Diabetes 1 Flashcards

1
Q

main use of glucose is as

A

brain fuel

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2
Q

brain accounts for
__ % of body weight
__% of basal metabolic rate
__% of whole-body glucose utilization

A

Brain accounts for:
2.5% of body weight
**25% **of basal metabolic rate
50% of whole-body glucose utilization

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3
Q

__ cannot synthesize or store glucose

A

brain cannot synthesize or store glucose

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4
Q

where does brain get glucose?

A

it gets a continuous supply from circulation

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5
Q

to maintain blood glucose concentration, we must coordinate glucose __ into circulation and __ out of circulation and into __

A

to maintain blood glucose concentration, we must coordinate glucose influx into circulation and efflux out of circulation and into tissues

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6
Q

3 sources of glucose

A
  1. intestinal absorption
  2. glycogenolysis
  3. gluconeogenesis
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7
Q

glycogenolysis

A

glycogen to glucose

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8
Q

gluconeogenesis

A

synthesis of glucose from non-carb sources

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9
Q

glucose metabolism pathway steps

A
  1. Glucose is phosphorylated and trapped in the cell
  2. Becomes glycogen
  3. Can become pyruvate (glycolysis) and then lactate, alanine, acetyl-Coa
  4. acetyl-Coa can make ketones, citrate, fatty acids (then stored as triglycerides)
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10
Q

3 types of cells in Islet of Langerhans (and what they secrete)

A

Beta-cell → insulin (70%)
Alpha-cell → glucagon (20%)
Delta and PP cells (10%)

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11
Q

hormone most active during:
absorptive state
postabsorptive state

A

hormone most active during:
absorptive state: insulin
postabsorptive state: glucagon

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12
Q

insulin site of action

A

liver
adipose
muscle

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13
Q

glucagon site of action

A

mainly liver

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14
Q

insulin
blood glucose conc
blood fatty acid conc
glycogen synthesis
glycogenolysis
gluconeogenesis

A

insulin
↓ blood glucose conc
↓ blood fatty acid conc
↑ glycogen synthesis
↓ glycogenolysis
↓ gluconeogenesis

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15
Q

glucagon
blood glucose conc
blood fatty acid conc
glycogen synthesis
glycogenolysis
gluconeogenesis

A

glucagon
↑ blood glucose conc
↑ blood fatty acid conc
↓ glycogen synthesis
↑ glycogenolysis
↑ gluconeogenesis

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16
Q

target tissues of insulin

A

liver
adipose
muscle

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17
Q

insulin __ blood glucose conc

A

insulin decreases blood glucose conc

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18
Q

insulin action

glucose uptake into tissues
glycolysis
glycogen synthesis
glycogenolysis (liver)
gluconeogenesis (liver & kidney)

A

increases glucose uptake into tissues
stimulates glycolysis
stimulates glycogen synthesis
inhibits glycogenolysis (liver)
inhibits gluconeogenesis (liver & kidney)

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19
Q

insulin
decreases __ concentration
reduces __ output
promotes __ deposition and __ lipolysis
increases __ synthesis and inhibits __ breakdown

A

insulin
decreases blood glucose concentration
reduces hepatic glucose output
promotes fat deposition and inhibits lipolysis
increases protein synthesis and inhibits protein breakdown

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20
Q

insulin action on the liver
main role is to inhibit

A

insulin action on the liver
main role is to inhibit glycogenolysis and gluconeogenesis

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21
Q

indirect effects of insulin on liver
decrease __ flux to liver
decrease __ secretion

A

indirect effects of insulin on liver
decrease free fatty acid flux to liver
decrease glucagon secretion

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22
Q

insulin action on adipose
less __ to be used to produce __

A

insulin action on adipose
less FA to be used to produce ketone bodies

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23
Q

what is the incretin effect?

A

More insulin is secreted in response to an oral glucose load than to a matched IV glucose load

24
Q

the incretin effect is mediated by __ and __

A

the incretin effect is mediated by GLP-1 and GIP

25
Q

GLP-1 is secreted by __ cells
GIP is secreted by __ cells

A

GLP-1 is secreted by L cells
GIP is secreted by K cells

26
Q

purpose of glucose counterregulation

A

prevent hypoglycemia to preserve brain function

27
Q

glucose counterregulation steps

A
  1. Insulin levels decrease (blood glucose 80-85)
  2. Glucagon is secreted (blood glucose 65-70)
  3. Epinephrine is secreted (blood glucose 65-70)
  4. Cortisol & growth hormone (blood glucose 65-70)
  5. Behavioral defense (blood glucose 50-55)
28
Q

sources of glucose during fasting

A
  1. free glucose (extracellular fluid (ECF) and liver)
29
Q

during prolonged fasting
__ becomes sole source of glucose
__ broken down to AAs to be used for __
glucose utilization by __ and __ ceases
glucose utilization by __ declines by half
__ levels rise; brain uses __ for fuel at high concentrations

A

during prolonged fasting
gluconeogenesis becomes sole source of glucose
muscle protein broken down to AAs to be used for gluconeogenesis
glucose utilization by muscle and fat ceases
glucose utilization by brain declines by half
ketone levels rise; brain uses ketones for fuel at high concentrations

30
Q

3 counterregulatory hormones

A

glucagon
epinephrine
cortisol and GH

31
Q

glucagon secretion is stimulated by decrease in __ levels (__ effect)

A

glucagon secretion is stimulated by decrease in pancreatic islet insulin levels (paracrine effect)

32
Q

glucagon is secondarily stimulated by increased __ input

A

glucagon is secondarily stimulated by increased sympathetic input

33
Q

glucagon primarily acts on __ and causes increased __ and __

A

glucagon primarily acts on liver and causes increased glycogenolysis and gluconeogenesis

34
Q

when is epinephrine critical?

A

when glucagon is deficient

35
Q

epinephrine is secreted from __ in response to __ signaling

A

epinephrine is secreted from adrenal medulla in response to CNS signaling

36
Q

epinephrine stimulate __ and __ gluconeogenesis
stimulates __ glycogenolysis

A

epinephrine stimulate hepatic and renal gluconeogenesis
stimulates hepatic glycogenolysis

37
Q

epinephrine reduces glucose uptake by __ and __

A

epinephrine reduces glucose uptake by muscle and fat

38
Q

epinephrine stimulates __ and limits __ from pancreatic islets

A

epinephrine stimulates glucagon and limits insulin from pancreatic islets

39
Q

cortisol and GH promote __ and reduce __ glucose utilization

A

cortisol and GH promote gluconeogenesis and reduce peripheral glucose utilization

40
Q

which counterregulatory hormones are not critical?

A

cortisol and GH

41
Q

gluconeogenesis
require __ (from liver and kidneys)
__ do 10-20% of glucose production

A

gluconeogenesis
require G6Pase (from liver and kidneys)
kidneys do 10-20% of glucose production

42
Q

renal glucose production is regulated by __ and __, but NOT __

A

renal glucose production is regulated by insulin and epinephrine, but NOT glucagon

43
Q

what is the primary glucose counterregulatory hormone?

A

glucagon

44
Q

diabetes prevalence in US

A

13%

45
Q

diabetes is leading cause of __ in US
diabetes increases risk of __ and __

A

diabetes is leading cause of blindness in US
diabetes increases risk of CVD and death

46
Q

diagnosing diabetes
fasting plasma glucose __ OR
2-hour plasma glucose __ during a __ oral glucose tolerance test OR
random plasma glucose __ with symtpoms of hyperglycemia OR
HbA1c __

A

diagnosing diabetes
fasting plasma glucose ** ≥126 mg/dl ** OR
2-hour plasma glucose ** ≥200 mg/dl** during a 75G oral glucose tolerance test OR
random plasma glucose ≥200 mg/dl with symtpoms of hyperglycemia OR
HbA1c ≥ 6.5%

47
Q

HbA1c reflects

A

Hemoglobin A1c reflects the average blood glucose concentration over a 2-3 month period.

48
Q

HbA1c is used to

A
  1. diagnose diabetes
  2. monitor blood glucose control in patients with diabetes
49
Q

HbA1c measures

A

glycated hemoglobin

50
Q

what is glycated hemoglobin

A

hemoglobin with glucose irreversibly attached

51
Q

type 1 diabetes

A

an autoimmune process in which β-cells are destroyed, resulting in absolute insulin deficiency (~5-10% of diabetes cases)

52
Q

type 2 diabetes

A

characterized by insulin resistance and β-cell dysfunction, resulting in relative insulin deficiency (~90% of diabetes cases)

53
Q

people with type 1 diabetes have no

A

beta cells

54
Q

ominous octet of hyperglycemia

A
  1. decreased insulin secretion
  2. decreased incretin effect
  3. decreased glucose uptake
  4. increased HGP
  5. increased glucagon secretion
  6. increased lipolysis
  7. increased glucose reabsorption
  8. NT dysfunction
55
Q

type 1 diabetes
age at onset
weight
family history
autoantibodies (present?)
insulin requiring
insulin sensitivity
rise of DKA

A

type 1 diabetes
age at onset: any, but majorty < 25
weight: typically lean but can be overweight
family history: infrequent (may be family history of autoimmune disease
autoantibodies (present?): present
insulin requiring: yes
insulin sensitivity: normal
rise of DKA: high

56
Q

type 2 diabetes
age at onset
weight
family history
autoantibodies (present?)
insulin requiring
insulin sensitivity
rise of DKA

A

type 2 diabetes
age at onset: any, but majority >25
weight: >80% overweight/obese
family history: frequent
autoantibodies (present?): absent
insulin requiring: variable
insulin sensitivity: decreased
rise of DKA: low