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GIGU - Week 2 > 21- Regulation of Food Intake > Flashcards

21- Regulation of Food Intake Flashcards

1
Q

Neuronal centers that control feeding and satiety are located within the hypothalamus and include…

A
    • Lateral Nucleus (LH)
    • Ventromedial Nucleus (VM)
    • Paraventricular Nucleus (PV)
    • Dorsomedial Nucleus (DM)
    • Arcuate Nucleus (Arc)
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2
Q

Crosstalk between ________ and ________ regulations is key to maintain energy balance. The hypothalamus receives many types of signals.

A

Neural

Hormonal

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3
Q

Most of the integration signaling regulating food intake and energy expenditure happens in the _______ _______.

A

Arcuate Nucleus

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4
Q

There are two pathways involved for food intake regulation in the Arcuate Nucleus. For this pathway, _______ is released by POMC (pro-opiomelanocortin) neurons. ______ binds to ______ present in second-order neurons (located in PVN). This pathway will decrease food intake.

A

alpha-MSH (alpha-melanocortin)
alpha-MSH (alpha-melanocortin)
MCR-4

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5
Q

The alpha-MSH pathway is an (ANOREXIGENIC/OREXIGENIC) pathway.

A

Anorexigenic

***Causing “anorexia” meaning loss of appetite!

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6
Q

There are two pathways involved for food intake regulation in the Arcuate Nucleus. For this pathway, hunger signals stimulate the release of _______ which binds to _______ in second-order neurons (located in PVN).

A

NPY (Neuropeptide Y)

Y1R

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7
Q

Along with NPY, ________ is also released, which is an antagonist of MCR-4. This is the receptor for alpha-MSH on the second-order neuron (decreases food intake).

A

AGRP (Agouti-related Peptide)

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8
Q

The NPY pathway is an (ANOREXIGENIC/OREXIGENIC) pathway.

A

Orexigenic

***Stimulates and increases appetite!

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9
Q

This disorder is early-onset of severe obesity, infertility (hypogonadotropic hypogonadism), hyperphagia, and infections.

A

Leptin or Leptin receptor gene deficiency

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10
Q

This disorder is early-onset of severe obesity, increased linear growth, hyperphagia, and hyperinsulinemia. Most common known genetic cause of obesity. Homozygous worse than heterozygous.

A

Melanocortin 4 receptor (MC4R) gene mutation

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11
Q

This disorder presents as neonatal hypotonia, slow infant growth, small hands and feet, mental retardation, hypogonadism, hyperphagia leading to severe obesity, and paradoxically elevated ghrelin.

A

Prader-Willi Syndrome

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12
Q

Prader-Willi Syndrome is caused by a partial deletion of _________ or loss of _________ expressed genes.

A

Chromosome 15

Paternally

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13
Q

This disorder presents with obesity, red hair, adrenal insufficiency due to ACTH deficiency, hyperproinsulinemia, hyperphagia, pale skin, and cholestatic jaundice.

A

POMC (Proopiomelanocortin) deficiency

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14
Q

Several peptides that stimulate satiety and decrease feeding activate receptors on ________ afferents. If this activity is blocked, the amount of material in the stomach no longer influences meal size.

A

Vagal

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15
Q

_______ is crucial in the interpretation and relaying of peripheral signals. Vagal signaling to the _______ is integrated with info received by the hypothalamus to produce the appropriate feeding behavior and metabolic processes.

A

NTS
NTS

***NTS = Nucleus of the Tractus Solitarius

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16
Q

What are the steps in the circuit that produces responses related to feeding behavior and metabolism.

A

Vagal —> NTS —> Hypothalamus

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17
Q

The _________ is able to regulate food intake in response to peripheral signals even in the absence of higher centers’ input.

A

Hindbrain

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18
Q

This area of the hypothalamus is the hunger center. Its neurons project throughout the brain and release the orexigenic peptides melanin-concentrating hormone (MCH) or orexins A and B.

A

Lateral Hypothalamic Area (LHA)

***Same as Lateral Nucleus (LH)

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19
Q

This area of the hypothalamus is the satiety center.

A

Ventromedial Hypothalamic Nucleus (VMN)

***Same as Ventromedial Nucleus (VM)

20
Q

This nucleus contains neurons that in turn project to both cerebral cortex and areas of the brainstem.

A

Paraventricular Nucleus (PVN or PV)

21
Q

_________ released from the GI tract, pancreas, and adipose tissue regulate feeding behavior.

A

Hormones

22
Q

This is secreted in the stomach by endocrine cells and binds to growth hormone secretagogue receptors (GHSR). It stimulates neurons that release NPY (increase appetite). It initiates the feeding response.

A

Ghrelin

23
Q

What are the actions of Ghrelin?

A
    • Increased appetite
    • Increased gastric motility
    • Increased gastric acid secretion
    • Increased adipogenesis
    • Decreased insulin secretion
24
Q

This hormone binds to receptors in POMC and NPY systems. It causes decreased appetite and increased metabolism.

A

Insulin

25
Q

Insulin (INHIBITS/STIMULATES) the NPY pathway, and (INHIBITS/STIMULATES) the POMC pathway.

A

Inhibits
Stimulates

***Remember, NPY stimulates food intake and POMC inhibits food intake!

26
Q

In patients with T1DM there is an (INCREASE/DECREASE) in food intake associated with decreased insulin.

A

Increase

***Remember, insulin decreases appetite so if there is less of it then the patient will have increased hunger!

27
Q

This hormone is released by I cells in the duodenum and elicits satiety.

A

CCK

28
Q

CCK acts on the Vagal —> NTS —> Hypothalamus circuit and decreases _________ secretion. It also decreases gastric emptying and increases gastric distention.

A

Ghrelin

***Remember, CCK elicits satiety and Ghrelin initiates food intake!

29
Q

This is released by L cells of the Ileum and colon following a meal.

A

PYY

30
Q

PYY binds to ______ in the hypothalamus. It inhibits ______ neurons and stops its inhibition (thus stimulating) _______ neurons.

A

Y2R
NPY
POMC

***Remember, NPY stimulates food intake and POMC inhibits food intake!

31
Q

This hormone is secreted by cells in adipose tissue, and is an appetite-suppressing hormone. It decreases appetite, increases metabolism, and decreases Ghrelin release.

A

Leptin

32
Q

Leptin binds to receptors in POMC and NPY systems. It (INHIBITS/STIMULATES) the NPY pathway and (INHIBITS/STIMULATES) the POMC pathway.

A

Inhibits
Stimulates

  • **Remember, NPY stimulates food intake and POMC inhibits food intake!
  • **Insulin works in the same way!
33
Q

In obese children with congenital _______ deficiency, subcutaneous administration of recombinant _______ reduces fat mass, hyperinsulinemia, and hyperlipidemia.

A

Leptin

Leptin

34
Q

Obesity in humans is often associated with high ________ levels and a failure to respond to exogenous forms of it (a resistance is developed).

A

Leptin

35
Q

Adiposity signals are involved in the long-term regulation of ________ balance, while gut peptides modulate ________ intake on a meal-by-meal basis.

A

Energy

Food

36
Q

This is a proglucagon derived peptide that is co-secreted with PYY from L cells in the intestine. It’s a type of incretin and its levels rise after a meal and fall during fasting. Reduces food intake.

A

GLP-1 (Glucagon-like Peptide-1)

37
Q

GLP-1 reduces food intake, suppresses ________ secretion, and delays gastric emptying.

A

Glucagon

38
Q

This is a proglucagon derived peptide that is released from L cells of the intestine in response to ingested food and in proportion to caloric intake. It has an anorectic effect, meaning it decreases appetite.

A

Oxyntomodulin

39
Q

This is secreted from cells in the pancreatic islets of Langerhans. It decreases food intake directly through Y4R in the brainstem and hypothalamus. May also act via the Vagus N. to produce anorectic effects (suppress appetite).

A

Pancreatic Peptide (PP)

40
Q

This is secreted by Alpha cells of the pancreatic islets. It increases blood glucose levels and insulin secretion. It reduces food intake.

A

Glucagon

***Remember, insulin suppresses appetite!

41
Q

This is stored and released with insulin in response to food intake. It has anorectic effects (via inhibition of NPY release).

A

Amylin

42
Q

This disease is characterized by self-starvation and excessive weight loss. Patients become severely malnourished and significantly emaciated, leading to endocrinological and cardiological dysfunctions, and abnormalities within the digestive, skeletal, and reproductive systems.

A

Anorexia Nervosa (AN)

43
Q

In patients with AN, there are __________ in genes involved in eating attitudes, the regulation of eating behavior, motivation, and reward mechanisms.

A

Polymorphisms

44
Q

In patients with AN, basal and pulsatile secretion of ________ is reduced in association with reductions in fat mass.

A

Leptin

45
Q

In patients with AN, ________ resistance appears to be a conducive factor to a restrictive diet.

A

Ghrelin

46
Q

In patients with AN, elevated levels of ________ might contribute to decreased nutrient intake and disordered eating psychopathology.

A

PYY

***Remember, PYY decreases appetite!

GIGU - Week 2 (10 decks)

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