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lecture 26 Flashcards

1
Q

what is type 1 diabetes?

A

-polygenic disorder
-autoimmune destruction of insulin producing cells

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2
Q

what is type 2 diabetes?

A

-polygenic disorder
-defects in insulin action (obesity)
-defects in glucose-induced insulin secretion

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3
Q

what are the complications with diabetes?

A

retinopathy (sight)
nephropathy (kidney function)
peripheral neuropathy (feet)
autonomic neuropathy (cardiovascular, gut)
macrovascular (heart attack, stroke)

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4
Q

which type of diabetes associates with obesity?

A

type 2

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5
Q

why does obesity increase diabetes risk?

A

-associated with insulin resistance and enlargement of islets
-balance between lifestyle and B cell compensation (genetics)

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6
Q

when does type 2 diabetes develop?

A

once beta cells can no longer compensate for insulin resistance

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7
Q

how is type 2 diabetes developed from unhealthy lifestyle?

A

-increased obesity
-increased insulin resistance
-susceptible beta cells
-beta cell dysfunction and failure
-hyperglycaemia
-type 2 diabetes

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8
Q

what is the therapy for type 2 diabetes?

A

-lifestyle changes (diet and increased exercise)
-drugs - mono therapy (metformin) or combination

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9
Q

how is carbohydrate absorption targeted?

A

-inhibiting carb digestion with alpha-glucoside inhibitors (AGIs)

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10
Q

what are AGIs?

A

competitive inhibitors
convert oligosaccharides to glucose
1st gen -> acarbose -> not abosrbed
2nd gen -> miglitol ->absorbed

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11
Q

what are the benefits of AGI?

A

-decreases intestinal glucose absorption
-decreases glycemic index of food
-decreases post prandial blood (glucose) and triglycerides
-no risk of hypoglycaemia (too low glucose levels)

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12
Q

what are the adverse effects of AGI?

A

-abdominal discomfort as undigested carbs move from small intestine to colon
-fermentation of undigested carbs in colon

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13
Q

how is renal glucose excretion increased?

A

-by inhibiting SGLT2 in kidney

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14
Q

what do SGLTs do?

A

They are symporters of glucose and sodium > use sodium gradient (‘active transporter’ > Na+ must be pumped out)

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15
Q

what is the function of SGLT2 inhibitors?

A

prevent reabsorption of glucose causing excretion in urine

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16
Q

where is SGLT2 expressed?

A

kidney

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17
Q

where is SGLT1 expressed?

A

kidney and intestine

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18
Q

what are the inhibitors of SGLT2?

A

-phlorizin (non selective naturally occuring)
-sergiflozin and dapagliflozin (selective inhibitor)

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19
Q

what does phlorizin do?

A

inhibits intestinal and renal absorption of glucose
lowers blood glucose
inhibits SGLT1 and 2

20
Q

what does sergiflozin and dapagliflozin do?

A

-cause inhibition of renal glucose re-absorption
-lower blood glucose
-weight loss
-inhibits SGLT2

21
Q

what are the adverse effects/risks of using SGLTs?

A

increased urine volume
risk of urinary tract infections (UTIs)
risk of genital fungal infections

22
Q

how is insulin secretion targeted?

A

sulphonylureas
GLP-1R agonists
DPP4 inhibitors

23
Q

how do sulphonylureas work?

A

-bind to SUR1
-close the K-ATP channel
-membrane depolarisation
-increase insulin secretion

24
Q

what are incretins?

A

intestinal peptides produced in response to food that stimulate insulin secretion
GIP and GLP1

25
Q

what is GIP?

A

-glucose dependent insulinotropic peptide
-secreted from K cells in small intestine
-inhibits gastric motility, stimulates insulin secretion
-has inhibitory effect on appetite

26
Q

what is GLP1?

A

-glucagon like peptide 1
-secreted from L cells of colon
-stimulates insulin secretion by beta cells
-suppresses appetite in brain
-used in treatment of obesity

27
Q

what is an example of a GIP agonist?

A

tirzepatide

28
Q

what is an example of a GLP-1 agonist?

A

-exenatide
-liraglutide
-semaglutide

29
Q

what is the mechanism of action of GLP-1 on islet beta cells?

A
  1. bind to GLP-1 receptor
  2. increases cAMP
  3. increases PKA
  4. increases cAMP guanine nucleotide exchange factor
  5. increased ca2+
  6. decreased K ATP channel
  7. increased insulin secretion
30
Q

what causes degradation of incretins?

A

DPP-4 (dipeptidyl peptidase 4)
cleaves the first 2 residues to become inactive

31
Q

what 2 forms does DPP4 exist as?

A
  1. membrane anchored extracellular enzyme
  2. soluble form (retains catalytic activity)
32
Q

what are the benefits of sulphonylureas?

A

-decreases blood glucose
-increases insulin secretion

33
Q

what are the risks of sulphonylureas?

A

-increased risk of hypoglycaemia
-increased weight gain
-increased cardiovascular events

34
Q

what are the benefits of GLP-1R agonists and DPP4 inhibitors?

A

-decrease blood gluciose
-increased insulin secretion
-decrease glucagon secretion
-no risk of hypoglycaemia
-decreased food intake and body weight

35
Q

what are the potential risks of GLP-1R agonists and DPP4 inhibitors?

A

pancreatitis or pancreatic cancer
gastric discomfort

36
Q

what are the two ways adipose tissue expands in obesity?

A
  1. fat cell hypertrophy (increases in cell volume)
  2. fat cell hyperplasia (increase in cell number/adipogenesis)
37
Q

what happens when adipocytes attain their max capacity of lipid storage?

A

lipid leaves are raised in blood and other tissues

38
Q

what are PPAR-gamma drugs?

A

favour adipocyte proliferation and further lipid storage
prevents damage by lipids in other organs

39
Q

what do TZDs do?

A

-decrease blood glucose
-decrease blood insulin
-decrease blood triglycerides
-increase insulin sensitivity

40
Q

what does PPAR gamma do?

A

transcription factors that promotes adipocyte proliferation and differentiation

41
Q

how is PPAR gamma activated?

A
  1. ligand binding to PPAR gamma
  2. heterodimer with retinoid acid receptor
  3. recruitment to PPRE on DNA promoter
  4. recruitment of co-activator (eg. P300-histone acetylase)
  5. acetylation of histones exposes chromatin
  6. increased transcription of PPAR gamma target genes
42
Q

what are the benefits of TZDs?

A

-lower blood glucose and insulin
-increased insulin sensitivity in obesity

43
Q

what are the risks of TZDs?

A

increases body weight
can cause liver damage
heart attack risk

44
Q

which TZD is currently in clinical use?

A

pioglitazone

45
Q

what are the biological effects of metformin?

A

-decreased hepatic glucose production
-increased fatty acid oxidation
-increased insulin sensitivity
-increased glucose utilisation

46
Q

what is the mechanism of metformin?

A
  1. enter cells via OCT1
  2. accumulates in energised mitochondria (-ve charge inside)
  3. inhibits complex I
  4. decreases ATP/ADP (decreases energy for gluconeogenesis)
  5. increases AMP (inactivates adenyl cyclase, prevents glucagon signalling, decreases gluconeogenesis)
  6. AMPK activation (increased fatty acid oxidation, decreased fatty acid synthesis)
47
Q
A

psc2002 (15 decks)

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