Carbohydrate metabolism and control of blood glucose Flashcards

1
Q

What is the enzyme required to make free glucose needed for glycolysis

A

Glucose 6-phosphatase

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2
Q

Outline the metabolism of carbohydrates

A
  • Occurs in the liver
  • Fructose and galactose are converted into glucose
  • Glucose is then converted to pyruvate via glycolysis
  • enters TCA cycle then used in oxidative phosphorylation
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3
Q

What are the processes by which fat and amino acids can be converted to glucose

A

Fat = Beta oxidation

Amino Acids = gluconeogenesis

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4
Q

How is glucose transported across cell membranes

A

Via facilitated diffusion so requires transporter proteins and rate of diffusion will reach a plateau

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5
Q

Where are the different glucose transporters located and what are their functions

A

GLUT1 - most tissues (brain and blood cells) controls basal glucose uptake
GLUT2 - Liver, kidney, pancreatic Beta cells, used to remove excess glucose from blood and control insulin release
GLUT3 - CNS, controls basal glucose uptake
GLUT4 - Skeletal muscle and adipose tissue, Insulin and exercise increase GLUT4 at the plasma membrane
SGLT - GI tract, different involves active sodium-glucose transporter

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6
Q

structure of insulin and where is it produced?

A
  • Polypeptide made of two amino acid chains connected by disulphide bridges
  • Pancreatic Beta cells in the islets of Langerhans produce the insulin
  • production is stimulated by high glucose
  • degraded by insulinase
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7
Q

what reaction does glucokinase catalyse

A

phosphorylates glucose to form glucose 6-phosphate

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8
Q

What is the mechanism of insulin secretion?

A

1) glucose enters GLUT2 receptor of beta-cell
2) once in the cell through the TCA cycle produces ATP
3) ATP closes the potassium channels which depolarises the cell resulting in the opening of calcium channels
4) Calcium entry into the cell is the insulin secretion signal
5) granules of insulin from ER, Golgi apparatus and free granules exocytose and enter bloodstream

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9
Q

what are the drugs and hormones regulating insulin and where do they act?

A

1) Sulfonylureas close the potassium channels without needing glucose production of ATP
2) GLP-1 (Glucagon-like peptide) acts as an insulin secretion signal instead of calcium
3) Somatostatin and norepinephrine inhibit insulin release from Islets

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10
Q

Factors regulating insulin secretion

A

1) Main control is blood glucose concentration, High = insulin produced
2) High blood amino acid concentration = insulin produced as AA’s are insulin secretion signal
3) GI hormones increase insulin e.g. gastrin CCK and GIP
4) parasympathetic stimulation increases insulin
5) sympathetic stimulation decreases insulin production

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11
Q

Metabolic actions of insulin

A

Adipose tissue: dec lipolysis, inc lipogenesis, inc glucose uptake
Striated muscle: inc glycogen synthesis, inc glucose uptake by inc GLUT4, inc protein synthesis
Liver: inc glycogen synthesis by increasing glycogen synthase, inc lipogenesis, dec gluconeogenesis, inc glucose uptake by increasing glucokinase

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12
Q

What enzymes are required for glycogen breakdown and synthesis

A
Glycogen phosphorylase (breakdown)
Glycogen synthetase (synthesis)
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13
Q

which hormones raise glucose

A

glucagon
adrenaline/noradrenaline - Alpha inc glycogenolysis (liver) and Beta inc lipolysis
cortisol - inc lipolysis and gluconeogenesis, dec glucose uptake
growth hormone - inc gluconeogenesis (liver) and lipolysis (adipose tissue), dec glucose uptake (muscle)

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14
Q

What do Islets of Langerhan secrete

A

Alpha cells secrete glucagon
Beta cells secrete insulin
Delta cells secrete somatostatin

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15
Q

How does glucagon stimulate glycogen breakdown

A

Glucagon binds to G-protein coupled receptor which creates a signalling cascade and amplification to increase cAMP and PKA (protein kinase A) which stimulate glycogen phosphorylase promoting glycogenolysis (glycogen breakdown into glucose)

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16
Q

What factors increase/decrease glucagon secretion

A
  • Decreased blood glucose and increased circulating amino acids (more gluconeogenesis) increase glucagon secretion
  • exercise increase glucagon
  • somatostatin inhibits glucagon secretion, somatostatin suppresses metabolism so nutrients can be used for longer (not broken down)
17
Q

Differences between type 1 and 2 diabetes?

A

1) insulin-dependent, Beta-cell dysfunction, cause (viral infection, autoimmune, hereditary) onset 14
2) non-insulin dependant, insulin resistance, obesity-related and onset adult
in Type one no insulin is being produced in type two insulin is not effective in cells

18
Q

Effects of hyperglycaemia

A

Tired, hungry, thirsty, frequent urination, weight loss, blurry vision, wounds won’t heal and tingly feet and hands

19
Q

Which transporter proteins are needed to transport glucose back into blood in the nephron

A

SGLT 1 or 2 transports sodium and glucose out of the tubule into the cell then GLUT2 transports back into the blood (sodium-potassium pump transports the sodium back into the blood)
If glucose concentration is too high proximal tubule can become overwhelmed and glucose can be excreted

20
Q

Which drugs decrease renal glucose reabsorption

A

Gliflozins helps decrease blood glucose levels

21
Q

What are polyuria and polydipsia

A

Polyuria is excessive urination
polydipsia is excessive water consumption
both can result from hypoglycaemia

22
Q

Impacts of glucotoxicity

A

Glucose reacts with and alters proteins, these proteins then cause problems in the cell which can eventually lead to tissue damage. Cause: atypical cellular messaging, chronic inflammation, Beta-cell dysfunction and endothelial dysfunction

23
Q

What causes metabolic acidosis and diabetic ketoacidosis

A

Lack of insulin which normally inhibits lipolysis means more fats are broken down into fatty acids and glycerol. Fatty acids undergo Beta-oxidation in the liver to create keto acids. Ketones decrease blood PH causing metabolic acidosis. H+ can also disrupt intracellular potassium causing hyperkalaemia

24
Q

What symptoms of hyperglycaemia are caused by increased depletion of body protein and fat

A
  • Weight loss
  • increased appetite
  • tissue wastage
  • asthenia (lack of energy)
    depletion is due to energy needing to be produced from these sources as no insulin
25
Q

Complications of diabetes

A
  • Major CVD risk factor
  • Retinopathy
  • Stroke
  • Nephropathy (damage to kidneys)
  • Neuropathy (damage to nerves)
26
Q

How is Diabetes diagnosed?

A

Check:

  • Urinary glucose
  • Fasting blood glucose
  • Fasting plasma glucose
  • Glucose tolerance
  • Presence of ketoacidosis