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Sophie - Applied Physiology & Pharmacology Year 2 > 56.1 Metabolic Homeostasis > Flashcards

56.1 Metabolic Homeostasis Flashcards

1
Q

Which cellular processes occur during growth?

A

Hyperplasia
Hypertrophy

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2
Q

What hormones regulate prenatal growth?

A

Growth hormone (GH)
Insulin like growth factors (IGF-1 and 2)
Foetal insulin
Placental growth hormones

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3
Q

What determines growth?

A

Environment: nutrition and emotional deprivation
Genetics

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4
Q

When is the lifetime of a human is the most rapid period of growth?

A

Prenatal growth within the uterus
(CONCEPTION TO BIRTH: Weight increases x 4.4x108 Length increases x 3850)

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5
Q

What is foetal programming?

A

A concept that suggests certain events occurring during critical points of pregnancy may cause permanent effects on the foetus and the infant long after birth

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6
Q

What are the consequences of nutrient restriction during the fetuses time in the womb later in life?

A

-Increased risk of insulin resistance
-Increased risk of obesity
-Increased risk of cardiovascular disease

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7
Q

What are the effects of a diabetic mother on infants? Why does this occur?

A

INCREASED BODY WEIGHT
Materal hyperglycaemia –> fetal hyperinsulinaemia –> increased fat deposits, length and body mass

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8
Q

What are the consequences on the new-born of nutritional restriction in utero?

A

= reduction in endocrine and paracrine IGF
= resetting of foetal development to accommodate nutritionally deprived environment
= insulin, IGF and GH resistance = slower growth rate = smaller baby with reduced nutritional demands

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9
Q

Name two conditions which come about as a result of congenitally affected foetal growth

A

Leprechaunism
Pancreatic agenesis

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10
Q

What causes leprechaunism?

A

Mutation in the insulin receptor gene = severe dwarfism as a result of not being able to take up glucose (hyperglycaemia)

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11
Q

What is pancreatic agenesis? What are the consequences?

A

Anatomical variation in the pancreas characterised by a partial or total loss of the body and tail
Results in a 50% reduction in body weight

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12
Q

Name two foetal conditions which occur as a result of malnutrition

A

Marasmus (loss of adipose tissue, low blood glucose)
Kwashiorkor (oedema and altered pigmentation)

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13
Q

What is the result of excessive GH secretion?

A

Giantism

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14
Q

What is the result of insufficient GH secretion?

A

pituitary dwarfism

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15
Q

Which cell type makes GH?

A

Somatotrophs in the anterior pituitary

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16
Q

Which hormone triggers the release of GH from the anterior pituitary?

A

GH releasing hormone which acts on somatotrophs

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17
Q

Which hormone exerts negative feedback on GH release?

A

IGF-1 (as GH triggers IGF-1 secretion which mediates the actions of GH)
Somatostatin

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18
Q

What are the effects of GH?

A

Lipolysis of adipose tissue
Stimulation of gluconeogenesis
Stops glucose uptake by muscle

Opposite to insulin

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19
Q

When is the majority of GH released?

A

At night during sleep

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20
Q

What is acromegaly? What are the symptoms?

A

An excess of GH AFTER puberty
Epiphyseal plates closed up = no longitudinal growth
Thickening of bones and soft tissues of the head, hands and feet

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21
Q

What are the hormones involved in control of energy metabolism that are mentioned in the spec?

A
  • IGF1 (insulin-like growth factor 1)
  • IGF2 (insulin-like growth factor 2)
  • Insulin
  • Growth hormone
  • Human placental lactogen (hPL)
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22
Q

Where is endocrine IGF-1 synthesised?

A

Liver

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23
Q

Where is autocrine/paracrine IGF-1 synthesised?

A

Muscle
Cartilage
Bone

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24
Q

What are the effects of IGF-1? (5)

A

Binds to receptor tyrosine kinase:
-Promotes uptake of amino acids
-Stimulates protein synthesis
-Stimulates glucose uptake to muscle tissue
-Inhibits apoptosis
-Promotes tissue expansion

25
Q

What stimulates IGF-1 production?

A

Insulin (Promotes a shift to greater rates of glucose breakdown, storage and uptake to provide nutrients for cellular growth.)
Growth hormone

26
Q

What is the result of pituitary dwarfism secondary to GH deficiency on IGF-1 and IGF-2 concentrations and why?

A

Less GH:
Decreased circulating IGF-1 which relies on GH to stimulate its synthesis and release
None/little effect on IGF-2

27
Q

Where is IGF-2 produced?

A

Thecal and granulosa cells during folliculogenesis

28
Q

How does the timing of peak concentrations of IGF-1 and 2 differ?

A

IGF-1 = peaks during puberty when growth is increasing (greatest growth rates observed when IGF-1 is peaking)
IGF-2 = mediates interuterine growth (peaks just before birth)

29
Q

What is the function of IGF-2?

A

Binds to IGF1 and IGF2 receptors
-Promotes granulosa cell differentiation during follicular phase
-Promotes progestrone secretion during luteal phase (works with LH)
-Promote growth in utero

30
Q

What effect does insulin, IGF1 and IGF2 all have on the body?

A

Hypoglycaemia

31
Q

What is the result of IGF-2 knockouts?

A

Impaired foetal growth
reduced placenta size

32
Q

What does excessive IGF-2 secretion result in?

A

Somatic overgrowth

33
Q

How does foetal insulin regulate IGF-1?

A

Placental glucose transfer causes release of foetal insulin
Foetal insulin acts on maternal liver to trigger IGF-1 release
Fetus grows

34
Q

What is the role of insulin?

A

Promotes a shift to greater rates of glucose breakdown, storage and uptake to provide nutrients for cellular growth. Induces the secretion of hepatic IGF1 for its pro-growth effects

35
Q

What is the function of human placental lactogen?

A

Similar structure and function to growth hormone (1% as potent but present at 50X higher)
Modifies energy state of the mother to facilitate energy supply to foetus
Anti-insulin properties
-reduces maternal insulin sensitivity = increase in maternal blood glucose
-increases lipolysis of free fatty acids
-reduces maternal glucose utilisation

36
Q

Which cells make hPL?

A

Secreted by syncytiotrophoblasts during pregnancy

37
Q

What are the hormonal changes which occur during starvation?

A

Decreased insulin and increased glucagon secretion

38
Q

What are the short term adaptations of the body to starvation?

A

Driven by glucagon:
-Gluconeogenesis in the liver
-Glycogenolysis
-Lipolysis and beta oxidation in adipocytes

39
Q

What are the long term adaptations of the body to starvation?

A

Preservation of glucose for tissues which require it: red blood cells, brain and adrenal medulla
-Gluconeogenesis (muscle tissue metabolised to generate amino acids for glucose production)
-Ketogenesis (for heart and brain and renal cortex)

40
Q

What are the symptoms of chronic malnutrition? (6)

A

Elevated ketogenesis
Hypoglycaemia
Weight loss
Stunted growth during childhood
Fatigue
Immune suppression

41
Q

What are the metabolic changes that occur during chronic malnutrition?

A

Growth slows or stops so that protein and energy can be used for maintenance of existing tissues

Increased lipolysis (raised plasma free fatty acids)
Ketogenesis
Gluconeogenesis

Reduction in thermogenesis

42
Q

What score is used to assess patients with malnutrition?

A

Malnutrition-inflammation score (MIS)

43
Q

How does the malnutrition inflammation score assess?

A

Assesses 7 components in patients with chonric kidney disease:
-changes in the dry weight of dialysis products
-dietary intake (appetite)
-appearance of GI symptoms
-tiredness and functional capacity
-occurrence of comorbidities
-examined (observable) decreases in subcutaneous fat or signs of muscle wasting, accompanied with BMI decreases
-lowered serum albumin/total iron binding capacity

44
Q

What do the hormones involved in energy metabolism all rely on?

A

NUTRITIONAL INTAKE
-amino acids and glucose trigger insulin secretion
-amino acids trigger GH secretion
-iodine required for thyroxine hormone

45
Q

What will cause body mass to increase?

A

Energy intake exceeding energy expenditure

46
Q

Which hormones are involved in the control of body weight?

A

LEPTIN
Hormones which regulate appetite (CCK, PYY and GLP-1)
Sex steroids (influence fat distribution to promote fat storage around the lower body = better resistance to excessive weight gain)

47
Q

Where is leptin produced?

A

Adipose tissue at a rate which is proportional to fat content and overall mass

48
Q

How does leptin regulate body weight?

A

Sensed by the POMC/CART neurons of the arcuate directly and via connections to the ventromedial ‘satiety’ centres of the hypothalamus

49
Q

Why may adipose tissue be thought of as an endocrine organ?

A

It secretes a hormone leptin in proportion to fat stores (BMI)

50
Q

Where are the two main places fat can be deposited?

A

Subcutaneously
Visceral

51
Q

What is the difference in the significance of subcutaneous and visceral fat deposition?

A

Visceral fat is more dangerous and associated with increased metabolic diseases (insulin resistance)
Subcutaneous fat = beige tissue instead of white and incorporates brown adipocytes for thermogenesis (protection against CVD and T2DM)

52
Q

Why do wild type mice paired to ob/ob mice cause ob/ob to lose weight?

A

High leptin secretions by wild type mouse are shared to wild type circulation resulting in a decreased feeding drive for ob/ob mouse causing it to lose weight

53
Q

Why does leptin have little effect on obese individuals?

A

Hyperleptinemia causes leptin resistance

54
Q

Which individual is more likely to have insulin resistance?

A

A = more visceral fat deposits than cutaneous fat
Correlates with T2DM
same BMI

55
Q

What BMI does someone have to have to be qualified as obese?

A

30

56
Q

What is the role of adipose tissue in inflammation in the development of diabetes?

A

Fat tissue contains 50% macrophages
When fat cells die - release inflammatory mediators which activate macrophages to engulf them
Attracts other immune cells and mount an immune response on the adipocytes
cause the fat tissue to become insulin resistant
TNF-alpha blocks insulin signalling (produced in obese patients with adipose tissue macrophages)

57
Q

What are the consequences of obesity?

A

Decline in health:
-Increased in T2DM
-Increased atherosclerosis (increased LDLs) and CVD
-Hypertension
-Thrombosis

58
Q

What is malnutrition?

A

Deficiencies, excesses or imbalances in a person’s intake of energy and/or nutrients.

Sophie - Applied Physiology & Pharmacology Year 2 (32 decks)

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