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Renal and Endocrine Biology > REB 8. Insulin > Flashcards

REB 8. Insulin Flashcards

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1
Q

What is the major characteristic of Diabetes Mellitus?

A

elevated fasting blood glucose levels - hyperglycaemia

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2
Q

What are the 3 types of Diabetes Mellitus?

A

[1] Type I - insulin deficiency
[2] Type II - insulin resistance (around 95%)
[3] Gestational Diabetes - 5% of all pregnancies

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3
Q

If Diabetes Mellitus is unmanaged overtime, what can it lead to?

A 
[1] Nerve Damage (Neuropathy)
[2] Renal Failure (Nephropathy)
[3] Heart Attacks
[4] Blindness (Retinopathy)
[5] Strokes
[6] Vascular Damage (Macroangiopathy) - leads to amputation
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4
Q

Where is insulin secreted? What is its primary function and what are its major targets?

A
  • secreted by beta cells of islet of Langerhans in pancreas
  • primary function is to facilitate uptake of glucose into body cells
  • adipose tissue and skeletal muscle are major targets of insulin
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5
Q

Which cells do not require insulin for glucose uptake?

A
  • brain cells
  • liver cells
  • kidney cells
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6
Q

What are the 3 major cell types in the Islets of Langerhans? Which one is the most prevalent?

A

[1] alpha cells - 20%
- secrete glucagon

[2] beta cells - 75%
- produce insulin

[3] gamma cells - 5%
- secrete somatostatin

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7
Q

What are some characteristics of the Islets of Langerhans?

A
  • 1 to 3 million islets per adult pancreas (1 to 2% of mass)
  • highly vascularized (allows secreted hormone good access to circulation)
  • innervated by sympathetic and parasympathetic neurons
  • nervous signals modulate secretion of insulin + glucagon
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8
Q

What are the functions of Somatostatin on the gastrointestinal system and anterior pituitary gland?

A

Gastrointestinal System:

  • suppresses release of insulin + glucagon (pancreatic hormones)
  • suppresses release of gastrin, cholecystokinin (gastrointestinal hormones)

Anterior Pituitary:
- inhibits the release of growth hormone (GH) and thyroid stimulating hormone (TSH)

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9
Q

What is the function of glucagon?

A

it opposes role of insulin and raises glucose levels - by enhancing gluconeogenesis and glycogenolysis

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10
Q

How is insulin synthesized/coded for? List the steps

A

[1] synthesized in beta cells

[2] mRNA translated as single chain precursor - Preproinsulin

[3] removal of the signal peptid by endopeptidases in the rough endoplasmic reticulum

[4] proinsulin has 3 domains:

(a) amino-terminal B chain
(b) carboxy-terminal A chain
(c) connecting peptide or C peptide (it is cleaved off - no physiological function)

[5] mature insulin has 2 unbranched peptide chains - linked by 2 disulphides

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11
Q

What are the 3 prohormone convertase enzymes involved in insulin processing?

A

[1] PC2
[2] PC3
[3] Carboxypeptidase E

then, insulin + C-peptide are packaged into golgi into secretory granules

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12
Q

What are the steps/procedure for insulin release?

A

[1] Glucose enters the cells through GLUT2 transporter

[2] Glucose is metabolized by the glucokinase enzyme (glucose to glucose-6-phosphate)

[3] this generates ATP (the ATP/ADP ratio increases)

[4] the increased ATP leads for the closure of ATP-sensitive K+ channels

[5] there is a decreased K+ efflux (potassium stays in cell) and this depolarises cell membrane

[6] there is the opening voltage-sensitive Ca2+ channel and the calcium ions enter the cells

[7] the increased intracellular calcium ions triggers the release of insulin-containing secretory granules
- insulin is released!

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13
Q

What may be a possible cause of hypoglycaemia? (general answer)

A

hyperinsulinism - high insulin levels

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14
Q

What are some causes of hypoglycaemia from excess endogenous insulin production/secretion?

A

[1] Insulinomas
- insulin secreting pancreatic tumours
[2] Congenital Hyperinsulinism
- genetic defects

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15
Q

What are some causes of hypoglycaemia that is not from endogenous insulin (from an external source)?

A

[1] Drug-Induced Hyperinsulinism (e.g. Sulfonylurea type 2DM treatment)

[2] Hypoglycaemia due to exogenous (injected) insulin

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16
Q

What are the 2 main forms of congenital hyperinsulinism?

A

[1] Transient Neonatal Hyperinsulinism

  • may be due to premature births
  • usually resolves itself in a few days or months

[2] Focal or Diffuse Hyperinsulinism

  • due to genetic defects
  • there are 3 types of this form of hyperinsulinism all dependent on a genetic mutation
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17
Q

What are the 3 types of genetic mutations that may occur leading to focal/diffuse hyperinsulinism?

A

[1] KATP channel disorders (mutations SUR1 Kir6.2 proteins in channel results in inappropriate insulin secretion)

[2] Glucokinase gain-of-function mutation (the “glucose-sensing enzyme” instructs the beta-cell to secrete insulin when there is a lower blood glucose than normal)

[3] Hyperammonaemic Hyperinsulinism (HI/HA) gain of function mutation glutamate dehydrogenase

  • beta cells secrete insulin when an increase ATP/ADP ratio triggers amino acid breakdown + formation of alpha-ketoglutarate
  • more insulin is secreted
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18
Q

What are some regulators of insulin release? (first name the 3 main categories)

A

[1] Nutrients

  • Glucose
  • Amino Acids (leucine, isoleucine, alanine + arganine)

[2] Paracrine Hormones

  • Glucagon
  • Somatostatin

[3] Gastrointestinal Hormones (Incretins)

  • Gastric Inhibitory Polypeptide (GIP)
  • Glucagon Like Peptide (GLP)
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19
Q

What are incretins?

A

Incretins are hormones produced in the small intestine during a meal that enter the vasculature and trigger insulin release by pancreatic beta cells

20
Q

Where is glucagon synthesized? [3]

A 
[1] Pancreas 
- Pancreatic Alpha Cells
[2] Intestine
- Intestinal Neuroendocrine L-Cells 
[3] Brain
21
Q

When is glucagon secreted? What triggers glucagon to be secreted?

A

[1] Low Blood Glucose
[2] Low Insulin - low insulin means low blood glucose
[3] Rise in Amino Acids after a protein meal (stimualates glucagon)
[4] adrenaline + noradrenaline

22
Q

What is the function of glucagon? What does it do?

A

[1] activation of hepatic glycogenolysis
- breakdown of glycogen

[2] activation of hepatic gluconeogenesis
- glucose is created

23
Q

What is the precursor for glucagon (which undergoes tissue-specific post-translational processing)?

A

Proglucagon

24
Q

Proglucagon is converted into what in the pancreatic alpha-cells?

A

[1] Glucagon
[2] Glicentin-Related Pancreatic Peptide
[3] MPF

25
Q

Proglucagon is converted into what in the intestinal neuroendocrine L-cells?

A

[1] Glucagon Like Peptide-I (GLP I)
[2] GLP II (biologically inactive)
[3] Glicentin

26
Q

What are the functions of Glucagon Like Peptide I?

A
  • potent stimulator of insulin secretion
  • stimulates somatostatin release for delta-cells of pancreas
  • inhibits glucagon from alpha cells
27
Q

What are the functions of Glicentin?

A
  • stimulator of insulin secretion
  • inhibits gastric acid secretion
  • regulates gut motility
28
Q 
What are the...
[1] Rapid
[2] Intermediate
[3] Delayed
principal actions of insulin?
A

[1] increases transport of glucose, amino acids and K+ into insulin-sensitive cells

[2]

  • stimulates entry of amino acids + protein synthesis
  • inhibits protein degradation
  • activates glycolysis + glyocogen synthesis
  • inhibits glycogenolysis + glucose-Genica enzymes

[3] increase in mRNAs for lipogenic + other enzymes

29
Q

What is the receptor type for insulin receptors? How many subunits are they made up of? Explain the characteristics of the subunits.

A 
Receptor Type: Tyrosine Kinase
It has 2 subunits:
[1] Alpha Subunit
- extracellular part
- contains the insulin-binding domain

[2] Beta Subunit

  • transmembrane domain
  • ATP Binding + Tyrosine Kinase Domains

*note: they are bonded by disulfides bonds

30
Q

What bond is between the alpha and beta subunit in the insulin receptor?

A

A disulfide bond

31
Q

When insulin binds to the insulin receptor what happens?

A

[1] autophosphorylation of the tyrosine on the beta subunits

[2] the activated receptor phosphorylates intracelullar proteins (e.g. IRS-1)

[3] signal pathways are activated
- has an influence on gene expression, metabolism and growth

[4] insulin then degraded by lysosomes

32
Q

What is the mechanism by which insulin facilitates glucose entry into both muscle and adipose tissue?

A

[1] after the insulin binds to the receptors, this causes the fusion of vesicles with the plasma membrane

[2] the fusion of vesicles then allows for the insertion of glucose transporters (GLUT4)

[3] when receptors are no longer occupied, they are recycled back into the cytoplasm

33
Q

Which glucose receptors are required for the brain and liver?

A

TRICK QUESTION
the brain and liver do not require insulin for glucose uptake
- they use a non insulin-dependent transporter (GLUT2 + GLUT3)

34
Q

Which glucose transporter is responsive to insulin and is in adipose tissue and striated muscle (skeletal + heart)

A

GLUT4

35
Q

What type of tissue are the GLUT4 receptors in?

A

[1] adipose tissue

[2] striated muscle (skeletal + heart)

36
Q

How is circulating insulin broken down? What is the half-life for insulin?

A
  • insulinase in the liver and kidneys break down circulating insulin
  • the half life of insulin is 4 to 6 minutes
    (degradation ensures that the insulin level is modulated)
37
Q

What are some disorders due to hypoglycaemia (excess insulin)?

A

[1] Insulinoma

[2] Persistent Hyperinsulinaemia and Hypoglycaemia in Infancy

  • ATP-sensitive K+ channels on beta cells are closed
  • glucokinase/glutamate dehydrogenase (gain of function mutation)
38
Q

What is a disorder of hyperglycaemia/insufficient insulin?

A

Diabetes Mellitus

39
Q

What are the 3 types of diabetes mellitus?

A

[1] Type I Diabetes

  • beta cell destruction (mostly immune mediated)
  • absolute insulin deficiency
  • onset most common in childhood and early adulthood

[2] Type II Diabetes

  • most common type (95%)
  • various degree of beta cell dysfunction and insulin resistance
  • associated with obesity and overweight

[3] Gestational Diabetes Mellitus

  • transient condition associated with pregnancy
  • can increase risk of mother developing type II
40
Q

Compare the times of onset between Type I and Type II diabetes.

A

Type I diabetes has a rapid onset.

Type II has a slow onset.

41
Q

What are the classical symptoms of Type I diabetes?

A 
[1] increased thirst (polydipsia)
[2] increased urination (polyuria)
[3] glycosuria
[4] weight loss with increased appetite
[5] fatigue 
[6] nausea 
[7] vomiting 
[8] diabetes ketoacidosis
42
Q

What are the classical symptoms of type II diabetes?

A 
[1] increased thirst (polydipsia)
[2] increased urination (polyuria)
[3] glycosuria 
[4] increased appetite 
[5] fatigue
[6] blurred vision
[7] slow-healing infections
[8] impotence in men
43
Q

What is diabetes ketoacidosis and how can it result?

A

Diabetes Ketoacidosis: uncontrolled diabetes may result in ketoacidosis (diabetic coma)

Steps:

  • when body cannot make insulin, the body cannot use glucose and breaks down fats for energy
  • when fats are broken down, ketones are produced in liver
  • if levels of ketones cannot be excreted in urine, they build up in blood which can lead to ketoacidosis
44
Q

What are the symptoms of ketoacidosis?

A
  • shortness of breath
  • breath that smells sweet
  • nausea and comforting
  • very dry mouth
45
Q

Why is plasma glucose concentration increased in diabetes Mellitus?

A
  • insulin regulates uptake of glucose
  • without insulin, glucose cannot be transported into the cells (the body interprets this as a lack of glucose)
  • gluconeogenesis, glycogenolysis and lipolysis resulting in increased blood glucose
46
Q

Why do patients with diabetes Mellitus have glycosuria?

A
  • normally, 100% of the glucose that is filtered is reabsorbed
    (glucose reabsorption involved transport proteins)
  • in hyperglycaemic people, the filtered glucose can exceed the capacity that the kidney tubules can reabsorb glucose (this is because the transport proteins become saturated)
  • result is glucose in urine
  • glucose draws water in the urine by osmosis
  • so hyperglycaemia causes a diabetic to produce a high volume of glucose-containing urine (polyuria)

Renal and Endocrine Biology (25 decks)

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