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VBMS 325 > Module 5- growth & lactation > Flashcards

Module 5- growth & lactation Flashcards

1
Q

where are hypothalamic factors released

A

stalk of anterior pituitary

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2
Q

what does GnRH stimulate

A

stimulates GH secretion

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3
Q

somatostatin

A

inhibits GH secretion

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4
Q

grehlin

A

regulator of GH secretion, secreted in response to empty stomach

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5
Q

T or F: stomach is an endocrine gland

A

T

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6
Q

where are receptors of GH found

A

pituitary gland

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7
Q

transcription vs translation

A

scription-DNA -> RNA
lation-RNA -> protein

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8
Q

T or F: GnRH stimulates transcription & translation

A

T

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9
Q

how is GH released? why?

A

GH is produced in cells in anterior pituitary & stored in vesicles
- vesicles allow a burst of hormone rather than taking a long time to make new

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10
Q

T or F: somatostatin can be found in GI tract & other tissues as well as endocrine

A

T

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11
Q

how many forms of somatostatin are there?

A

2

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12
Q

BST

A

bovine somatotropin- used to improve milk production in E.coli

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13
Q

where are GH receptors located (5)

A

liver, adipose, bone, muscle & gonads

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14
Q

T or F: GH receptors in mammary epithelium

A

F

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15
Q

T or F: GH is pulsatile

A

T

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16
Q

why can you not take a single of GH & tell what the cows status is

A

b/c GH is pulsatile so it fluctuates so much and is not coordinated

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17
Q

where is grehlin made

A

stomach lining

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18
Q

where are ghrelin receptors located

A

hypothalamus

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19
Q

what stimulates IGF-1?

A

GH

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20
Q

how is IGF-1 produced/stored?

A

no vesicles, it is released slowly in several hours

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21
Q

what is the major source of IGF-1?

A

liver

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22
Q

anabolic vs mitogenic

A

a-synthesize proteins
m-cell perforation

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23
Q

IGF-1 plays role in ( ) growth while IGF-2 plays role in ( ) growth

A

pre/post natal, utero/post natal

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24
Q

IGF-1 has ( )% amino acid identity with insulin

A

50%

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25
Q

what are the 3 main tissues that express IGF-1

A

liver, uterus & ovary

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26
Q

why are IGF binding proteins used?

A

b/c we do not use vesicles

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27
Q

what is most abundant binding protein in blood? function?

A

IGFBP-3, protects IGF from degradation

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28
Q

what are the 2 main binding proteins secreted from liver? function?

A

IGFBP 1 & 2, reduce tissue availability of IGFs

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29
Q

direct vs indirect effects of GH

A

direct-act directly on receptors
indirect-things that IGF-1 does that stimulates GH

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30
Q

anti-lipogenic

A

stops making new fat & encourages breakdown of fat, GH inhibits insulin

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31
Q

lipolytic

A

breaks down fat, stimulates lipolysis = stimulates effect of epinephrine = releases energy from adipose tissue

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32
Q

what does GH need to stimulate more release when in a negative energy balance for anabolic/mitogenic functions of IGF-1

A

epinephrine

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33
Q

GH makes epinephrine ( ) potent

A

potent

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34
Q

insulin is ( ) potent in stimulating glucose uptake

A

less

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35
Q

GH secretion ( ) with grehlin

A

increases

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36
Q

low nutrition does what do IFG-1

A

liver makes less IGF-1 = less negative feedback to pituitary = stimulation of more GH

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37
Q

what 5 things occur in GH/IGF-1 levels during low nutrition?

A

1) increased GH from more grehlin
2) reduced number of GH receptors on liver b/c of lower protein synthesis
3) reduced IGF-1 secretion b/c of less receptors
4) increased IGFBP 1 & 2 and increased IGFBP-3
5) stimulates release of energy from adipose tissue for energy needs

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38
Q

example of direct & indirect effects of malnutrition on GH/IGF-1

A

direct: lipolytic, antagonizing insulin

indirect: reduced IGF-1

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39
Q

why are males larger than females

A

testosterone is more potent than estrogen in IGF-1 = increases GH pulsatility = more GH activity

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40
Q

effects of stress on IGF-1

A

increased cortisol = decrease in liver GH receptors = growth is reduced = lower effectiveness of IGF-1

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41
Q

effects of illness on IGF-1

A

cytokine hormone stimulates immune response when sick = directly reduces amount of liver production of IGF-1 = no appetite

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42
Q

nutrition & steroid effects on IGF-1

A

estradiol is more capable of stimulating IGF-1 in well fed animals

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43
Q

why does IGF-1 peak in high nutrition not low nutrition animals

A

b/c low nutrition directly inhibits the production of IGF-1 because of the lack of GH receptors on liver in low nutrition states

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44
Q

T or F: IGF-1 has no stimulating effects on animals with lack of management & feeding levels & stress

A

T

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45
Q

steroid impacts for cattle effects on GH

A

increases GH receptors on liver = increases GH pulsability

  • does not work in monogastrics
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46
Q

why do plasma IGF-1 levels drop at day 21 & day 60 in pigs?

A

1) weaning is at 21 days = stress = cortisol increases = blocks GH receptors in liver = decline in IGF-1
2) change in environment = not eating = reduced nutrition = reduced IGF-1
3) exposure to pathogens= fighting change in gut microbiome b/c no milk anymore = cereal grains are different substrate for bacteria = immunosuppression = reduced appetite = loss of GH receptors on liver = drop in IGF-1
4) day 60: nursery -> grower barn = change in diet & environment = drop in IGF-1

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47
Q

why peak in GH at day 24?

A

1) low IGF-1 levels = reduced negative feedback = more GH
2) stomach is empty = makes ghrelin hormone = stimulates GH secretion
3) GH increases to make energy to support/maintain body function when they are not consuming feed

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48
Q

leptin

A

hormone that suppresses appetite by acting on hypothalamus & limits desire to eat

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49
Q

4 leptin functions

A

1) suppresses appetite
2) increases energy use
3) permits LH surge
4) Increases immune cell activity

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50
Q

what occurs with a mutation that no longer makes leptin

A

obese, hypoactive & low metabolic activity

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51
Q

where is leptin secreted

A

adipocytes

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52
Q

2 main drivers of leptin secretion

A

1) adiposity- increased with increased adipose size
2) energy balance- when no food = decreased leptin release

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53
Q

T or F: leptin is 2x higher in females than males

A

T

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54
Q

role of leptin cattle (2)

A

1) adds fat cover in finishing
2) as animals mature = reduce muscle growth & increasing fat growth

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55
Q

T or F: as you add fat, your appetite decreases

A

T

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56
Q

T or F: a reduction in appetite causes use of energy towards heat production but not for reproductive cycling

A

T

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57
Q

cattle genotype for leptin

A

wildtype = T allele = codes for cysteine (normal)

C allele= codes for arginine = reduced function

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58
Q

why does the T allele for leptin allow normal function?

A

b/c it codes for cysteine which has disulfide bonds to support protein binding

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59
Q

T or F: reduced function leptin ( C allele) changes the easy ability for fat cover

A

T

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60
Q

how is leptin managed?

A

genotypically- feeding & management are optimized to a particular genotype

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61
Q

myostatin

A

paracrine (local) hormone that results in double muscling phenotype if absent

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62
Q

what is the most common cattle breed for double muscling

A

belgian blue

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63
Q

how many myostatin mutations have been identified

A

5

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64
Q

what does double muscling mean

A

double the muscle fibers

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65
Q

where do most of the myostatin effects occur? why is it hard to occur?

A

Utero, hard to control with use of drugs

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66
Q

what test can be done for myostatin gene identification in humans

A

CRISPR

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67
Q

lactation

A

production of milk by the mammary gland, characteristic of all mammals

68
Q

4 functions of lactation

A

1) provide milk
2) passive immunity of antibodies via colostrum
3) help gut development
4) promote beneficial intestinal bacteria

69
Q

what nutrient is found in milk that promotes the growth of beneficial bacteria

A

polysaccharides (carb)

70
Q

what is the mammary gland composed of

A

alveoli (spheres) that are made of a single layer of glandular cells

71
Q

glandular cell function

A

synthesize milk & secrete it into the lumen

72
Q

milk is an ( )

A

ultrafiltrate

73
Q

how many L of blood transfers through mammary gland to get 1 L of milk?

A

600L

74
Q

what are proteins, glucose & amino acids made into in milk

A

caseins / milk fats

75
Q

T or F: blood moves rapidly through the gland

A

T

76
Q

mammary vein

A

vein that passes along abdomen to gland that returns milk back to the circulatory system
- like a garden hose

77
Q

each alveolus is surrounded by

A

myoepithelial (muscle cells) - looks like a spider

78
Q

myoepithelial cell function

A

contract & force milk out of lumen of alveoli into a duct system

79
Q

alveoli are arranged in groups called

A

lobules that turn into lobes

80
Q

udder cistern

A

where milk is collected when it is forced into the duct system

81
Q

movement of milk

A

alveoli -> lumen -> duct system -> utter cistern -> teat cistern -> teat canal (where milk exits)

82
Q

where does milk exit out of

A

teat canal

83
Q

what causes myoepithelial cells to contract?

A

oxytocin

84
Q

where is oxytocin released from

A

posterior pituitary gland

85
Q

the bovine suspensory system

A

bovine udder is composed of 4 separate mammary glands

86
Q

suspensory ligaments

A

hold udder in place & supports the weight of the mammary gland

87
Q

what would occur without suspensory ligaments

A

udder drag low = more susceptible to mastitis or injury

88
Q

how much does the udder weigh

A

20 kg

89
Q

ampullae in mammary gland

A

provide limited milk storage, similar to udder cistern

90
Q

mammogenesis

A

mammary gland development

91
Q

lactogenesis

A

initiation of milk synthesis

92
Q

galactopoiesis

A

milk synthesis

93
Q

when does mammogenesis occur

A

adolescence in begging of reproductive cycling during 1st cyclw

94
Q

life cycle of dairy cow
0 days, 60-90 days, 305-320 days, 60 day

A

0=calving
60-90=re-breeding then lactation
305-320= drying off
60 day= dry period & breed again

95
Q

when is peak lactation

A

during 1st nine weeks

96
Q

how does drying off occur?

A

as lactation progresses, myoepithelial cells die = loss of milk synthesis capacity

97
Q

drying off

A

stopping production of milk, lasts 2 months

98
Q

T or F: female calf is born with rudimentary mammary system

A

T

99
Q

mammary system at birth

A

udder has teat & gland cisterns but duct system is not really developed

100
Q

mammary gland birth -> pre-pubertal period

A

mammary gland growth is isometric (grows at same time as rest of body), very little duct developement

101
Q

how can overfeeding impact mammary gland formation

A

increased deposition of fat in mammary gland = limits further development of duct system

102
Q

mammary gland at time of puberty

A

estrogen, progesterone & cortisol are released

103
Q

what does estrogen & progesterone do for mammary gland growth?

A

estrogen- growth of cistern in ducts
progesterone-growth of alveoli

104
Q

T or F: you cannot take a heifer that has not reached puberty & inject her with hormones to start producing milk

A

T

105
Q

mammary gland during pregnancy

A

duct system develops & alveoli develop towards end of pregnancy

106
Q

mammary gland around time of calving

A

1) surge of prolactin & decrease in progesterone
2) lactose synthesis

107
Q

what is milk volume driven by?

A

lactose

108
Q

how is lactose secreted

A

secreted into lumen & water follows by osmosis

109
Q

T or F: caseins/proteins do not follow lactose by osmosis

A

T

110
Q

what is lactose

A

small soluble sugar

111
Q

what does a surge in prolactin cause?

A

drives initiation of lactogenesis

112
Q

what hormone is high during pregnancy

A

progesterone

113
Q

what is galactopoiesis driven by in cattle vs other spcies

A

cattle- GH
other- prolactin

114
Q

what are the 3 most important hormones for milk synthesis

A

1) prolactin
2) GH
3) IGF-1

115
Q

T or F: prolactin is higher during longer photoperiods

A

T

116
Q

sow milk production increases with

A

litter size

more suckling = more prolactin = drives milk synthesis

117
Q

peak milk yield

A

4-8 weeks then slowly declines

118
Q

lactation curve

A

increase number of secretory cells after parturition = increased activity

119
Q

what does decreased epithelial cell number mean

A

apoptosis

120
Q

what to select for if you want a higher persistance

A

reduced apoptosis

121
Q

milk let down is a ( ) reflec

A

neuro-hormonal

122
Q

milk let down reflex

A

suckling / massing udder stimulates nerves in tit to send signal to posterior pit for oxytocin release = myoepithelial cells squeeze alveoli = forces milk out of duct system

123
Q

how long does it take before milk let down occurs

A

1 min

124
Q

when is peak of milk let down? how long does it last before all oxytocin is released?

A

peak is 2-3 min, lasts 6-8 mins before all oxytocin is released

125
Q

what can inhibit milk let down

A

stress = vasoconstriction = no oxytocin release

126
Q

fat in milk is 99% ( )

A

triglycerides

127
Q

homogenization

A

rapid mixing of milk to turn large globules (float) into small globules so they stay mixed to avoid separation of milk

128
Q

2 milk proteins

A

casein & whey

129
Q

the epithelial cell of mammary gland

A

secretory vesicle is full of milk fat = pushed through plasma membrane of cell = plasma membrane forms surface of fat globule

130
Q

how is fat in milk stored

A

in a globule that is surrounded by plasma membrane

131
Q

what 2 components of milk are released into the lumen

A

lactose & proteins

132
Q

what are solids in milk

A

what comes out at the bottom (protein & fat) when you spin milk rapidly in centrifuge

133
Q

what type of milk is produced if there is less lactose

A

more concentrated b/c less lactose = draws less water into milk protein via osmosis

134
Q

T or F: lactoferrin has health benefit

A

T

135
Q

how are immunoglobins transported

A

taken from blood & moved into lumen across the epithelium

136
Q

what is the primary source of immunoglobin for neonate

A

colostrum

137
Q

4 factors affecting milk fat composition

A

1) milk fat %
2) milk fat composition
3) milk protein %
4) colostrum vs mature milk

138
Q

colostrum has ( )x protein & ()x fat as mature milk

A

40x, 1.5x

139
Q

what occurs if you freeze colostrum

A

freeze immune cells but can still have a healthy calf

140
Q

what type of immunoglobin is colostrum mainly?

A

IgG

141
Q

is IgA absorbed? why or why not?

A

not typically b/c it s very resistant to degradation in gut- present in mature milk

142
Q

how does IgA work?

A

has 4 binding sites which are capable of joining pathogens together to inhibit their movement towards epithelium & supporting their removal via peristalsis

143
Q

lactoferrin

A

binds iron to make it more available for neonate

144
Q

why is iron given as an injection, not oral in neonates?

A

it can overwhelm lactoferrin & cause E.coli scours

145
Q

what is the most limiting nutrient for bacteria/pathogens

A

iron

146
Q

bacterostatic vs bacterocidal

A

static-prevents growth
cidal-kills

147
Q

oligosacchardies

A

short complex sugar, is preferred nutrient for beneficial bacteria

148
Q

how do beneficial bacteria take advantage of oligosaccharides

A

use it as a substrate

149
Q

de novo synthesis

A

make on own

150
Q

what type of synthesis does C4-C16 use

A

de novo

151
Q

how are short & long chain FA made

A

short-synthesized in mammary gland & secreted
long-taken from diet or adipose tissue

152
Q

ruminant vs monogastric milk composition

A

ruminant- higher in saturated fat
monogastric-reflects what the diet is - can be unsaturated or satured- no modulating effects

153
Q

northern seal milk composition

A

do not eat during lactation = all fats comes from adipose

154
Q

elephant milk synthesis

A

de novo synthesis

155
Q

how many times a day should a cow be milked to increase milk yield

A

3x

156
Q

4 effects of mastitis

A

1) infiltration of immune cells from blood into gland
2) destruction of alveoli
3) reduced milk production
4) negative economic impacts

157
Q

why does milk production decrease with mastitis

A

neutrophils squeeze between 2 cells to get into alveoli to clear infection, they damage the epithelial cells

158
Q

mastitis pathway

A

bacteria finds way through teats and duct system and then get into alveoli

159
Q

somatic cells

A

cells with full chromosome

160
Q

what does a high level of somatic cells in a dairy cow mean?

A

infection in the gland

161
Q

how long is milk production reduced with mastitis

A

until there is drying off & another round of parturition for mammary gland growth

162
Q

a somatic cell count <100,000 is (good/bad)

A

bad

163
Q

what is the largest economic loss from mastitis from

A

reduced production

164
Q

T or F: peak lactation is 6th lactation

A

T

165
Q

hormone levels in mammogenesis

A

decrease progesterone, increase estrogen & cortisol, no change in prolactin

166
Q

hormone levels in lactogenesis

A

peak production in estrogen, cortisol & prolactin, decrease progesterone

167
Q

hormone levels in galactopoiesis

A

decrease progesterone, estrogen, cortisol & prolactin

VBMS 325 (17 decks)

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