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Physiology Y2 > Growth and Development > Flashcards

Growth and Development Flashcards

1
Q

Distinguish isometric and allometric growth.

A

Isometric growth – young animal is very similar to the adult animal just scaled up.

Allometric growth – proportions change during growth, not just a smaller version of the adult. Animals are adapted in relation to their size.

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2
Q

How is physiological function influenced by size?

A
  • Temperature regulation
  • Movement
  • Diffusion – inefficient over large distances
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3
Q

What is physiological scaling of body mass and metabolic rate?

A

As body mass increases, metabolic rate per g of animal decreases. Related at least in part to heat loss but more to do with surface area to volume ratio. Small animals are able to do gas exchange by diffusion over a cell membrane but larger more complex organisms have adapted CVS and respiratory systems as physiological adaptations.

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4
Q

What are the 5 cellular changes for growth and development?

A

Hypertrophy - cell becomes larger in some way.

Hyperplasia - mass increases by cell division.

Migration - cells to different parts of the body

Differentiation

Apoptosis – controlled cell death, important in forming the mature CNS.

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5
Q

What is the result of a failure to control growth?

A

Regeneration – proud flesh, which is where the phase of regeneration called granulation becomes exaggerated, impairing the recovery of function.

Cancer – failure of growth control.

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6
Q

Name 3 factors that influence growth and so development.

A

Nutrition
Environment
Genetics

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7
Q

What are the growth waves in different tissues?

A

1 = head, brain, metatarsus, kidney fat

2 = neck, bone, tibia-fibula, intermuscular fat

3 = thorax, muscle, femur, subcutaneous fat

4 = loin, fat, pelvis, intramuscular fat

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8
Q

How are growth waves affected by poor nutrition?

A

Both growth and development happen but more slowly, but order of growth curves is the same.

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9
Q

What affects nutrition?

A

Composition of diet and the influence of food availability:

  • Effects reflect competition for limited food resources
  • Animals weaned at 21 days
  • Fed ad lib after weaning
  • Affects during early development not reserved
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10
Q

How do genetics affect growth and development?

A
  • Effects of breeding on conformation
  • Gender differences in growth rates
  • Effects of breeding on weight gain: broiler chickens
  • Influence of parental gender on growth: shire mare, larger offspring (birth size is key). Growth is determined more by the breed of mare than breed of stallion.
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11
Q

Describe an example of genetics and breeding affecting conformation.

A

Wild boar are heavier in the shoulder, smaller on the back legs and shorter body than commercial pigs. Genetic influence on body shape and so growth. Is changed too much, there are repercussions on animal’s health, as they are not adapted to deal with this size and shape.

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12
Q

What controls body size?

A

Some genes responses for differences between breeds are known: large study in dogs across more than 80 breeds. Correlation between versions of some genes and breed size. IGF1 expressed in each dog measured. Smaller breeds express a form of IGF1 that larger dogs have a different form of.

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13
Q

How does temperature affect growth and development?

A

Environmental temperature changes in body shape even for litter mates that will later heat loss from the body’s surface. In pigs, cold results in short limbs and torso, stunted tail, snout and ears.

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14
Q

What are the adverse effects of microflora?

A
  • Cleary infection that causes vomiting or diarrhoea will reduce growth and can kill young animals – economic disaster
  • Even if they survive, growth will be retarded for a variable period
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15
Q

Give a summary of growth.

A

In young animals, growth is mainly by hyperplasia, increasing the number of cells rather than cell size. Growth can be measured in a qualitative, body proportions and function, and quantitative, weight and height, way. Growth requires fuel and building blocks – nutritional diet. This is driven by hormones and growth factors.

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16
Q

How is growth hormone released?

A
  • From the anterior pituitary some somatotroph cells.
  • Cells are stimulated to produce growth hormone by growth hormone releasing hormone, which is released from the arcuate nucleus of the hypothalamus.
  • There are negative and positive feedback effects.
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17
Q

What is the effect of somatostatin on growth hormone?

A

There are cells in the periventricular nucleus of the hypothalamus that release somatostatin. Somatostatin also acts on some isotopes in the anterior pituitary and acts to prevent the release of growth hormone.

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18
Q

What are the direct effects of growth hormone?

A
  • Acts to increase blood glucose by acting on the liver and skeletal muscle
  • Causes gluconeogenesis, glycogenolysis, increased protein synthesis and decreased lipogenesis in adipose tissue
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19
Q

What are the indirect effects of growth hormone?

A
  • Locally, growth hormone causes the release of IGF-1, which acts on many different tissues to cause growth
  • Growth factor can cause much larger quantities of IGF-1 to be released from the liver and into the bloodstream, so can have more widespread effects on the body.
  • Can also act as a negative feedback: IGF-1 released from the liver will feed back to the cells of the arcuate nucleus and cause a decrease in the amount of growth hormone releasing hormone released, which reduces the overall amount of growth hormone.
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20
Q

What is the relationship between weight and insulin like growth factor-1?

A

IGF-1 levels correlate with adult body size. Data shows differences in types of poodle, body weight correlated with amount of IGF-1.

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21
Q

What growth do farm animals have focus on?

A
  • Ratio of fat to skeletal muscle
  • Rapid growth selection
  • Animals now have increased body size, altered body composition and rapid growth rate
  • Often leading to long bone abnormalities
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22
Q

Describe the process of the effect of growth hormone and insulin-like growth factor-1 on bone growth.

A
  1. Growth hormone released
  2. Binds to receptors on pre-chondrocytes
  3. Differentiation of these cells and occurs at the proximal zone of the growth plate
  4. Causes cells to become early chondrocytes at the intermediate zone of the growth plate
  5. Early chondrocytes produce IGF-1, which acts locally
  6. Clonal expansion caused
  7. Terminal differentiation, causing cells to mature and form part of the bone matrix
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23
Q

What is the role of plasma IGF-1?

A

Plasma IGF-1 is GH dependent and mediates local growth.

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24
Q

What is bone growth regulated by?

A

IGF-1 – mitogenic, recruitment of precursor cells and maintenance of differentiated state by increasing differentiation and clonal expansion

Glucocorticoids – permissive/presence required for normal cell processes. But in pharmacological doses can result in bone loss and stimulation of catabolism.

Androgens – testosterone surge during puberty induces closure of growth plate. Pre-pubertal castration increases long bone growth.

Growth factors – local (autocrine/paracrine), in all tissues, mitogens, not tissue specific, growth and remodelling of bone, such as fibroblast growth factors.

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25
Q

Distinguish red and white skeletal muscle.

A

White – fast twitch. For sprinting, fine motor control and reflexive action.

Red – slow twitch, myoglobin containing. Sustained contraction, such as posture.

Ratio of red and white is genetically determined. In reality, muscle fibres are intermingled.

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26
Q

Define myogenesis.

A

Myogenesis – myoblasts proliferate, differentiate and fuse to generate myofibres.

27
Q

How is muscle growth regulated?

A
  • IGF-1 – Increase glucose and amino acids uptake. Decrease proteolysis and increases protein synthesis to cause hypertrophy. Effects on muscle precursor cells by increasing myoblast proliferation and causing hypoplasia during development.
  • Glucocorticoids – permissive but in pharmacological doses there can be glucose sparing and protein catabolism. Steroid treatment leads to muscle atrophy or poor growth.
  • Growth factors – such as myostatin and FGF
  • Beta-adrenergic agonists – repartitioning agents (redirect nutrients to skeletal muscle and not adipose tissue). Increase rate of weight gain by increasing protein deposition.
  • Androgens and oestrogens – increased protein deposition, first growth promoters used oestrogens in ruminants.
28
Q

What are the properties of brown adipose tissue?

A
  • Role in heat production and so weight control
  • Location is species specific
  • Richly vascularised and many mitochondria for energy reproduction
  • Responds to environmental and nutritional cues – hyperplasia with cold exposure
29
Q

What are the properties of white adipose tissue?

A
  • Role in energy storage
  • Diffuse in several locations
  • Sites are species specific – subcutaneous fat in pigs versus beef cattle
  • Endocrine function
  • Adipogenesis from stem cells
  • Hypertrophy induces hyperplasia
30
Q

Describe the endocrine function of white adipose tissue.

A
  • Secretes factors with importance endocrine functions
  • Importance of the endocrine function illustrated by metabolic consequences of both too much and too little
  • Secretes factors that are involved in appetite regulation, energy homeostasis, the immune response and vascular development. Such as leptin, which has a major role in body weight regulation.
31
Q

How is adipose tissue growth regulated?

A
  • GH and IGF-1 – reduction of fat mass due to inhibition of lipogenesis and stimulation of lipolysis to fuel growth
  • Insulin – lipogenesis. Stimulates proliferation, differentiation and maintenance of differentiated adipocytes.
  • Glucocorticoids – stimulate accumulation of visceral fat
  • Growth factors
32
Q

Describe the body composition of farm animals.

A

Farm animals have very little control of feed intake, the farmer will ensure that nutrition is optimises and that the ultimate production of desirable meat product is produced in the most economic way.

33
Q

Describe body composition of wild animals.

A

Animals in the wild have food sources that are more difficult to come by, that may alter at different times of the year, so survival mechanisms will favour energy storage, weight gain and fat accumulation, not at the detriment of the animal, as weight gain and intake will be tightly regulated.

34
Q

Describe body composition of domestic animals.

A

Pets have similar physiology to animals in the wild but diets are determined by owners. This can cause problems such as overweightness and obesity, skin fold thickness, dimensional evaluation and BCS.

35
Q

What are aetiologies of obesity in pets?

A

Increased dietary fat
Improved palpability
Age of indoor animals
Exercise
Neutering
Glucocorticoids

36
Q

What are some associated co-morbidities of obesity in pets?

A

Osteoarthritis
Heart disease
Renal problems
Diabetes
Respiratory

37
Q

What are the signals from the periphery to control weight and body composition?

A

Nutrient signals – fatty acids, glucose and amino acids

Nerve signals – gastric distension

Hormonal signals – insulin, leptin, ghrelin, PYY and CCK

38
Q

What are the signals on the satiety cnetre?

A
  • Glucose and so insulin
  • CCK, which correlates to fat content of meal
  • Stomach distension
  • Body fat stores
  • Smell of desirable food
  • Sight of desirable food
39
Q

What is the effect of ghrelin on the satiety centre?

A

From stomach. Levels increase during fasting. Stimulates feeding centre and promotes eating.

40
Q

What is the effect of leptin on the satiety centre?

A

From white fat. Levels proportion to fat reserves and stimulates satiety centre and inhibits easting.

41
Q

What is the effect peptide YY/PY on the satiety centre?

A

From epithelium of small and large intestines. Release proportional to the size of a meal. Stimulates satiety centre and inhibits eating.

42
Q

What is the effect of CCK on the satiety centre?

A

From epithelium of small intestine. Release is proportional to fat content of meal. Stimulates satiety centre and inhibits eating.

43
Q

How does satiety have hypothalamic regulation?

A
  • Alpha-MSH – melanocyte stimulating hormone. It is cleaved from the POMC precursor protein.
  • AGRP – agouti-related peptide
  • NPY – neuropeptide Y
  • POMC – proopiomelanocortin
  • MCH – melanin concentrating hormone
44
Q

What is the effect on NPY on satiety?

A

If cells in the arcuate nucleus of the hypothalamus are stimulated to release NPY, this then stimulates a group of second order neurones to increase the activity of eating, usually by bringing about the sensation of hunger.

45
Q

What is the effect of POMC on satiety?

A

If cells in the arcuate nucleus of the hypothalamus are stimulated to release POMC, this acts on a different group of second order neurones to depress feelings of hinger to inhibit feeding.

46
Q

What are the effects of leptin and ghrelin on satiety?

A

Leptin acts to cause release of POMC to inhibit feeding.

Ghrelin acts to cause release of NPY to encourage eating.

47
Q

How do mutations of leptin cause obesity?

A
  1. Leptin level in the blood is proportional to fat mass
  2. Blood brain barrier
  3. Leptin receptor – leptin level in CNS is dependent on transport into the CNS from the blood, leptin does not cross the membrane, as it is a protein.
48
Q

Describe the POMC satiety signals.

A
  • Leptin stimulates alpha-MSH and beta-MSH release
  • Alpha and beta-MSH both stimulate MC4 receptor
  • MC4 receptor stimulation reduces eating
  • AgRP inhibits MC4 receptor
  • Gamma-MSH has a role in release of luteinising hormone
49
Q

What are the factors contributing to puberty?

A

Hormonal
Genetic
Environmental
Nutritional

50
Q

What are the variabilities of age in the onset of puberty between species?

A

Mouse – 7 weeks
Gilt – 5-8 months
Filly – 1-2 years
Elephant and human – 1-1.5 decades

51
Q

What are the variabilities of age in the onset of puberty within species?

A

Mouse and rat – 2-2.5 months
Gilt – 5-8 months
Queen – 5-16 months due to season
Bitch – 5-18 months due to breed
Lamb – 6-16 months due to season
Heifer – 6-18 months due to breed
Filly – 10-24 months due to breed and season

52
Q

What are the influences of sex on puberty?

A

Large peaks of LH are normal oestrous but between these there are much smaller more regular peaks of LH. The release of LH and testosterone occurs every 4-5 hours.

53
Q

What must occur in the hypothalamus-pituitary axis for puberty to occur?

A
  • Pulsatile increase in GnRH, steady increase will not cause puberty.
  • Sex hormones also feed into kisspeptin 1 neurones and these alone are not enough to cause puberty
  • Seasonal changes, day length and so light affects puberty. Light acts on the suprachiasmatic nucleus and so the pineal gland, which causes the release of melatonin, which also acts on kisspeptin 1 neurones
  • SCN may also have a direct effect on kisspeptin 1 cells also
54
Q

What are the effects of leptin on energy reserves and puberty?

A
  • Reproductive function is sensitive to the state of energy reserves, such as females need threshold energy reserves to successfully face pregnancy and lactation.
  • Initiation of puberty is strongly influenced by the nutritional level received during the prepubertal period after weaning, such as low nutrient intake results in delayed onset of fertility.
  • Energy reserves are signalled by leptin. Signal produced by white fat to indicate that there is a certain amount of fat in the body.
55
Q

How does leptin deficiency link to infertility?

A
  • Leptin-deficient mice and humans show lock of puberty
  • Variable degree of hypogonadotropic hypogonadism and infertility
  • Lack of GnRH
56
Q

What is the purpose of kisspeptin 1 neurones?

A

Kisspeptin 1 neurones can coordinate all the signals and cause kisspeptin release, which acts on the GnRH neurones, causing GnRH release. Sex steroids can have positive and negative effects on kisspeptin neurones.

57
Q

Describe the hypothalamic-gonadal axis in females.

A

In females, oestradiol inhibits ARC/arcuate nucleus of the hypothalamus via negative feedback. Oestradiol stimulates AVPA/anteroventral periventricular nucleus in positive feedback and is involved in GnRH/LH surge in proestrus.

58
Q

What does the expression of kisspeptin allow?

A

Expression of kisspeptin from the kiss1 gene and its receptor GPR54 appear to be the key for pulsative GnRH release.

59
Q

What is the role of vets in meat production?

A
  • Vets need a basic understanding of what ‘products’ farmers are aiming to produce
  • Farmers will look for advice from their vet about how to optimise production, minimise environmental impact, get the best price for their animals, meet market specification
  • Vets may have specific roles in breeding advice, procedures (castration), production systems and nutrition, optimising slaughter weigh/age and manipulations (growth promotion)
60
Q

Distinguish late and early maturation.

A

Early maturing – these tend to put on fat quicker, but are less heavy, they tend to be steers or heifers, and tend to be native UK breeds

Late maturing – these take longer to reach the 15 -20% fat target but kill out heavier. They are usually continental breeds or bulls.

61
Q

Define maturing.

A

The likelihood of putting fat on without increasing energy density of diet.

62
Q

Define allometry.

A

The relationship of the growth of 1 part of an organism to the growth of another part or the growth of the whole organism.

63
Q

What are growth promoters?

A

Hormonal compounds used to change growth rate, feed utilisation and body composition in livestock, or products to modify gut flora.

64
Q

Give 7 examples of growth promoters.

A

Growth hormone
Sex hormones
Catecholamines
Antimicrobials
Bovine somatotropin
Oestrogen and androgens
Beta-adrenergic agonists

Physiology Y2 (14 decks)

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