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IDT Spring > Diabetes Lec 1-3 > Flashcards

Diabetes Lec 1-3 Flashcards

1
Q

diabetes mellitus is the most common metabolic disease characterized by?

A

hyperglycemia

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2
Q

T/F 1 in 4 US adults with diabetes don’t know they have it

A

true

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3
Q

what effect does overload of glucose metabolites and end products have due to diabetes?

A

increased oxidative and inflammatory stress, damage epithelial cells, and damage myelin sheaths

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4
Q

define macrovascular disease

A

disease of large blood vessels, including coronary arteries, aorta, and arteries in brain/limbs

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5
Q

define microvascular disease

A

disease involving small blood vessels

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6
Q

what are examples of microvascular diseases and which one is the most common?

A

retinopathy (most common), diabetic kidney disease, peripheral neuropathy, and autonomic neuropathy

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7
Q

what is the goal of comprehensive care?

A

preventing long-term macrovascular and microvascular complications in addition to glycemic control

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8
Q

preprandial (fasting) plasma glucose levels:
normal, prediabetic, and diabetic

A

n: <100
pre: 100-125
diabetes: over 126

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9
Q

peak postprandial (after meal) plasma glucose levels:
normal, prediabetic, and diabetic

A

n: <140
pre: 140-199
diabetes: over 200

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10
Q

Glucose is used for ATP production and building blocks for _______ and substrates for ________

A

biopolymers, glycosylation

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11
Q

A1C levels:
normal, prediabetic, and diabetic

A

n: <5.7%
pre: 5.7-6.5%
diabetic: >6.5%

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12
Q

describe how carbs are broken down into glucose in the small intestine

A

pancreatic a-amylase is secreted into the small intestine to breaks down polysaccharides to glucose
additionally, intestinal a-glucosidase breaks down saccharides to glucose

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13
Q

what are the glucose polymers?
what disaccharides do they breakdown into?
what monosaccharides to disaccharides break down into and via which enzymes?

A

starch and glycogen
maltose, sucrose, and lactose
maltase -> 2 glucose, sucrase -> 1 glucose + 1 fructose, lactase -> 1 glucose + 1 galactose

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14
Q

what are non-pharm ways of helping w/ glycemic control?

A

low-carb diet (not for pts w/ eating disorder or renal disease), and avoid added sugar. a-glucosidase inhibitor (for GI discomfort)

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15
Q

T/F GLUTs require ATP to function

A

false non-energy dependent

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16
Q

describe GLUT1

A

present in all tissue mediating basal glucose uptake

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17
Q

describe GLUT2

A

major transporter in intestinal, hepatic and renal cells with low affinity for glucose

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18
Q

describe GLUT3

A

major transporter on neurons with a high affinity for glucose

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19
Q

describe GLUT4

A

transporter in skeletal muscle and adipose tissue

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20
Q

T/F SGLTs are non-energy-dependent

A

false, they are energy-dependent

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21
Q

where do we find SGLT1? SGLT2?
what is SGLT1s role?

A

in intestinal and renal cells
in renal cells
actively transports glucose from the lumen into small intestine epithelial cells

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22
Q

how does glucose exit small intestine epithelial cells?

A

passive diffusion via GLUT2

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23
Q

glucose reabsorption occurs in the epithelial cells of?

A

the kidneys

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24
Q

SGLT2 transports ____ of glucose from the proximal tubule lumen into the epithelial cell

A

90%

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25
Q

SGLT1 transports ____ of glucose from the proximal tubule lumen into the epithelial cell

A

10%

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26
Q

glucose exits the kidney epithelial cell via passive facilitated diffusion via?

A

GLUT2 and GLUT1

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27
Q

what is the purpose of an SGLT2 inhibitor?

A

used for glycemic control: causes more glucose to be excreted via the urine

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28
Q

describe the different processes of glucose metabolism

A

glycolysis: glucose breakdown into 2 pyruvate molecules.
aerobic respiration: pyruvate breakdown to CO2 in Krebs cycle and oxidative phosphorylation
anaerobic respiration: pyruvate conversion to lactate

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29
Q

describe glycogenesis and glycogenolysis in the liver
When is glycogenesis activated?

A

glycogenesis: glucose is phosphorylated to become G6P, which is converted to G1P, a building block for glycogen synthesis
Activated during rest periods and by insulin in response to high glucose levels
glycogenolysis: glycogen is broken down to G6P to generate glucose for export into the bloodstream

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30
Q

(Liver) increased ____ indicates excessive glucose uptake. which promotes _______ and inhibits ________; glucose inhibits ________

A

G6P, glycogenesis, glycogenolysis, glycogenolysis

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31
Q

describe glycogenesis and glycogenolysis in the skeletal muscle

A

glycogenesis (same as liver): glucose is phosphorylated to become G6P, which is converted to G1P, a building block for glycogen synthesis (occurs at rest)
glycogenolysis: glycogen is broken down to F6P to generate ATP for energy in the skeletal muscle (occurs during exercise)

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32
Q

(Skeletal muscle) increased ___ indicates sufficient energy, which promotes ________ and inhibits ________; ATP inhibits _________

A

G6P, glycogenesis, glycogenolysis, glycogenolysis

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33
Q

describe lipogenesis in the liver (lipid synthesis)

A

glucose enters liver cell via GLUT2 and undergoes glycolysis. pyruvate is oxidized to citrate (start of lipogenesis) and is converted to acetyl-CoA, which is converted into fatty acid. Fatty acids are esterified into triglycerides, which are packaged to form VLDL for adipose tissue to take

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34
Q

describe lipogenesis and lipolysis in the adipose tissue

A

lipogenesis: VLDL and chylomicrons break down to fatty acids to go into adipocytes and convert to triglycerides. glucose also enters adipocytes via GLUT4 and undergoes glycolysis and oxidation to generate fatty acids which become triglycerides
lipolysis: triglycerides become glycerol and fatty acids which enters blood stream.

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35
Q

describe gluconeogenesis (glucose synthesis) in the liver and kidneys
what is it the reverse process of?

A

lactate, glycerol, amino acids, and fatty acids enter liver to help with forming glucose which enters the bloodstream and is taken up by the brain for ATP production
glycolysis

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36
Q

describe ketogenesis in the liver and adipose tissue

A

ketogenesis converts Acetyl-CoA into ketone bodies where they can undergo ketolysis to produce ATP

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37
Q

Glucose Homeostasis: Prandial State
-Nutrient absorption in the GI tract causes an increased circulating glucose level
- Glucose stimulates the release of intestinal hormones and neural stimuli to control pancreatic hormone secretion
- Total body glycolysis increases to generate energy
- The liver, skeletal muscle, and adipose tissue take up glucose for storage via increased glycogenesis and lipogenesis
- The production of glucose, fatty acids, and ketone bodies via glycogenolysis, gluconeogenesis, lipolysis and ketogenesis is decreased

A

.

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38
Q

Glucose Homeostasis: Fasting State
- Absence of nutrient absorption from the GI tract causes a decreased circulating glucose level
- Low glucose level causes the neural stimuli to stop pancreatic hormone secretion
- Glycogenolysis and gluconeogenesis increase in the liver to supply glucose
- Lipolysis and ketogenesis increase in the adipose tissue and liver to generate fatty acids and ketone bodies for energy production
- The storage of glucose via glycogenesis and lipogenesis is decreased
* Glycemic control
- Basal insulin maintaining fasting blood glucose
- Bolus insulin preventing prandial elevation and correcting acute elevation of blood glucose

A

.

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39
Q

Which of the following does not increase blood glucose? (the rest do)
a. absorption/reabsorption
b. glycolysis
c. glycogenolysis (liver)
d. gluconeogenesis

A

b

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40
Q

Which of the following does not decrease blood glucose? (the rest do)
a. glycolysis
b. glycogenesis
c. glycogenolysis (liver)
d. lipogenesis

A

c

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41
Q

what are islets of langerhans?

A

groups of pancreatic cells secreting insulin and glucagon which consists of A cells (glucagon) , B cells (insulin and amylin) , Delta cells (somatostatin) , PP cells (pancreatic peptide), and epsilon cells (ghrelin)

42
Q

Glucagon stimulates ______ and _______ secretion
Insulin inhibits ______ secretion
Somatostatin inhibits _______, _____, and __________ secretion
Ghrelin inhibits _______ and _____ secretion
Pancreatic polypeptide inhibits ______ secretion

A

insulin, somatostatin
glucagon
glucagon, insulin, pancreatic polypeptide
glucagon, insulin
glucagon

43
Q

Pancreatic hyperglycemic factor:
-proglucagon is cleaved to generate _________ in alpha (A) cells
-glucose _____ glucagon production by stimulating _____ and _____ secretion
-fatty acids _______ glucagon production
-amino acids ________ glucagon production
-neurotransmitters ______ glucagon secretion in response to hypoglycemia
-

A

glucagon
inhibits, insulin, somatostatin
inhibit
stimulate
stimulate

44
Q

what is the mechanism of action of glucagon?

A

regulates energy delivery during the fasting state. Glucagon binds to G-protein coupled receptors on hepatocytes and increases cAMP production to to increase blood glucose levels by:
stimulating glycogenolysis
-activating gluconeogenesis

also increases blood ketone body level by limiting lipogenesis and activating ketogenesis

45
Q

how does glucagon activation effect the heart and gut?

A

increases heart rate and force of contraction while relaxing gut smooth muscle

46
Q

what are the different ways that glucagon-like peptide 1 (GLP-1) is produced?

A

-proglucagon cleaved to generate GLP-1 and GLP-2
-glucose and fatty acids stimulate GLP production
-parasympathetic stimulation in response to food consumption promotes GLP production

47
Q

GLP-1 targets the ______, whereas GLP-2 targets the ________ and _______

A

pancreas, GI tract, brain

48
Q

what is the mechanism of action of GLP-1?

A

regulates postprandial blood glucose levels with the pancreas as the major target organ. it binds to G protein-coupled receptor and increases cAMP production which increases intracellular calcium to decrease blood glucose levels by:
stimulating glucose-dependent insulin and somatostatin secretion to inhibit glucagon production
-inhibit gastric emptying and gastric acid secretion

49
Q

what enzyme inactivates GLP-1?

A

Dipeptidyl peptidase 4 (DPP-4)

50
Q

what drug classes do we use to increase the effects of GLP-1?

A

GLP-1 agonists and DPP-4 inhibitors

51
Q

what is the mechanism of action of glucose-dependent insulinotropic polypeptide (GIP)?

A

regulates postprandial blood glucose level with the pancreas as the major target organ. GIP binds to G protein-coupled receptors to increase cAMP production to increase intracellular calcium to decrease blood glucose levels by:
-stimulating glucose-dependent insulin secretion to inhibit glucagon production
-prevent beta cell apoptosis and stimulate beta cell growth
-promote adipocyte differentiation and lipogenesis

52
Q

what enzyme inactivates GIP?

A

DPP-4

53
Q

Amylin is produced and stored with insulin in the ________ cells

A

Beta

54
Q

________ stimulates Amylin production

A

Glucose

55
Q

T/F factors affecting insulin production also affect Amylin production

A

True

56
Q

What is Amylins mechanism of action?

A

-regulate appetite during prandial state by binding to G protein-coupled receptor and increases cAMP production
-decrease blood glucose levels by inhibiting glucagon production
-inhibit gastric emptying and intestinal motility, and improve satiety

57
Q

Somatostatin is produced by ______ cells and endocrine cells

A

Delta

58
Q

What factors stimulate somatostatin secretion?

A

Glucose, glucagon, and GLP-1

59
Q

What are the 2 ways somatostatin regulates blood glucose levels?

A

Inhibits glucagon production via somatostatin receptor 2 (SSTR2) on ALPHA cells
Inhibits insulin production via SSTR5 on BETA cells

60
Q

Somatostatin inhibits pancreatic secretion, gastric emptying, and gastric acid secretion

A
61
Q

Pancreatic polypeptide is produced by?

A

PP (F) cells

62
Q

Pancreatic polypeptides regulate ________ during the _______ state

A

Digestion, prandial

63
Q

Mechanism of pancreatic polypeptides?

A

Bind to G protein-coupled receptors and increase cAMP production and regulates pancreatic secretions and gall bladder contraction

64
Q

Ghrelin is stimulated by ______ and is produced by _______ and ________ cells

A

Fasting, epsilon, endocrine

65
Q

Mechanism of ghrelin?

A

Regulate food intake by binding to G protein-coupled receptors to increase cAMP. Also induce gastric emptying and gastric acid secretion, and increase appetite

66
Q

Of the following, select all that cause a decrease in blood glucose
A. Glucagon
B. Glucagon-like peptide 1 (GLP-1)
C. Amylin
D. Ghrelin
E. Somatostatin
F. Insulin
G. GIP

A

B, C, F, G

67
Q

Of the following, which one increases blood glucose?
A. Pancreatic polypeptides
B. Ghrelin
C. Glucagon
D. GIP
E. GLP-1

A

C

68
Q

insulin is produced by the pancreas; what is another term for describing insulin and what cells in the pancreas produce it?

A

pancreatic hypoglycemic factor
beta cells

69
Q

Proinsulin is formed in the pancreas and is made up of?
How does it form into insulin?

A

single-chain polypeptides A, B, and C
A and B are cross-linked to generate insulin, leaving a residual C-peptide

70
Q

T/F proinsulin does not lower blood glucose levels until it is cross-linked and cleaved into insulin

A

False, it has mild hypoglycemic action

71
Q

what processes does BASAL insulin inhibit? when is/isn’t basal insulin released?
what is the purpose of BOLUS insulin?

A

glycogenolysis, gluconeogenesis, and ketogenesis

during the bodies’ fasting state, it stops after dietary glucose from meals
to decrease blood glucose levels after meals

72
Q

after bolus insulin secretion, glucose enters the beta cell via ______ and undergoes ______ and __________________ to generate ATP

A

GLUT2, glycolysis, oxidative phosphorylation

73
Q

how is the ATP generated by glucose used in the pancreas to cause insulin secretion?

A

ATP-dependent K channels close to cause cell depolarization via sodium entering cell. Sodium triggers voltage-gated Ca channels to open and increase intracellular Ca release. This causes insulin to be released into the plasma which is facilitated by cAMP

74
Q

what drug class involving targeting potassium channels would effect insulin secretion?
what precautions should be taken if using this type of drug?

A

K channel blockers: a drug that inhibits K channel will increase insulin secretion into bloodstream

avoid fasting, prolonged exercise, and alcohol consumption

75
Q

what drug class involving targeting cAMP would effect insulin secretion?

A

any drug class that increases cAMP

76
Q

what is the significance of insulin binding to tyrosine kinase receptors?

A

it causes receptor autophosphorylation which phosphorylates downstream intracellular proteins. It activates PI3 kinase to activate AKT which drives the movement of GLUT4 containing vesicles to the cell membrane for glucose transport into the cell

77
Q

what receptor does Foxo1 inhibit to prevent expression of enzymes involved in glucose and fatty acid metabolism? how does insulin play a role in this pathway?

A

peroxisome proliferator-activated receptor (PPAR)

insulin activates AKT which inhibits Foxo1 in order to allow gene expression for cell growth and division

78
Q

what drug class targeting PPAR would be used to help with glycemic control?
what exactly does it do?
adverse reactions?

A

PPARy agonist
increase insulin sensitivity
edema, heart failure

79
Q

which organ is reached first after insulin secretion?

A

the liver

80
Q

The roles of insulin in the liver include:
-induce insertion of additional ______ into cell membrane to facilitate glucose transport
-promote glycogenesis and inhibit _________
-promote glycolysis and inhibit ___________
-promote lipogenesis and inhibit __________________
-promote protein synthesis and inhibit _____________

A

GLUT2
glycogenolysis
gluconeogenesis
fatty acid oxidation/ketogenesis
protein degradation

81
Q

____________ is the main site of insulin-mediated glucose disposal

A

skeletal muscle

82
Q

** insulin has a similar role in skeletal muscle as it does in the liver. it also promotes amino acid transport and induces translocation of ________ into the cell rather than GLUT2 as in the liver

A

GLUT4

83
Q

__________ is the third major insulin-sensitive tissue involved in the regulation of body fuel

A

adipose tissue

84
Q

AMP-activated protein kinase (AMPK) has what function in the liver? skeletal muscle?
It also increases the _____ sensitivity of cells

A

liver: promotes fatty acid oxidation while inhibiting gluconeogenesis and lipogenesis
skeletal: promotes glucose uptake and fatty acid oxidation while inhibiting protein synthesis

insulin

85
Q

decreased ____ and increased ____ levels activates AMPK, which activates _______ pathways and inhibits _______ pathways

A

ATP, AMP, catabolic, synthetic

86
Q

type 1 diabetes usually presents in childhood and results from autoimmune destruction of ___________

A

pancreatic beta cells

87
Q

in type 1 diabetes beta cells do not produce ______ , whereas alpha cells have increased _______ production

A

insulin, glucagon

88
Q

why are patients with type 1 diabetes at a higher risk of diabetic ketoacidosis?

A

fatty acids are used for energy production and ketogenesis since your body can not transport glucose into cells

89
Q

what test can be used for type 1 diabetics to determine if they’re still producing insulin?

A

C-peptide test

90
Q

describe type 2 diabetes
what happens to beta cells?

A

usually occurs in adulthood and results from insulin deficiency and insulin resistance
beta cells insulin secretory capacity decreases over time

91
Q

which antigen is seen in type 1 diabetics but not in type 2?

A

human lymphocyte antigen

92
Q

T/F beta cell destruction does not initially occur in type 2 diabetes

A

true

93
Q

define gestational diabetes
-what can occur in early pregnancy?
-what can occur as pregnancy progresses?
-what can occur in late pregnancy?
-how do we treat it?

A

type of diabetes that results from glucose intolerance during pregnancy
-placental hormones can increase lipogenesis and beta cell proliferation
-placental hormones can increase lipolysis and insulin resistance, but inhibit glycogenesis
-in late pregnancy, glucose levels elevate and if the body can’t compensate with increased insulin secretion it can cause hyperglycemia and gestational diabetes
-manage symptoms with lifestyle modifications and insulin

94
Q

identify 2 placental hormones which increase the risk of gestational diabetes:
A. Leptin
B. TNFb
C. Prolactin
D. Estrogen/Progesterone

A

A and D

95
Q

identify 2 placental hormones which increase the risk of gestational diabetes:
A. Adiponectin
B. Lactogen
C. TNFa
D. PFK2

A

B and C

96
Q

identify 2 placental hormones which increase the risk of gestational diabetes:
A. TNFb
B. Growth hormone
C. Ceterone
D. Corticosterone

A

B and D

97
Q

T/F monogenic diabetes is an inherited type of diabetes

A

true

98
Q

T/F maturity-onset diabetes of the young is caused by an autosomal recessive gene mutation (MODY)

MODY2 results from an abnormal _________ enzyme

A

false, an autosomal dominant gene mutation

glucokinase

99
Q

how do monogenic and MODY diabetes effect someone?

A

they cause limited glucose-stimulated insulin secretion but not insulin resistance

100
Q

secondary diabetes is caused by complications of certain conditions, what are examples of how secondary diabetes occurs?

A

-disease of pancreas, such as pancreatitis
-drugs that damage beta cells, interfere with insulin release, induce insulin resistance, impact glucose metabolism or cause autoimmunity
-infections that damage beta cells, such as mumps
-ethanol that is toxic to pancreas: chronic alcoholic pancreatitis

101
Q

GLP-1, voltage-gated Ca channel, cAMP, PPARy, and AMPK promote or inhibit the actions of insulin secretion?

A

promote

102
Q

a-glucosidase, SGLT-2, DPP-4, and ATP-dependent K channel promote or inhibit the actions of insulin secretion?

A

inhibit

IDT Spring (22 decks)

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