11.2 - Metabolic And Endocrine Control During Special Circumstances Flashcards

1
Q

What fuel sources are normally available in the blood and available under special conditions?

A

Normally

  • glucose
  • fatty acids (except in RBC, brain and CNS)

Special conditions

  • amino acids from muscle mass, converted to glucose or ketone bodies
  • ketone bodies from fatty acids, used when glucose short as brain can use it
  • lactate, made in anaerobic metabolism in body
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2
Q

What happening 2 hours after feeding?

A

Immediate metabolism supported by glucose

Speed up growth and repair process

Make glycogen as rapidly as possible

Increase fat stores

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3
Q

What happens 2-10 hours after feeding?

A

Glucose and fats no longer being absorbed

Maintain blood glucose by drawing on glycogen stores
Support other metabolic activity with fatty acids released from stores
Preserve blood glucose for brain

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4
Q

What happens 8-10 hours after feeding?

A

Glycogen stores depleted = need to make more glucose

Continue to support metabolism with fatty acids

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5
Q

What happens during starvation?

A

Need to reduce protein breakdown

Fatty acid metabolism produces ketone bodies

Brain becomes able to metabolise ketone bodies = reduces need for glucose.

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6
Q

What do anabolic hormones do?

A

Promote fuel storage e.g insulin

Lack of insulin = catabolic state

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7
Q

What do catabolic hormones do?

A

Promote release from stores and utilisation

E.g glucagon, adrenaline, cortisol, growth hormone and thyroid hormone

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8
Q

What does insulin stop and promote?

A

Stop

  • gluconeogenesis
  • glycogenolysis
  • lipolysis
  • ketogenesis
  • proteolysis

Go

  • GLUT4 transporter for muscle uptake
  • glycolysis
  • glycogen synthesis
  • protein synthesis
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9
Q

What does feeding promote?

A

Amino acid uptake and protein synthesis in liver and muscle

Promotes lipogenesis and storage. Of fatty acids as triacylglycerol in adipose

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10
Q

What do you get from fasting?

A

Glycogenolysis
Lipolysis
Gluconeogenesis - glycerol from fat provided. Kidney also starts doing this also.

Cortisol is released which prevents most cells from using glucose and fatty acids are preferentially metabolised.

Liver starts making ketone bodies and brain starts to utilise these sparing glucose requirement from protein

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11
Q

What are the two main phases of metabolic adaptation during pregnancy?

A

Anabolic

  • early pregnancy
  • increase in maternal fat stores and small increase in insulin sensitivity
  • nutrients stored to meet futur demands of rapid foetal growth

Catabolic

  • late pregnancy
  • decreased insulin sensitivity (increased resistance)
  • tissues use fatty acids to save glucose
  • increased resistance to insulin = increase maternal glucose and free fatty acid conc
  • allows greater substrate availability for foetal growth.
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12
Q

What’s the fetoplacental unit?

A

Placenta, fetal adrenal glands and fetal liver make an endocrine entity called the fetoplacental unit

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13
Q

What hormones does the placenta release to control the maternal hypothalamic pituitary axis?

A

Hypothalamic

  • CRH
  • GnRH
  • TRH
  • GHRH

Pituitary like

  • ACTH
  • Human chorionic gonadotropin
  • human chorion thyrotropi
  • human placental lactogen
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14
Q

What happens to insulin levels in the second half of pregnancy?

A

Maternal insulin increases

Anti insulin hormones increases at a faster rate

Therefore the insulin/anti insulin ratio falls

Cells therefore have decreased insulin sensitivity

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15
Q

What are anti insulin hormones?

A

cause transient hyperglycaemia after meals because Of increased insulin resistance

Hypoglycaemia can occur between meals and at night because of the continuous fetal draw of Glucose

NB: maternal ant pit becomes desensitised to CRH so more ACTH and cortisol is around

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16
Q

Whats insulin secretion like in pregnancy?

A

Increased appetite = more glucose in ingested

Oestrogen and progesterone increase sensitivity of maternal pancreatic B cells to blood glucose

  • B cell hyperplasia
  • B cell hypertrophy

Leads to increased insulin synthesis and secretion
If B cells don’t respond normally, blood glucose may become seriously high and gestational diabetes may develop

17
Q

What are the underlying causes of gestational diabetes?

A

1) autoantibodies similar to those characteristic of type 1 DM
2) genetic susceptibility to maturity onset of diabeties
3) B cell dysfunction in setting of obesity and chronic insulin resistance

18
Q

What are the clinical implications of gestational diabetes?

A
  • Increased incidence of miscarriage
  • Incidence of congenital malformation is 4x higher
  • Fetal macrosomia (large body) = could get shoulder dystopia (shoulder gets stuck during birth)
  • Associated with gestational hypertension and preeclampsia
  • risk minimised if diagnosed and managed
19
Q

What makes someone more at risk of gestational diabeties?

A

Higher insulin resistance before pregnancy

Also age as fat to lean body mass ratio increases and insulin resistance increases with age (over 25)

BMI over 25 kg/m2

More common in Asians, black and Hispanic groups

If you have gestational diabetes during pregnancy will probably develop type 2 later in life.

20
Q

What’s the management for gestational diabeties?

A

Dietary modification

Insulin injections if persistent hyperglycaemia

Regular ultrasound scans to asses fetal growth

21
Q

What metabolic responses occur during excersise?

A

Increased energy demands met by mobilisation of energy stores

Glucose supply to brain maintain

End products of metabolism are removed asap

22
Q

How are atp stores replenished in exercise ?

A

Muscle creatine phosphate stores rapidly replenish

Glycolysis supplied atp - 2 per glucose

  • using muscle glycogen in intensive excersise that’s anaerobic
  • oxygen can be supplied from complete oxidation of glucose and glycogen stores from muscle and liver in long excersise e.g jogging

Oxidative phosphorylation - but needs oxygen

23
Q

What’s the role of the liver in blood glucose conc?

A

Excersise increases hepatic blood glucose production through glycogenolysis and gluconeogenesis

Liver recycles lactate produced by anaerobic metabolism

Rate of glucose production from liver is insufficient to meet full demands,
Needs to be maintained for brain

EXTRA

Muscle takes glucose from GLUT4 from insulin and GLUT 1 (always active )
Excersise also have insulin independant process of glucose uptake

24
Q

How are fatty acids used as fuel?

A

In aerobic conditions

  • slow release from adipose tissue
  • limited carrying capacity in blood
  • capacity limited by uptake across mitochondrial membrane

Low rate of atp production but high capacity for sustained production

25
Q

How is energy produced in a sprint?

A

Anaerobic respiration and muscle store of glycogen , helps to spare blood glucose for brain

26
Q

How is energy used in 1500 m distance race?

A

Three phases

  • initially creatine phosphate and anaerobic glycogen metabolism
  • long middle phase in which ATP is made aerobically from muscle glycogen
  • anaerobic metabolism of glycogen and produce lactate
27
Q

How is energy made in a marathon?

A

Aerobic mainly, uses muscle and liver glycogen and fatty acids

Insulin levels slowly fall
Glucagon Levels rise and do their thing

Adrenaline for glycogenolysis and lipolysis and more growth hormone for lipolysis and gluconeogenesis

Cortisol rises slowly for lipolysis and gluconeogenesis

28
Q

What are the benefits of excersise?

A
  • less adipose more muscle
  • glucose tolerance improves
  • more insulin sensitive tissues
  • less blood triglycerides
  • blood pressure falls
  • psychological effects