D

Supraoptic

Ans. C

Explanation:

Ans. is ‘C’ i.e., Ventromedial

The ventromedial nucleus is located in the basomedial hypothalamus, and is a critical node of the neural circuitry of female sexual behavior – so, not surprisingly . This ventromedial hypothalamus is classically known as a “satiety center


Q. 16

Which of the following increases appetite ‑

 A

Insulin

 B

Leptin

 C

α-MSH

 D

Neuropeptide Y

Q. 16

Which of the following increases appetite ‑

 A

Insulin

 B

Leptin

 C

α-MSH

 D

Neuropeptide Y

Ans. D

Explanation:

Ans. is ‘d’ i.e., Neuropeptide Y



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