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Physiology > Insulin & Glucagon > Flashcards

Insulin & Glucagon Flashcards

1
Q

What occurs during the anabolic phase of homeostasis? What is this phase also known as?

A

Synthesis of compounds constituting the body’s structure (e.g. protein and glycogen synthesis)

AKA: Fed state

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2
Q

What is the relationship between caloric intake and demand during the anabolic phase? Is energy stored or mobilized?

A

Caloric intake > demand

energy storage

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3
Q

What occurs during the catabolic phase of homeostasis? When does it occur?

A

Oxidative processes that release energy (e.g. Ox phos and ETC)

4-6 hours after food ingesting; lasts until person eats again

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4
Q

What is the relationship between caloric intake and demand during the catabolic phase? Is energy stored or mobilized?

A

Caloric intake < demand

energy mobilization

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5
Q

What are the endocrine and exocrine products of the pancreas?

A

Endocrine: insulin, glucagon, somatostatin

Exocrine: digestive enzymes and HCO3-

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6
Q

What are endocrine sections of the pancreas called?

A

Islets of Langerhans

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7
Q

Label the cell types of an islet of Langerhans

A
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8
Q

What do α cells secrete?

A

Glucagon

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9
Q

What do β cells secrete?

A

Insulin

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10
Q

What do δ cells secrete?

A

Somatostatin

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11
Q

What are the functions of the A & B chains of insulin?

A

A: species-specific sites

B: biological activity

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12
Q

Where is the C-peptide cleaved from the A and B chains of insulin?

A

Golgi

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13
Q

What is the half-life of insulin? How is it cleared from the body?

A

4-6 minutes

cleared by receptor-mediated endocytosis and lysosomal insulinases

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14
Q

Why do diabetics have to administer themselves more insulin than is needed for metabolism?

A

~50% of insulin in a single pass through the liver

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15
Q

What kind of receptors are insulin receptors? How do they function when insulin binds?

A

Tyrosine kinase-containing receptors

Dimerizes and triggers autophosphorylation of β subunits; phosphorylates cytoplasmic insulin receptor substrate (IRS-1 & IRS-2)

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16
Q

What would cause a downregulation of insulin receptors (3)?

A

Obesity

High carbohydrate intake

Insulin resistance

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17
Q

What would cause an upregulation of insulin receptors (1)?

A

Fasting

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18
Q

What are the two signal transduction pathways that insulin activates? What do they stimulate?

A

Mitogen-activated protein (MAP) kinase pathway: promotes cell growth and DNA synthesis

Phosphatidylinositol-3-kinase pathway: inserts GLUT4 to membranes of skeletal muscle and adipose tissue; stimulates glycogen, lipid, and protein synthesis

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19
Q

How much insulin does an average adult pancreas secrete?

A

~40-50 units/day

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20
Q

What is a normal basal level of insulin secreted daily?

A

10 μU/mL (50% of total daily insulin)

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21
Q

What does “bolus insulin” refer to?

A

Insulin secreted outside of the basal level

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22
Q

Secretion of insulin is biphasic. How do insulin levels change during each phase?

A

Early phase: initial burst of insulin in the first 10 minutes after a meal; fusion of docked granules

Late phase: slower rise of insulin release; mobilization from a reserve pool

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23
Q

What amino acids can stimulate insulin secretion (3)?

A

Alanine

Lysine

Arginine

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24
Q

What is the function of incretins? Where are they secreted from? Example?

A

Amplify glucose-induced insulin release

Secreted from intestines

Ex: gastric inhibitory peptide & GLP-1

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25
Q

Does acetylcholine stimulate or inhibit insulin secretion?

A

Stimulate

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26
Q

Does Epi or NE have a greater inhibitory effect on insulin secretion?

A

Epi

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27
Q

What is the difference between SGLT and GLUT transporters?

A

SGLTs are coupled to sodium and GLUTs are not

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28
Q

How many glucose transporters are encoded in the human genome?

A

14

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29
Q

Where are SGLT1 transporters located?

A

Intestinal and renal epithelium

30
Q

Where are SGLT2 transporters located?

A

Renal epithelium

31
Q

Where are GLUT1 and GLUT3 transporters located? Under what conditions are they active?

A

Located everywhere

Always on

32
Q

Where are GLUT2 transporters located? When are they active?

A

Located on pancreatic β cells and hepatic cells

Only active at high [glucose]; bidirectional transport

33
Q

Where are GLUT4 transporters located? When are they activated?

A

Located on skeletal muscle, heart, and adipose tissue

Activated when insulin binds to its receptor

34
Q

Where are GLUT5 transporters located? What do they transport?

A

Located on the brush border of small intestinal cells (enterocytes)

Transport fructose

35
Q

Explain the cascade of events that occur in a pancreatic β cell that leads to secretion of insulin (4).

A
  1. Glucose enters through GLUT2 and generates ATP
  2. ATP-sensitive K+ channel closes (coupled to sulphonylurea receptor)
  3. Trapped K+ depolarizes membrane and Ca2+ influxes
  4. Insulin secreted
36
Q

Why can administration of sulphonylureas lead to hypoglycemia?

A

Triggers insulin secretion independent of glucose

Inhibits ATP-sensitive K+ channel, leading to depolarization

37
Q

Skeletal muscle, adipose tissue, and the heart are responsible for ___% of the body’s glucose metabolism. Of the three ______ takes up 80%

A

40%

Skeletal muscle

38
Q

What happens to GLUT4 transporters when insulin binds to its receptor?

A

Upregulation of GLUT4

New transporters added to the cell membrane from the Golgi

39
Q

What are the two triggers for diabetic ketoacidosis?

A

Lack of insulin

Increased counterregulatory hormones due to stress

40
Q

How much insulin is necessary to inhibit lipolysis and the generation of ketone bodies?

A

1-2 μU/mL

41
Q

How much insulin is necessary to affect glucose metabolism in the liver and muscle?

A

25-50 μU/mL

42
Q

How much insulin is necessary to stimulate glucose uptake into fat?

A

10 μU/mL

43
Q

How is hyposecretion (diabetes mellitus) characterized (2)?

A

Abolsute relative deficiency of insulin

Absolute relative excess of glucagon

44
Q

What are the major characteristics of hyperglycemia (3)?

A

Polyuria

Polydipsia

Polyphagia

45
Q

Why does hyperglycemia cause polyuria?

A

Excess glucose is greater than glucose renal tubular maximum, which acts as an osmotic diuretic

46
Q

Why does hyperglycemia cause polydipsia?

A

Dehydration occurs due to osmotic diuresis

47
Q

Why does hyperglycemia cause polyphagia?

A

Insulin inhibits feeding, so lack of insulin could increase appetite

Intracellular glucose is low, which signals starvation

48
Q

To be diagnosed with diabetes, someone must meet one of four criteria. What are they?

A

Diabetes symptoms w/ blood glucose of 200 mg/dL

Fasting blood glucose ≥ 126 mg/dL

2-hour oral glucose tolerance test ≥ 200 mg/dL

Hemoglobin A1c ≥ 6.5%

49
Q

What fasting blood glucose is considered pre-diabetic?

A

100-125 mg/dL

50
Q

How many people in the US have diabetes and how many are pre-diabetic?

A

34.2 million with diabetes

88 million pre-diabetic

51
Q

What ethnic groups have the highest rates of diabetes?

A

Pacific Islanders and Native Americans

52
Q

What viruses cause someone to develop type 1 diabetes? (3)

A

Coxsackie B4

Mumps

Rubella

53
Q

Antibodies to what three antigens can lead to type 1 diabetes?

A

Insulin

Glutamic acid decarboxylase

Islet antigen-2

54
Q

What are the symptoms of diabetic ketoacidosis? Does it occur more commonly in type 1 or type 2 diabetes?

A

Type 1

abdominal pain

nausea

vomiting

55
Q

Are sulfonylureas used to treat type 1 or type 2 diabetes? Explain.

A

Type 2

Sulfonylureas trigger insulin secretion, even in the absence of glucose. Type 1 diabetics cannot produce insulin, so sulfonylureas would not work.

56
Q

What are four challenges that increase the risk of type 2 diabetes?

A

Decreased AMP-kinase (AMPk) activity

Increased persistent organic pollutants (POPs)

“Thrifty” genotypes

Increased cortisol

57
Q

What is the function of AMP-kinase?

A

“Metabolic switch”; switches between ATP-consuming processes (ie. GNEO) and ATP-generating processes (ie. lipid oxidation)

58
Q

What two inflammatory proteins are released from adipose tissue in response to them becoming overfat (“angry fat”). What process do they interfere with?

A

Tumor necrosis factor (TNF-α)

IL-6 (from macrophages)

Interfere with insulin-receptor signaling, ultimately leading to type 2 diabetes

59
Q

Based on the graph of the oral glucose tolerance test, which line represents someone with diabetes mellitus?

A
60
Q

What is the function of metformin?

A

Insulin sensitizer

61
Q

What is the key way to prevent diabetes?

A

Weight loss

62
Q

What are some long-term complications of type 2 diabetes (6)?

A

Coronary artery disease

Cerebrovascular disease

Peripheral vascular disease

Retinopathy

Nephropathy

Neuropathy

63
Q

What is the “albatross around your neck” when it comes to treating diabetes? Why?

A

Hypoglycemia

Imbalance between diabetes meds and food intake/activity

Hypoglycemia leads to more hypoglycemia

64
Q

What are the counterregulatory hormones to insulin (5)? Which has the greatest effect (*).

A

Growth Hormone

Cortisol

Epinephrine

Norepinephrine

*Glucagon

65
Q

What are the three major functions of glucagon?

A

**Mobilization of glucose (glycogenolysis and GNEO)

Lipolysis

Ketogenesis

66
Q

What is the insulin/glucagon (I/G) ratio in the fed state vs fasting state?

A

Fed I/G: 30

Fasting I/G: 2

67
Q

What are the major and minor regulators of glucagon secretion (6)?

A

Major:

Hypoglycemia

Minor:

Dietary amino acids

Epinephrine

SNS

Cortisol

Growth hormone

68
Q

What is GLP-1?

A

Glucagon-like peptide-1

In the intestines, alternative processing of proglucagon –> GLP-1

69
Q

What are the signs and symptoms of a glucagonoma (5)?

A

5 D’s

Depression

Diabetes

Declining weight

Deep vein thrombosis

Dermatitis

70
Q

What are the short term and long term treatments for a glucagonoma (2)?

A

Short term: somatostatin analogs (ie. octreotide)

Long term: surgery

Physiology (11 decks)

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