Lecture 9 Flashcards

1
Q

What is Homeostasis?

A

The process by which a system (such as the body) maintains a relatively constant internal milieu
Temperature/Blood concentrations
Blood pH/ p

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2
Q

What is the Set Point?

A

Set point is the point of optimal physiological functioning. Physiological and behavioral function must be maintained within a narrow range around set point.

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3
Q

What are the four steps required for Homeostasis?

A

Reference value: Set point
Detection mechanism: to detect deviation from set point
Mobilization: To return to set point
Negative Feedback: Shut down mobilized process once homeostasis is reached

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4
Q

What is Hypovolemic thirst?

A

Hypovolemic thirst refers to a kind of thirst provoked by low blood volume.
Ex. when bleeding from a wound.

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5
Q

What is osmotic thirst?

A

Osmotic thirst is caused by cellular dehydration- which can occur after ingesting a salty snack.

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6
Q

Dehydration and ADH/ Vasopressin Response.

A

ADH/AVP is release from the Anterior pituitary in response to Cerebral osmoreceptor dehydration and reduction of blood volume -via baroreceptors

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7
Q

What is caused by the release of ADH/AVP?

A

Retention of water in kidneys

Vasoconstriction

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8
Q

How do Cerebral osmoreceptors respond to mild and extended dehydration?

A

In mild dehydration: Sends signal to paraventricular nucleus (PVN) and supraoptic nucleus (SON) to produce AVP/ADH, which stimulates water retention
In extended dehydration: stimulates drinking

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9
Q

How do Baroreceptors respond to low blood volume?

A

Baroreceptors stretch receptors in walls of blood vessels and stimulates PVN and SON to produce AVP/ADH, release from post pituitary to increases blood pressure

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10
Q

What is stimulated by Hypovolemia in the kidneys?

A

Drop in blood pressure signals the brain and the kidneys to produce renin to converts angiotensinogen (from blood) to angiotensin I, II, and III.

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11
Q

What are some characteristics of the peptide hormone Insulin?

A

It is released by beta cells of pancreas in response to food cues or when blood glucose rises. In the liver, it converts glucose to glycogen. Prevents breakdown of glycogen and mobilization of fat stores. Is the ONLY hormone to promote energy storage.

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12
Q

Describe Metabolism: Fasting state

A

The metabolic system’s top priority is the BRAIN. the Brain can only process glucose via blood (ketones as last resort)
During fasting, glucose is diverted to brain at expense of rest of body, which metabolizes fatty acids into glucose.

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13
Q

What are non-food sources of energy and their characteristics?

A

Glucagon is released from alpha cells of pancreas when blood glucose is low. It stimulates glycogenolysis and Lipolysis in liver
During stress, cortisol and epinephrine stimulate production of glucose in liver (gluconeogenesis), and breakdown of fat.

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14
Q

What are some Orexigenic Neurotransmitters and where are they release from?

A

NPY (Neuropeptide Y) and AgRP (Agouti-related protein) both released from ARC, act on paraventricular nucleus of the hypothalamus (PVN) to induce feeding behavior.

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15
Q

What are some Anorectic neurotransmitters?

A

CART (cocaine and amphetamine-regulated transcript) and

POMC, which makes α-MSH(melanocyte-stimulating hormone) both might inhibit eating

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16
Q

What are some characteristics of the peptide hormone Ghrelin?

A

It is released by GI tract when the stomach is empty. It is stimulated by chronic stress and inhibits reproduction by acting on HPG Axis.
Activates the reward system and acts in ARC hypothalamus to promote feeding

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17
Q

What are Neuropeptide Y (NPY) and Agouti related protein (AgRP)?

A

They are orexigenic peptides that stimulates feeding behavior. Released from neurons in ARC hypothalamus.

18
Q

Orexin and Melanin-concentrating hormone (MCH)

A

Both increase feeding and metabolism
Inhibited by leptin
Activated by ghrelin
Orexin also called hypocretin stimulates wakefulness (narcolepsy)

19
Q

Describe Leptin?

A

Its a adipokine (released by fat cells) peptide hormone. Not the “satiety” hormone but the “starvation” hormone. Leptin treatment does not curtail obesity (usually).

20
Q

Control of food intake: Insulin

A

When insulin levels drop, hunger ensues. Insulin reaches the hypothalamus via CSF. In baboons there is an increased of CSF insulin after meal.
ICV insulin reduced food intake. Insulin may serve as signal of amount of fat. Obese people have more circulating insulin and Insulin receptors in ARC.

21
Q

what is POMC?

A

POMC is a hormone precursor normally produced by the pituitary gland and hypothalamus in the brain.

22
Q

POMC involvement in food inhibition

A

Leptin and insulin activate receptors in ARC, to produce POMC. POMC is broken down into opioids and melanocortins (α-MSH and ACTH) POMC and α-MSH activate receptors in PVN suppressing feeding.

23
Q

CART involvement in food inhibition

A

Leptin activates receptors in ARC to secrete CART. CART activate receptors in PVN to suppresses feeding

24
Q

Hypothalamic control of inducing feeding

A

When leptin and insulin are low and ghrelin is high the NYP/AgRP are activate, suppressing POMC/CART and inducing feeding

25
Q

Hypothalamic control of feeding inhibition

A

When leptin or insulin are high, the POMC/CART is activated, leading to α-MSH release, inhibiting NYP/AgRP and feeding.

26
Q

Short term regulation of feeding by CCK

A

Cholecystokinin (CCK) is released by gut to aid digestion (via vagus nerve). CKK inhibits feeding in hungry animals.

27
Q

Short term regulation of feeding by Amylin

A

Amylin is released from pancreatic β cells with insulin and delays gut emptying. Acts on brainstem to inhibit feeding.

28
Q

Chronic stress and Hunger

A

In chronic stress CRH/CRF stimulates ACTH, prompting glucocorticoids to activate the stress response. Consumption of sugar and fat increased. Abdominal fat is stored and NPY secretion increased.

29
Q

Gonadal Steroids and feeding: Estrogen

A

Estrogen blocks the increased of body fat and decreased physical activity in overiectomaized rats. During periods of low estrogen (cycling) food intake is high.

30
Q

Pregnancy, Menopause and feeding

A

During Pregnancy progesterone is high which leads to high feeding
Menopause: in female and male fat distribution (subcutaneous to visceral).

31
Q

What is stimulated by Angiotensin II?

A

Angiotensin II stimulates drinking behavior and stimulates the release of aldosterone which promotes sodium retention in kidneys and water retention

32
Q

CRH effects on NPY.

A

CRH inhibits NPY function. Stress interrupts negative feedback of CRH on NPY leading to obesity

33
Q

What are the functions of Neuropeptide Y (NPY) and Agouti related protein (AgRP)

A

Released from the ARC hypothalamus onto paraventricular nucleus (PVN) and lateral hypothalamic area (LHA). Interacts with receptors in PVN to prompt feeding. It is stimulated by low leptin/insulin levels.

34
Q

How does leptin suppress feeding ?

A

It acts on arcuate nucleus of the hypothalamus to suppress feeding. It is released in proportion to amount of fat and it drops dramatically when lipolysis takes place.

35
Q

Short term regulation of feeding by Bombesin.

A

Bombesin is released by gut (via brain)

Administration of bombesin reduces feeding and has a additive effect with CCK

36
Q

Short term regulation of feeding by Peptide tyrosine-tyrosine

A

Peptide tyrosine-tyrosine (PYY)
Released from ilium and colon to inhibit NPY and AgRP neurons. Obese adults show decreased PYY in response to meals and when fasting.

37
Q

What is Aldosterone?

A

Aldosterone regulates the balance of water and electrolytes in the body. Stimulates the kidney to excrete potassium into the urine and retain sodium.

38
Q

How do the liver and Gastro-intestinal Tract signals travel?

A

Signals from liver and gut travel via vagus nerve to brainstem to terminate meal.
Low levels of adiposity can block signal to increase consumption after satiety.

39
Q

Physiological feeding experiments with rats

A

Transplant a stomach into a rat and feeding transplanted stomach stops feeding, even if normal stomach is empty
Blood infusion from recently fed rat inhibits feeding  blood borne agent.

40
Q

Short term regulation of feeding and Peptide tyrosine-tyrosine (PYY)

A

PYY is released from ilium and colon to inhibit NPY and AgRP neurons, inhibiting feeding.
Obese People show decreased levels of PYY in response to meals and when fasting.

41
Q

Acute stress and hunger

A

During acute stress CRH/CRF prompts ACTH, which stimulates cortisol inhibiting CRH/CRF release decreasing feeding behavior.