(12) Nutrition

Question 1

(The Effects of Nutrition on the Estrous Cycle)

1. Under nutrition primarily affects what? having what effect?
2. increased nutrition has what as primary target?

Answer 1

1. the hypothalamus, reducing GnRH secretion (then reflected in pituitary/ovary function)
2. ovary (HP axis secondarily affected by altered feedback)

Question 2

(Under Nutrition/Negative Energy Balance)

(Short term energy restriction)

1. Short term severe under nutrition in previously well fed female monogastric animals causes an almost immediate decrease in what?

restored easily?

(Long term malnourishment)

1. quick turn around when fed?
2. what percentage body fat required for male spermatogenesis?

for opitmal female cyclicity?

Answer 2

1. GnRH and LH levels (in ruminants takes longer cause ferm keeps going in the rumen)

yeah

1. not always

This has lead to the concept that there is a certain degree of “fatness” that is necessary for normal reproduction and has been the basis of body condition scoring in cattle (also horses and sheep) herd health programs. This concept is known as the “critical body fat hypothesis” and it is still fairly widely accepted.

2. 12-14%

22% (3:1 lean:fat)

However, when individuals are kept well below these levels of body fat for long periods they may resume fertile cyclicity without any improvement in body condition. There appears to be a degree of adaptation available, or put another way, the “degree of fatness” and the reproductive control axis can be separated from each other. This dissociation can also be shown experimentally and has lead to the more recent concept that, while fatness and the reproductive axis are associated, the association is not a directly causal one. There may also be species variation in the relative importance for thin animals of replacing minimal body fat levels vs. getting some acute increases in available calories; and this may depend on reproductive strategies and life history of the species. The theory that looks at more acute changes in caloric availability as controlling GnRH secretion is borrowed from the control of eating behavior and is called the “metabolic fuels hypothesis”.

Question 3

(Signaling Metabolic Status and altering Hypothalamic GnRH Secretion)

(Peripheral signals of metabolic state)

(leptin)

1. peptide hormone secreted from what?
2. fasting does what?
3. food intake does what?

Answer 3

1. white adipose

more fat = more leptin

although affected by other short term things

2. reduces leptin
3. increases leptin

(leptin functions as a marker of both long-term nutrition and relatively short-term metabolic changes.)

Question 4

(Leptin)

Leptin sits with a foot in both metabolic fuels and critical body fat hypotheses.

1. Within the reproductive system the peptide appears to function as a permissive signal for what?
2. In good condictions and good leptin levels…
3. 1 leptin inhibits what that inhibit what?
4. 2. stimulates what that does what?
5. When fat stores decline or the animal is fasted, what happens?

Answer 4

1. pulastile secretory activity of GnRH neurons
2. NPY nerouns that inhibit GnRH neurouns (allowing GnRH secretion)
3. 2. KNDy kisspeptin system which directly stimulates GnRH pulses

(Leptin appears to be the major permissive controller of these neurons. Thus low leptin levels decrease KNDy neuron activity, kiss secretion, and thus GnRH.)

3. circulating leptin levels drop and the GnRH pulse generator is suppressed

Question 5

(Ghrelin)

1. is a peptide hormone secreted by what?
2. secretion does what with fasting?

has transient surge in anticipation of what?

3. In ways is the opposite of what?
4. recent evidence it suppresses what?

Answer 5

1. the stomach in an endocrine manner
2. increases

food (by the same cholinergic system that causes anticipatory increases in salivation and gastric acid secretion)

3. leptin - levels inverse to body condition
4. kisspeptin sysem and thus GnRH

(this isn’t real clear though…)

Question 6

(Insulin-like Growth Factor 1 (IGF-1))

1. While some is produced locally in astrocytes, the great majority of hormone fluctuations for IGF-1 seen by the hypothalamus are due to what?
2. IGF-1 can do what two things?
3. Under conditions of restricted feeding what happens to levels?

Answer 6

1. circulating levels produced by the liver in response to growth hormone stimulation
2. directly enchance secrtion by GnRH neurons

act indirectly by increasing kiss secretion from KNDy neurons

3. IGF-1 levels decrease and so do these stimulatory inputs

Question 7

(Insulin)

1. Insulin levels fluctuate throughout the day in response to glucose, but its overall concentration is also directly proportional to what?
2. While in culture insulin can increase GnRH secretion directly, in vivo its greatest contribution may be indirect, by doing what?

Answer 7

1. amount of adipose tissue in body
2. inhibiting NPY neurons

Question 8

(Gut Fill)

1. Neural sensory inputs from the gastrointestinal tract via the what? provide information on gut fill to control food intake

Answer 8

1. vagus

(It is postulated that these may also have a minor role in controlling the GnRH pulse generator, but evidence suggests that it is the caloric content (absorbed) of the meal, rather than gut fill/distension that mediates the reproductive effects)

Question 9

(Metabolic Fuels Hypothesis)

1-2. This hypothesis hinges on the bodies ability to detect changes in metabolic fuels that are available for oxidation. There are 2 parts to this:

what are they?

(what are the fuels being detected)

1. most important is what?
2. what else is important possibly?

(What sites detect the info about metabolic fuel oxidation?)

1. what is it?

Answer 9

1. the fuel (calories in some form) has to be present in body in sufficient quantitiy
2. has to be available for oxidation in tissues
3. glucose

(deficiency in glucose oxidation = glucoprivation)

2. fatty acids availbe for oxidation (lack = lipprivation)
3. area postrema (AP) located in hindbrain (inhibiting glucose oxidation in this area inhibits reproduction)

Question 10

(Signaling the Hypothalamo-Pituitary Axis)

How does this info from hindbrain influence GnRH neurons?

(GnRH neurons appear to be inhibited by neuronal transmission from the hindbrain in at least 2 ways:)

1. Neuronal projections from the hindbrain inhibit GnRH neurons directly using what?
2. NPY and CA neurons from the hindbrain active what that do what?
3. NPY may act indirectly by doing what?

Answer 10

1. neuropeptide Y (NPY) and catecholamines (CA: NE and E) as NT
2. corticotropin releasing hormone (CRH) neurons which then inhibit GnRH neurons
3. suppressing KNDy neurons

Question 11

(Direct Effects of Energy Deprivation on the Ovary?)

While the effect of energy deficit on reproduction is primarily mediated at the level of the hypothalamus, there are some possible effects directly mediated at the level of the ovary. There may be species differences in the degree of direct ovarian involvement, research suggests little to none of the following occur sheep but they have been demonstrated in lactating dairy cows.

Question 12

(Direct Effects of Energy Deprivation on the Ovary?)

(Follicle Growth)

(Insulin and Insulin-like Growth Factors (IGF))

1. IGF and insulin have synergistic actions with the gonadotropins (especially increasing sensitivity to FSH) to do what?

Answer 12

1. promote granulosa cell proliferation (= follicle growth ➔ mainly IGF) and steroidogenesis (= estrogen production ➔ mainly insulin).

(In states of severe under nutrition, levels of growth hormone and IGF are uncoupled, growth hormone levels increase but those of IGF-1 fall. Falling IGF-1 during under nutrition has a potentially direct ovarian role in reducing cyclicity. In times of under nutrition insulin levels are also reduced.)

Question 13

(Direct Effects of Energy Deprivation on the Ovary?)

(Oocyte Viability)

1. Oocytes taken from cows in poor body condition have decreased fertilization rates and lower developmental competence (fewer fertilized ones form blastocysts) compared to those from cows in good body condition.

Question 14

Direct Effects of Energy Deprivation on the Ovary?

Corpus Luteum Function

Small preovulatory follicles with poor steroidogenic capacity due to under nutrition, give rise to small, poorly steroidogenic corpora lutea.

1. this is exacerbated by what?

Answer 14

1. by low luteinizing hormone levels (from a nutritionally suppressed H-P axis) reduce CL progesterone production - affect primarily at H-P axis with 2° ovarian effect.

Question 15

(Increasing Energy to Increase Reproduction)

1. Effects of negative energy balance were mediated at the level of the hypothalamus, improving nutrition beyond normal act at what level?
2. results in what?

Answer 15

1. mediated at the ovarian/follicle level with some secondary input from the H-P axis

(does not stimulate the HP axis to further increase GnRH secretion)

2. increase in number of mature follicles that develop per cycle (thus number of ovulations and increased litter size)

(it isn’t that ovaries need a lot of energy…. the fact that body overall has alot of energy is what encourages them to grow)

Question 16

(Increasing Energy to Increase Reproduction)

1. stimulatory effects seen before eating but continue after weight gain…. thus nutiritional effects have been divided into 3 categories
2. seen before weight change detecatble
3. seen while weight is increasing
4. body weight maintained at high level

Answer 16

1. acute effect
2. dynamic effect
3. static effect

Question 17

(Increasing Energy to Increase Reproduction)

1. Under conditions of acutely increased nutrtion, what happens to glucose, insulin, and leptin?
2. glucose and insulin increased –> ?

what does this do to estradiol secretion from follicles?

3. leptin increased

what does this do to estradiol secretion from follicles?

4. Intrafollicular IGFBP increased = ?

what does this do to estradiol secretion from follicles?

5. what is the upshot of decreased estradiol production?

Answer 17

1. all increased

(and according to the model intrafollicular levels of IGF binding proteins are also increased (remember from follicular dominance that these render IGF inactive).)

2. increased glucose uptake into follicles

This suppresses estradiol secretion from follicles

3. This suppresses estradiol secretion from follicles
4. less free IGF

This suppresses estradiol secretion from follicles

5. ss feedback inhibition of FSH secretion. With less inhibitory feedback the FSH levels are higher and more follicles are supported through the selection process.

(So while the ovary is the primary target of increased nutrition, the feedback loops involving the hypothalamo-pituitary-ovarian axis are critical to the result of increased number of ovulations.)

Question 18

(Flushing)

This is an old technique of increasing ovulation rate in sheep and other polyovular species. It works by using the acute phase of the mechanism above. The females are put on a high plane of nutrition (>NRC recommendations) 2-3 weeks prior to breeding. However flushing only works in undernourished ewes and only brings them up to the reproductive level of normally conditioned animals. It is a short-term tool that allows them to achieve but not to exceed their genetic potential.

Question 19

(Sodium Ionophores (eg monensin))

1. these do what?
2. affects glucose/insulin how?
3. has been shown to do what (relative to reproduction?)

Answer 19

1. Alters rumen microflora and results in shift away from acetate and butyrate and toward propionate as the product of fermentation.
2. This is gluconeogenic, which in turn increases insulin.
3. Has been shown to increase pituitary sensitivity to GnRH and improve reproductive performance, especially under less than ideal nutrition.

Question 20

(Dietary Fat)

1. feeding fat to ruminats results in what?
2. it increases what?

(n-6:n-3 ratio)

1. high n-3 (fish oil) does what?
2. resulting in what?

Answer 20

1. ncreased propionate production. With similar effects to ionophore feeding
2. granulosa proliferation, increases medium sized follicle population and improves breeding performance independent of any effect on energy balance.

(There may also be increases in follicular and luteal steroidogenesis.)

1. decrease prostaglandin formation by uterine endometrium and decrease sensitivty of CL to prostaglandins that are released
2. longer estrous (diestrus) cycle and increased embryo survival

(Relatively high n-3 levels may also reduce the risk of pre-term labor by reducing levels of circulating inflammatory cytokines.)

Question 21

(Protein)

1. extremely low protein diets will cause what in monogastrics?

however most effects are where?

2. In ruminants, excess protein and non-protein nitrgoen result in what?

affect on cyclitcity?

on ovarian follicles?

Answer 21

1. cessation of estrous cycle

further down the reproductive axis

(Specific amino acid deficiencies are important in monogastrics with increased embryonic, fetal and neonatal losses.)

2. increased urea and ammonia levels (

don’t have affect on cyclitiy)

decreased oocyte quality with reductions in fertilization rates and blastocyst formation

(It is also hypothesized that increased uterine urea levels and decreased pH cause increased embryonic death. (These last results are somewhat controversial.))

Question 22

Other Nutritional Influences
Specific vitamin and mineral deficiencies are also more likely to cause embryonic and neonatal losses than to affect female cyclicity. However, copper and iodine deficiencies are reported to cause irregular or suppressed estrous cyclicity.

Question 23

(The Effects of Stress on Reproduction)

1. stress = ?
2. stressor = ?

Answer 23

1. loss of homeostasis
2. stimulus that threatens homeostasis

As such, stressors provide the animals with information on adverse environmental conditions. We saw previously that reproduction represents a significant energetic crunch, but one which is fairly predictable in terms of timing (such as late pregnancy and lactation). It makes sense for an animal, in the face of an adverse environment (stress) to temporarily avoid committing to the future increased metabolic load that reproduction requires. Unsurprisingly, stress is generally inhibitory to reproduction.

Question 24

(Examples of Stress Effects on Different Stages of Reproduction)

(Stress effects on breeding)

1. what is effect on GnRH and LSH on cows and ewes following transport stress?
2. Captive wild animals that have high cortisol and low sex steroid levels are not reproductively successful until what happens?
3. A change in an individual=s social status within the group can be important. In some situations only the dominant or alpha pair will breed.
4. Couples emotionally stressed about infertility have lower success in assisted reproductive programs. Women IVF patients with higher blood pressure and heart rate in response to a stress test had fewer fertilized oocytes and transferable embryos than those with low stress scores.

Answer 24

1. reductions
2. the situtation normalizes

Question 25

(Stress and Gestation)

1. In pregnant women, exposure to psychosocial stressors at 28-30 weeks of gestation shortens the pregnancy and lowers birth weights.

Crowding
We saw in the Lee-Boot effect an example where crowding altered female reproductive cyclicity. Stress may also be involved in the spectacular population fluctuations of lemmings. Some lemming populations vary widely in number over 3-4 years. The result is densities of 0.5 - 125 animals per hectare. Following number increases there are crashes, the reason for which is unknown, but one of the dominant theories is an overwhelming social stress. This would result in immunocompromised animals, with death from overwhelming parasite and microbial infection.

Question 26

(How Stress Acts to inhibit reproductive function)

1. Analogous to the hypothalamo-pituitary gonadal (HPG) axis for reproduction, the stress system consists of a what?
2. Corticotropin releasing hormone (CRH) from the hypothalamus, causes release of what?

which acts on adrenal gland to do what?

3. The HPG and HPA interact at several levels, but the dominant effect appears to occur at the level of what?

Answer 26

1. hypothalamo-pituitary adrenal (HPA) axis.
2. ACTH from the pituitary

stimulate release of the corticotropins

3. the hypothalamus

Question 27

(How Stress Acts to inhibit reproductive function)

(Effects of stress on tonic GnRH secretion)

1. stressful situations cause release of what and what in the hypothalamus?
2. CRH predominates in response to what?
3. What is secreted along with CRH in response to more intense stressors?
4. While receptors for CRH and AVP have been demonstrated on GnRH cell bodies, most of the inhibitory effects appear to be mediated by what?

Answer 27

1. CRH and arginine vasopressin (AVP)
2. weak stressors
3. AVP
4. activation of inhibitory interneurons whuch use opiods and GABA to affect the activation of GnRH neurons

Question 28

(How Stress Acts to inhibit reproductive function)

Effects of stress on generation of the LH surge

1. Acute stress can prevent the occurrence of the pre-ovulatory LH surge. Less severe stressors can delay its occurrence and decrease its amplitude.
2. effects represent what?

Answer 28

2. combo or reduced GnRH secretion and resulting decreased LH secretion

Question 29

(How Stress acts to inhibit reproductive function)

(Extrahypothalamic Sites of HPA-HPG Axis Interaction)

1. There are also reports of CRH acting directly on what?

Answer 29

1. pituitary and gonad - and for gonadal actions of ACTH and cortisol

(At present the studies are confusing and our most consistent information is that for CRH (and AVP) acting within the hypothalamus.)

Question 30

(Overriing the inhibtion of stress)

When responding to environmental stress by inhibiting reproduction, an organism is essentially deciding that by avoiding the additional costs of breeding at present they increase their (or future offsprings) chance of surviving and engaging in successful reproduction in the future when the stressor is removed. However, in some instances it makes sense to override or ignore the stressful aspects of the current environment and breed anyway, changing the trade-off of survival as an individual with the chance to pass on your genes

occurs in what five situations?

Answer 30

• Old individuals that have little chance of future reproductive success.
• Seasonal breeders, especially those with very short breeding seasons.
• Species where both partners provide parental care (loss of one parent is less important).
• Semelparous species where there is only one breeding period followed by death.
• Dominant animals in social groups where only the dominant pair breed and dominance is temporary.

Question 31

The Stressful effects of Reproduction
Males and females are often stressed differently by reproduction. Especially in polygynous species where males compete to mate, but then have no role in care of the offspring.
For males mating is a stressful business. They need to grow and maintain the secondary sex characteristics that will let them attract females and intimidate or fight rivals. They may have to defend a territory or mates against rivals and perform courtship displays. All of these things are taxing, stressful and take resources from homeostatic areas like the immune system.
The stress of rutting in reindeer increases glucocorticoids, which decreases immune function, making the animals prone to high parasite burdens.
An extreme example is the brown antechinus, a small marsupial. Males of this species are involved in a frenzy of fighting other males and prolonged mating bouts with females. The result is increased glucocorticoids, involution of lymphoid tissues, reduced immune function, parasitism and death in their first year.
In females the stresses arise during pregnancy and lactation. It is usually hypothesized that reduced immunologic function in pregnancy is required to avoid rejection of the fetus. However, it may be that the energetic demands of pregnancy cause nutrient repartitioning that results in the reduced immunologic competence. A reduction in parasite resistance and increased shedding of parasite eggs is a well-recognized phenomenon after birth and during early lactation.