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Physiology > ENDO V Insulin and Glucagon > Flashcards

ENDO V Insulin and Glucagon Flashcards

1
Q

what secretes glucagon

A

alpha cells

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2
Q

what secretes insulin

A

beta cells

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3
Q

what secretes somatostatin

A

delta cells

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4
Q

what secretes pancreatic polypeptide

A

F cells

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5
Q

what does the pancreas contain

A

islets of langerhans

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6
Q

how much of the islets of langerhans do alpha and beta cells make up

A

about 85%

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7
Q

what is the majority of the pancreas composed of and what does it do

A

acinar cells that produce digestive enzymes

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8
Q

what is the exocrine portion of the pancreas

A

the acinar cells

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9
Q

what is the endocrine portion of the pancreas

A

islets of langerhans

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10
Q

what is insulin secretion associated with

A

energy abundance

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11
Q

what is insulin made of

A

two amino acid chains connected by disulfide linkages

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12
Q

what happens to insulin when A and B chains are split

A

functional activity of insulin molecule is lost

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13
Q

do proinsulin and C peptide have any insulin activity

A

no

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14
Q

what does insulin circulate bound to

A

nothing

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15
Q

what is the half life of insulin

A

6 mins

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16
Q

where is insulin formed

A

in beta cells

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17
Q

what is the process of insulin formation

A

starts as proinsulin then in the golgi proinsulin is cleaved into c-peptide and insulin

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18
Q

what are incretins

A

hormones produced by the digestive system that stimulate insulin secretion before plasma glucose is elevated

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19
Q

what are examples of incretins

A

GLP-1 and GIP

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20
Q

what is the mechanism of insulin secretion

A

-glucose enters the cell via GLUT 1 and GLUT 2 transporter
- glucose is converted into pyruvate and used to make ATP in the mitochondria
-ATP enters the ATP sensitive K+ channel and closes it which causes depolarization
- this opens VG Ca2+ channels and calcium enters the cell.
-cAMP is signaled and signals secretory granules to excytose insulin and C peptide

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21
Q

what is the sulfonylurea receptor (SUR) (K+ ATP channel)

A

binding site for some drugs that act as insulin secretagogues for treatment of type 2 diabetes

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22
Q

what is the key regulator of insulin secretion

A

glucose levels

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23
Q

what glucose levels stimulate insulin synthesis

A

greater than 3.9 mmol/L

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24
Q

what else besides insulin regulate insulin secretion

A

amino acids, ketones, various nutrients, GI peptides and NTs

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25
Q

in the beginning of insulin secretion what insulin is released

A

pre formed insulin

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26
Q

after 10-20 minutes of insulin secretion what insulin is released

A

pre formed insulin and newly synthesized insulin

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27
Q

what is normal fasting blood glucose

A

80-90 mg/ 100 ml

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28
Q

at what levels of blood glucose does insulin secretion rise

A

above 100 mg/100 ml

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29
Q

what blood glucose is peak secretion of insulin

A

400-600 mg/100 ml

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30
Q

can insulin be secreted past 400-600 mg/ 100 ml of blood glucose

A

no

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31
Q

what is the relationship between glucagon and blood glucose levels

A

glucagon levels decrease as blood glucose levels increase

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32
Q

what type of receptor is the insulin receptor

A

tyrosine kinase linked receptor

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33
Q

what is the FAST target cells response to insulin binding to its receptor

A

increased glucose uptake especially by muscle cells and adipocytes due to translocation of vesicles containing GLUT 4 to the membrane

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34
Q

what does the membrane become more permeable to when insulin binds to its receptor

A

amino acids, potassium and phosphate ions

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35
Q

what is the SLOWER target cells response to insulin binding and how long is this

A

10-15 minutes, change in enzyme activity leading to changes in metabolism

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36
Q

what is the SLOWEST target cells response to insulin binding and how long is this

A

hours-days, changes is gene expression and growth

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37
Q

what happens to insulin when it binds

A

it forms a dimer

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38
Q

what are the results of insulin

A

-glucose transport
- protein synthesis
-fat synthesis
-glycogen synthesis
- growth and gene expression

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39
Q

what are the effects of insulin on muscle

A

-increases glucose uptake and metabolism - anabolic effect
- increases glycogen storage in skeletal muscle
- increases protein synthesis and inhibits protein degradation

40
Q

what is the permeability of resting muscles to glucose

A

slightly permeable

41
Q

what is the relationship between insulin and growth hormone to promote growth

A

synergism

42
Q

what does lack of insulin cause

A

protein depletion and increased plasma amino acids

43
Q

what is the effect of insulin on the liver

A

promotes uptake and storage of glucose as glycogen

44
Q

what is the mechanism of increasing uptake and glucose storage in the liver

A

-increased glycogen synthase leading to glycogen synthesis
- decreased breakdown of glycogen by inhibiting liver phosphorylase
-increases glucose uptake

45
Q

what is the effect of insulin on gluconeogenesis

A

inhibitory

46
Q

what does insulin promote conversion of excess glucose into

A

fatty acids

47
Q

what is the mechanism of insulin promoting fat synthesis and storage

A

-increased glucose transport into liver TG+ lipoprotein released from liver
-activates lipoprotein lipase in the capillary walls of adipose tissue, splitting triglycerides into fatty acids, and absorption into adipocytes

48
Q

what are the essential effects of insulin for fat storage in adipose tissue

A

-inhibits action of hormone sensitive lipase (HSL)
-enhances glucose transport into adipocytes
-alpha glycerol phosphate
- glycerol and fatty acids -> TG

49
Q

what does lipoprotein lipase do

A

brings more lipids into adipocytes

50
Q

what does lack of insulin cause in adipocytes

A

lipolysis and release of FFA and increases plasma cholesterol and phospholipids concentrations

51
Q

what does HSL do

A

exports triglycerides from adipocyte into the blood

52
Q

what are the major target tissues of insulin

A

muscle, liver, adipose tissue

53
Q

what is the effect of insulin on ketoacids in plasma

A

decreased ketoacids

54
Q

what is the effect of insulin on amino acids in plasma

A

decreased

55
Q

what causes increased insulin secretion

A

-increased blood glucose
-increased blood FFAs
-increased blood AAs
- incretins
-glucagon, GH, cortisol which all increase blood glucose
- PNS stimulation, AcH
-Beta adrenergic stimulation
- insulin resistance, obesity,
-sulfonylurea drugs

56
Q

how do incretins work when binding to receptor

A

increase cAMP in beta cell

57
Q

how do sulfonylurea drugs work in beta cell

A

close K ATP channel in beta cell

58
Q

what caused decreased insulin secretion

A
  • decreased blood glucose
  • fasting
  • somatostatin
    -alpha adrenergic activity
    -leptin
59
Q

glucagon is the hormone of “_____”

A

starvation

60
Q

what is the relationship between blood glucose and glucagon

A

inverse

61
Q

what is glucagon secretion stimulated by

A

hypoglycemia, epinephrine (Beta 2), vagus nerve

62
Q

what is the primary target tissue of glucagon

A

liver to increase blood glucose

63
Q

how does glucagon increase blood glucose in the liver

A

-stimulating glycogenolysis and inhibiting glycogen synthesis
- increasing gluconeogenesis
-increases blood fatty acid and ketoacid levels to provide more substrates for gluconeogenesis

64
Q

what are the ketoacids released by the liver

A

acetone, acetoacetate, beta-hydroxybutyrate

65
Q

what is diabetes mellitus

A

metabolic disorder characterized by hyperglycemia due to insufficient insulin or cellular resistance to insulin

66
Q

what is the difference between a normal individual and a DM individual’s blood glucose levels

A

with DM it takes longer to reduce blood glucose levels and glucose levels dont reach the control level

67
Q

which type of diabetes is hypoinsulinemia

A

type 1

68
Q

what are symptoms of DM

A

-polyuria
-polydipsia
-polyphagia
- extreme fatigue
-blurry vision
-cuts/bruises slow to heal
-weight loss (type 1)
-tingling, pain, or numbness in hands and feet (type 2)

69
Q

approximately 25% of patients with type 1 DM initially present with___

A

diabetic ketoacidosis, hyperglycemia greater than 250 fasting blood glucose

70
Q

how is DM diagnosed

A

casual plasma glucose greater than 200 mg/dl and hyperlgycemia symptoms

71
Q

what is fasting plasma glucose in normal individuals vs DM

A

normal- 100
DM- 126

72
Q

what is normal and DM A1C

A

normal- less than 5.6
DM- greater than 6.5

73
Q

what is the pathophyiology of DM type 1

A

-autoimmune destruction of pancreatic beta cells

74
Q

what percentage of diabetes cases are type 1

A

5-10%

75
Q

what are the risk factors for type 1 diabetes

A

-genetic predisposition
-environmental triggers stimulate autoimmune response such as viral infections or chemical toxins

76
Q

when does type 1 onset

A

usually less than 40, non- obese younger patients

77
Q

when does hyperglycemia occur in type 1 DM

A

when 80-90% of cells destroyed

78
Q

what does hyperglycemia in type 1 DM lead to

A

-polyuria
-polydipsia
- polyphagia
-glucosuria
-weight loss
-fatigue
-hyperkalemia due to lack of insulin which normally activates the sodium potassium pump

79
Q

what is diabetic ketacidosis due to

A

increased lipolysis to fatty acids to produce ketoacids

80
Q

what is DKA a response to

A

a cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess such as glucagon, catecholamines, cortisone and GH

81
Q

what is the pathophysiology of DKA

A

-osmotic diuresis and dehydration (hyperglycemia)
- metabolic acidosis (accumulation of ketones)
- fluid and electrolyte imbalances

82
Q

what type of diabetes does DKA occur with

A

type 1

83
Q

what causes DKA

A

-trauma
-stress
-infection
-reduced daily insulin injections

84
Q

what are signs and symptoms of DKA

A

-fruity breath
- nausea/abdominal pain
-dehydration
-tachycardia
-lethargy
-coma
-kussmaul respirations

85
Q

what is the goal of kussmaul respirations

A

blow off CO2 to reverse acidosis

86
Q

what are the three categories of DKA and explain each

A

-mild (pH 7.25-7.3) individual is alert
- moderate (pH 7-7.25) individual is drowsy
- severe (pH less than 7) individual will be in a stupor or coma

87
Q

what does acidosis do to neuronal function and why

A

depresses it because it block inward current of Na+ and Ca2+

88
Q

what is type 2 DM

A

fasting hyperglycemia despite availability of insulin - insulin resistance

89
Q

what are risk factors for type 2 DM

A

-history of diabetes in parents or siblings
- obesity
- physical inactivity
-race/ethnicity
-women
-patients with hypertension

90
Q

what is the pathophysiology of T2DM

A

-hyperinsulinemia due to insulin resistance
-beta cell dysfunction with impaired insulin secretion
-due to down regulation of insulin receptors in target tissues and insulin resistance

91
Q

what occurs in metabolic syndrome

A

-obesity
-insulin resistance
- fasting hyperglycemia
- lipid abnormalities
-hypertension

92
Q

what do individuals with metabolic syndrome have increased risk for

A

CVD (atherosclerosis) and insulin resistance

93
Q

what are complications of both type 1 and type 2 DM

A

-retinopathy
-nephropathy
-neuropathy
- vascular disease
- myopathies

94
Q

what are oral manifestations of DM

A
  • periodontal disease
    -salivary and taste dysfunction
    -oral bacterial and fungal infections
    -oral mucosa lesions
    -diminished salivary flow and burning mouth syndrome
  • delayed mucosal wound healing
    -xerostomia
95
Q

what is the effect of diabetes on periodontal disease and treatment

A

diabetes leads to periodontal disease and vice versa. treatment of periodontal disease may improve glycemic control

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