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Repro Bio 2 > Nutrition/stress on estrous/repro > Flashcards

Nutrition/stress on estrous/repro Flashcards

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1
Q

what does under-nutrition affect

A
  • affects hypothalamus

- reduces GnRH secretion, which is reflected in pituitary/ovarian function

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2
Q

what does increased nutrition do

A
  • ovary is primary target

- H-P axis is secondarily affected by altered feedback

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3
Q

short term energy restriction

A
  • monogastrics: almost immediate decrease in GnRH and LH levels
  • ruminants: same effect but takes several days
  • effects are reversed when normal nutrition restored
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4
Q

long term malnourishment

A
  • starting on normal ration will not always quickly restore circulating gonadotropin levels or reproductive activity
  • “critical body fat hypothesis” –> need some fat for reproduction (males 12-14%, females 22%)
  • degree of adaptation available if kept at low body fat for a while
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5
Q

what is leptin

A
  • peptide hormone secreted from white adipose tissue
  • circulating levels correlated with fat stores (more fat = more leptin)
  • functions as a marker of long-term nutrition and relatively short-term metabolic changes
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6
Q

leptin and reproductive system in good conditions

A
  • leptin inhibits NPY neurons –> inhibitory directly and indirectly on GnRH
  • leptin stimulates KNDy kisspeptin system –> stimulates GnRH pulses (low leptin decreases KNDy, kisspeptin, and therefore GnRH)
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7
Q

what happens to leptin and GnRH when fat stores decline

A

circulating leptin levels drop and GnRH pulse generator is suppressed

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8
Q

what is ghrelin

A
  • peptide hormone secreted by stomach in endocrine manner
  • secretion increases with fasting
  • transient surge in anticipation of food
  • circulating levels are inversely related to body condition (opposite of leptin)
  • suppresses kisspeptin and therefore GnTH
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9
Q

insulin-like growth factor 1 (IGF-1)

A
  • fluctuations due to circulating levels produced by the liver in response to growth hormone stimulation
  • directly enhances secretion by GnRH neurons, increases kiss secretion rom KNDy neurons
  • levels decrease with restricted feeding
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10
Q

insulin

A
  • fluctuates in response to glucose
  • overall concentration is directly proportional to amount of adipose tissue in the body
  • inhibits NPY neurons
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11
Q

gut fill?

A
  • neural sensory inputs from GI tract via vagus nerve provide info on gut fill to control food intake
  • minor role in controlling GnRH pulse generator?
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12
Q

metabolic fuel hypothesis

A
  • hinges on the body’s ability to detect changes in metabolic fuels that are available for oxidation
  • the fuel (calories) has to be present in the body in sufficient quantity
  • it has to be available for oxidation in tissues
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13
Q

what are the fuels being detected in metabolic fuel hypothesis

A
  • glucose (circulating and able to get into tissues)

- fatty acids

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14
Q

what site(s) detect the information about metabolic fuel oxidation

A

area postrema (AP) located in the hindbrain –> inhibiting glucose oxidation here inhibits reproductive axis

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15
Q

signaling the hypothalamo-pituitary axis

A
  • GnRH neurons inhibited by neuronal transmission from hindbrain in at least 2 ways
    1) neuronal projections form hindbrain inhibit GnRH neurons directly using neuropeptide Y and catecholamines
    2) NPY and CA neurons activate CRH neurons –> inhibit GnRH neurons
    3) NPY suppresses KNDy neurons
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16
Q

direct effects of energy deprivation on ovary (list)

A
  • follicle growth
  • oocyte viability
  • CL function
17
Q

follicle growth during energy deprivation

A
  • insulin and IGF-1 have synergistic action with gonadotropins
  • GH increases, IGF-1 decreases –> reduces cyclicity
18
Q

oocyte viability during energy deprivation

A

-decreased fertilization rates and lower developmental competence

19
Q

CL function during energy deprivation

A
  • small preovulatory follicles with poor steroidogenic capacity –> small, poorly steroidogenic CL
  • exacerbated by low LH levels
20
Q

increasing energy to increase reproduction

A
  • improving beyond normal does not stimulate H-P axis to further increase GnRH secretion
  • positive influence is mediated at the ovarian/follicle level with some secondary input from the H-P axis
  • results in an increase in the number of mature follicles that develop per cycle and thus the number of ovulations and eventually in increased litter size
21
Q

3 divisions of nutritional effects

A
  • acute effect: seen before body weight change is detectable
  • dynamic effect: seen while body weight is increasing
  • static effect: seen when body weight is maintained at a high level
22
Q

what happens to hormones during conditions of acutely increased nutrition

A
  • glucose/insulin increased –> increased glucose uptake into follicles –> suppresses estradiol secretion from follicles
  • leptin increased –> suppresses estradiol secretion from follicles
  • IGFBP increased –> less free IGF –> suppresses estradiol secretion from follicles
23
Q

result of decreased estradiol production from follicles during increased nutrition

A

less feedback inhibition of FSH –> FSH levels higher –> more follicles supported

24
Q

flushing

A
  • increases ovulation rate in sheep
  • slightly undernourished ewes put on a high plane of nutrition 2-3wks prior to breeding
  • allows them to achieve but not exceed their genetic potential
25
Q

sodium ionophores (monensin)

A
  • alters rumen microflora and shifts away from acetate/butyrate towards propionate
  • propionate is gluconeogenic –> increases insulin
  • increases pituitary sensitivity to GnRH and improve reproductive performance
26
Q

dietary fat

A
  • feeding some fat to ruminants increases propionate production (gluconeogenic)
  • increases medium sized follicle population, improves breeding performance
  • ratio of n6:n3 unsaturated fats are important
  • high n-3 can reduce prostaglandin/sensitivity to it –> longer estrous cycle, increased embryo survival
27
Q

protein

A
  • low protein diets cause cessation of estrous cycles in monogastrics
  • specific amino acid deficiencies are important in monogastrics
  • ruminants: excess protein and NPN result in increased urea and ammonia levels –> no effect on cyclicity
28
Q

other nutritional influences

A
  • vitamin/mineral deficiencies cause embryonic and neonatal losses
  • Cu, I deficiencies cause irregular/suppressed estrous cyclicity
29
Q

examples of stress effects on reproduction

A
  • cows/ewes: reduced GnRH, LH after shipping
  • captive wild animals: high cortisol, low sex steroids
  • change in social status
  • IVF patients
30
Q

stress and gestation

A

pregnant women stressed at 28-30wks shortens pregnancy and lowers birth weight

31
Q

hypothalamic effects of stress

A
  • release of CRH and vasopressin
  • CRH predominates in response to weak stress
  • vasopressin secreted with CRH with more intense stress
  • most of inhibitory effects mediated by activation of inhibitory interneurons –> use opioids and GABA to affect activation of GnRH neurons
32
Q

effects of stress on generation of LH surge

A
  • acute stress can prevent occurrence of pre-ovulatory LH surge
  • less severe stressors can delay its occurrence and decrease its amplitude
  • effects represent a combination of reduced GnRH secretion from hypothalamus and reduced LH secretion in response to GnRH
33
Q

overriding inhibition of stress (when it’s a good idea)

A
  • old individuals
  • seasonal breeders
  • both partners provide parental care
  • semelparous species (die after breeding)
  • dominant animals where only dominant animals breed and dominance is temporary

Repro Bio 2 (9 decks)

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