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NUTR3360 > Quiz 3- module 6 part 1 > Flashcards

Quiz 3- module 6 part 1 Flashcards

1
Q

T/F: in T2D late stages, individuals have high glucose and high insulin levels when in a fasted state.

A

False, they have LOW insulin levels because the pancreas has fatigued

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2
Q

In the insulin-resistant stage of an individual with T2D, glucose levels are _______ and insulin levels are _____ in a fasted state. (low, high or normal)

A

normal, high.

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3
Q

What is the HOMA model used to estimate?
there are 2 diff subtypes, say what specific thing each estimates

A

Insulin Sensitivity/secretion
- uses fasting glucose and insulin values
HOMA-IR= estimates insulin sensitivity
HOMA-Beta = estimates insulin secretion

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4
Q

THE GOLD STANDARD OF ASSESSING INS SENSITIVITY: 3 questions
1. In general, how do the clamps work?
2. How does the glucose clamp work and what is it used for?
3. How does the insulin clamp work, and what is it used for?

A
  1. Plasma concentrations of either glucose or insulin are “clamped at high level by balancing endogenous and infused glucose
    • assesses insulin secretion by beta cells
    • more glucose infused= greater insulin secretion
  3. assesses peripheral insulin senstivity, more glucose infused = greater insulin sensitivity
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5
Q

CLAMPS OVERALL

A
  • plasma concentrations of glucose or insulin are clamped at high levels by balancing endogenous (blood) & infused glucose
  • either assess insulin secretion by beta cells (glucose clamp) or insulin sensitivity (insulin clamp)
  • more glucose infused = greater insulin secretion/sensitivity
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6
Q

Oral Glucose Tolerance Test (OGTT)

A
  • used to diagnose diabetes or prediabetes
  • patient fasts overnight, consumes 75g of glucose, blood drawn over 2 hours.
  • determines glucose clearance time, (glucose tolerance)
  • rapid clearance=tolerant ; slow=intolerant
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7
Q

Rank the methods of assessing insulin sensitivity;
___ OGTT
___ Fasting Values (HOMA)
___ Clamps

A
  1. clamps
  2. OGTT
  3. HOMA
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8
Q

if you were to look at an OGTT (hours vs bl glucose levels) comparing a T2D, Obese (insulin sensitive), pre diabetic, and healthy individuals, what would be the trends?

A

*T2D: highest, plateaus around 1 hour
* initial spike then downhill curve trend for the rest
Obese/prediabetic: obese slightly lower but levels match after 3 hours
normal: lowest levels

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9
Q

Hepatic Glucose Production (HGP)
Blood Glucose levels maintained through a balance of 3 things:

A
  1. intestinal absorption from dietary CHOs
  2. uptake by peripheral tissues
  3. uptake, storage and production by liver
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10
Q

Which organ plays a major role in blood glucose homeostasis in mammals? How?

A

LIVER
1. GLYCOGENESIS: uptake and stoage of glucose
2. GLYCOGENOLYSIS; GLUCONEOGENESIS: release of glucose.
- release is sensitive to hormones (insulin, glucagon etc)

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11
Q

The _____ is responsible for ___% of blood glucose in the fasting state

A

Liver; 90%

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12
Q

Hormonal Regulation of HGP:
Insulin release will _____ (suppress/elevate) HGP and _____ (inhibit/activate) release of glucagon from pancreatic alpha cells. Glucagon _____ (inhibits/activates) HGP.

A
  • suppress
  • inhibit
  • activates/stimulates
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13
Q

Steps of insulin release from beta cells:

A
  1. Glucose enters pancreatic b cell via GLUT2
  2. Undergoes glycolysis, INC cellular ATP
  3. High ATP shuts down ATP-sensitive channels, causing depolarization
  4. Depolarization results in calcium flooding inside B-cell
  5. Insulin released from granules into blood
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14
Q

What is RRP vs RP in phases of insulin release

A

RRP= PHASE 1= readily releasable pool
RP= PHASE 2= reserve pool

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15
Q

What happens in obese individuals regarding RRP and RP? What is increased?

A

Normal kinetics of RRP and RP but increased B-cell mass

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16
Q

What happens in impaired glucose tolerance individuals regarding RRP and RP?

A

RRP depleted
RP normal

17
Q

What happens in T2D individuals regarding RRP and RP? Why?

A

RRP lost or problem with insulin exocytosis
RP depleted
Pancreatic fatigue

18
Q

What happens after a CHO meal in individuals with T2D?
- blood glucose:
- insulin:
- glucagon;
How about after insulin injection?
- blood glucose
- glucagon

A

blood glucose very high
insulin low
glucagon remains high
after injection,
glucose reduced
glucagon still remains high

19
Q

why does glucagon remain high in T2D after CHO meal, even after insulin injection?

A

because it is injected into periphery, not the portal vein.

20
Q

Hormonal Regulation of Blood glucose, answer for both fasted and fed states in NON T2D
Insulin is ____ (high/low), glucagon _____ (high/low).
____ responsible for maintaining bl glucose levels
________ clears blood glucose

A

FASTED:
low, high, HGP, basal insulin
FED:
high, low, dietary glucose levels, insulin

21
Q

Hormonal Regulation of Blood glucose, answer for both fasted and fed states in T2D
Insulin is ____ (high/low/injected), glucagon is _____ (high/low).
____ & _____ cause blood glucose levels to be high
insulin is _____ (sufficient/insufficient) at clearing blood glucose

A

FASTED:
low, high, HGP, insulin injection
FED: insulin injected, high, Dietary glucose & HGP, insufficient

22
Q

How is HGP DIRECTLY regulated?

A

Insulin released by pancreas secreted into portal vein
-promotes hepatic glucose uptake via GLUT2 and production of glycogen
- inhibits gluconeogenic enzymes

23
Q

How is HGP INDIRECTLY regulated?

A

Inhibiting: glucagon secretion from a-cells, FFA release from adipose
Altering adipokine secretion (adiponectin inhibits HGP)
Regulating hypothalamus-liver axis

24
Q

What is MODY? Is it clinically the same as T2D? Why arent they called the same thing?

A

Maturity onset diabetes of the young (monogenic diabetes)
Clinically the same
EXCEPT, develops early in life from genetic mutations

25
Q

Genetics of MODY:
mode of inheritence
type of mutation

A
  • autosominal dominant inheritance
  • nonsense mutation in glucokinase
26
Q

genetic mutations that prevent ____ uptake and storage as glycogen are associated with severe, early onset diabetes, characterized by severe ______.
a) insulin, hyperglycemia
b) glucose, hypoglycemia
c) glucose, hyperglycemia
d) insulin, hypoglycemia

A

c) glucose, hyperglycemia

27
Q

LIRKO mice:
- what does it stand for
what happens before vs after OGTT (glucose injection)

A

Liver-specific insulin receptor knockout
before: high blood glucose, very high insulin
after ogtt: high blood glucose

28
Q

Loss of insulin signally in the liver (LIRKO mice) causes significant ______ in blood glucose levels
(increase or decrease)

A

inrease

29
Q

HGP and expression of genes involved in gluconeogenesis ______ (are/are not) suppressed by insulin in LIRKO mice. The livers of LIRKO mice think they are in a ______ (fasted/fed) state.

A

are not
fasted

30
Q

LIRKO mice have ____ levels of gluconeogenic genes and ____ levels of glycolytic genes

A

high
low

31
Q

In LIRKO mice, is insulin able to suppress HGP like it does in normal?

A

no

32
Q

Study conducted to see if over expressing glucoskinase would improve metabolic disorders seen in mice with an insulin receptor mutation: what was seen?

A
  • increased glucose metabolism in liver and can compensate in part for the disorder (reduced steatosis)
33
Q

Name 4 methods to assess glucose tolerance and insulin sensitivity

A

fasting glucose/insulin levels
HOMA-IR
OGTT
clamps

34
Q

Insulin release from pancreatic B cells

A
  • coordinated process consisting of two phases (RRP, RP)
  • suppresses glucagon secretion from pancreatic a-cells
35
Q

Regulation of HGP by insulin and glucagon involves regulation of
a) glycogenesis
b) glycolysis
c) Beta oxidation
d) FA transport
e) gluconeogenesis
f) 2 of above
g) all
h) 3 of above
i) 4 of above

A

3: a, b, e

36
Q

T/F: Regulation of HGP is both indirect and direct

A

true

NUTR3360 (6 decks)

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