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Physiology and Disease > 13 - Metabolic challenges to homeostasis > Flashcards

13 - Metabolic challenges to homeostasis Flashcards

1
Q

lysis

A

break down

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2
Q

genesis

A

make new

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3
Q

glyco

A

glycogen

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4
Q

gluco

A

glucose

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5
Q

glycogenolysis

A

conversion of glycogen to glucose

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6
Q

gluconeogenesis

A

production of new glucose (from a few amino acids, glycerol, lactic acid etc)

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7
Q

glycogenesis

A

storage of glucose as glycogen

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8
Q

anabolism

A

synthesis

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9
Q

catabolism

A

breakdown

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10
Q

effects of insulin (3)

A
  • promotes anabolism
    1. increased glucose uptake
    2. increased conversion of glucose to glycogen (glycogenesis)
    3. increased protein and lipid synthesis (excess glucose beyond glycogen storage goes to adipose storage)
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11
Q

effects of glucagon (3)

A
  • promotes catabolism
    1. increased liver glycogen breakdown -> glucose (glycogenolysis)
    2. increased glucose production (glucogenesis)
    3. lipid break down (lipolysis)
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12
Q

where does insulin act?

A

many sites, predominantly skeletal muscle, liver and adipose tissue

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13
Q

insulin action

A

promotes insertion of glutamate transporter GLUT4 into membrane (e.g. skeletal muscle). GLUT4 transporters facilitate glucose uptake down concentration gradient

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14
Q

local glucose sensing

A

sensed by pancreatic a/B cells (dependant on cellular ADP:ATP levels)

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15
Q

central glucose sensing

A

sensed by glucose-sensitive neurons in the hypothalamic nuclei

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16
Q

indirect glucose sensing

A

sensed indirectly from hormonal signals in digestive system (e.g. small intestine and liver)
- signals sent to vagus nerve or hypothalamus and brain stem via blood

17
Q

plasma glucose response to eating (a meal) (2)

A
  1. plasma glucose and insulin rise rapidly after a meal over course of 1-2 hours
  2. plasma glucose decline followed by insulin
    - allows dynamic bodily response to move towards anabolism
18
Q

5 phases of glucose metabolism (5)

A
  1. fed state (glucose acquired from dietary source)
  2. early fasting: glycogenolysis (glucose acquired by lysing glycogen stores in liver)
  3. late fasting: gluconeogenesis (glucose synthesised from sugars, lipids and some amino acids)
  4. early starvation: fatty acid oxidation becomes dominant, ketone bodies also used in TCA/Krebs cycle
  5. late starvation: fatty acid and ketone bodies used to exhaustion, amino acids from muscle proteins then metabolised
19
Q

how are glucose reserves allocated in late stages (4/5) of glucose metabolism?

A

last remaining glucose reserves used in brain, RBCs and kidneys (rest of body moves to fatty acids/ketone bodies)

20
Q

diabetes mellitus

A

metabolic disorder: genetic and environmental risks, defects in insulin signalling, elevated blood glucose, glucosuria (glucose in urine)

21
Q

type 1 diabetes mellitus (2)

A
  1. aggressive autoimmune loss of pancreatic B cells, usually early onset
  2. very low insulin levels, requires replacement
22
Q

type 2 diabetes mellitus (3)

A
  1. resistance to insulin, can involve high circulating insulin (hyperinsulinemia)
  2. progressive loss of pancreatic B cells
  3. usually later onset, usually contributed by diabetogenic diet and genetic risk
23
Q

metabolic effects of diabetes mellitus (type 1/2) (6)

A
  1. decreased cellular uptake of glucose - poor cellular use of glucose
  2. increased catabolism/ decreased anabolism
  3. increased gluconeogenesis
  4. increased glycogenolysis
  5. increased protein and lipid breakdown
  6. increased protein glycation (sugar molecule binding to protein)
24
Q

protein glycation example (2)

A
  1. sugar molecule binding to proteins
  2. e.g. haemoglobin - associated with vascular, renal and nerve inflammatory damage
25
Q

net metabolic effect of diabetes mellitus

A

increased circulating plasma glucose and impaired normal metabolic function

26
Q

diabetic ketoacidosis

A

decreased blood pH due to accumulation of acidic ketone byproducts

27
Q

cause of diabetic ketoacidosis

A

ketone bodies metabolised to enter krebs cycle when glucose uptake is poor

28
Q

symptoms of diabetic ketoacidosis (3)

A
  1. extreme hunger/thirst
  2. dizziness/ delirium
  3. risk of death without treatment
29
Q

insulin replacement therapy for type 1/2 diabetes (2)

A
  1. type 1 = lifelong
  2. type 2 = generally late-stage
30
Q

treatments for diabetes mellitus (4)

A
  1. insulin replacement therapy
  2. strict diet management
  3. metformin (reduces liver gluconeogenesis)
  4. SGLT inhibitors (inhibit glucose absorption in intestines (SGLT1)/kidneys (SGLT2)
    - overall aim = restore homeostatic control of glucose
31
Q

glucagon-like peptide 1 (2)

A
  1. hormone (many different actions, similar to insulin)
  2. receptors for GLP1 in brain decrease food intake
32
Q

ozempic

A

GLP1 receptor agonist (mimics effects)

33
Q

ozempic effects (3)

A
  1. decreases appetite and food seeking
  2. increased insulin signalling
  3. significant weight loss in clinical trials
34
Q

cholecystokinin (3)

A
  1. hormone, released in multiple sites (including small intestine), stimulates pancreatic juice/bile secretions
  2. signals satiety via parasympathetic vagus nerve
  3. CCK administration decreases food intake in rats
35
Q

cholecystokinin signalling via vagus nerve (2)

A
  1. appetite suppressing effect reduced by cutting vagus nerve (vagotomy)
  2. suggests CCK signalling to PNS important for controlling feeding
36
Q

set point model for energy homeostasis and feeding (4)

A
  1. set point: weight may have some form of set point signal
  2. comparator: compares set point signal to actual signal, affected by ‘incentive’
  3. error signal: difference between set point and actual weight activates negative feedback response via endocrine, autonomic or behavioural systems
  4. controlled variables and feedback detectors: changes such as blood glucose then fed back

Physiology and Disease (13 decks)

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