Lect 22 Flashcards

1
Q

Type I diabetes is caused by

A
  • immune mediated destruction of B-cells
  • absolute insulin deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

peak onset of Type I diabetes

A

11-13 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three main clinical manifestations of type I diabetes? which are induced by hyperglycemia and which is induced by insulin deficiency

A
  1. polydipsia
    • hyperglycemia-induced: H20 is osmotically attracted from cells
  2. polyuria
    • hyperglycemia-induced: acts as osmotic diuretic
  3. polyphagia
    • insulin deficiency: depletion of cellular stores of fluel produces cellular starvation and increases in hunger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

type I diabetes can lead to what threatening condition

A
  • diabetic ketoacidosis
    • insulin deficiency leads to glucagon excess -> glucagon promotes fatty acid oxidation -> excessive oxidation leads to formation of keytone bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

define metabolic syndrome

A

name for a group of risk factors that occur together and increase the risk for coronary artery disease, stroke, and type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Genetics + aging + obesity and inactivity can lead to

A

insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what conditions are associated with insulin resistance

A
  • type II diabetes
  • HTN
  • dyslipidemia
  • atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

type 2 diabetes ranges from what two etiologies

A
  • insulin resistance
  • insulin secretory defect with insulin resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

insulin resistance seen in type II diabetes occurs mainly in what organ

A

muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

insulin resistance seen in type II diabetes MOA

A
  • reduction in insulin receptor content
    • decrease in tyrosine kinase activity
  • defects in IRS-1, IRS-2 (Insulin receptor substrate)
    • decreased glucose transport
    • defective vesicular transport to surface membranes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does type II diabetes effect the liver

A
  • glucose exceeds the capacity of the liver leading to increased storage of fatty acids and hepatic steatosis and nonalcoholic steatotic hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

glucose uptake in the liver is due to what transporter

A

Glut2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does the liver take in glucose without insulin?

A
  • glucose uptake in liver is due to glut 2
  • liver takes up glucose -> glycogen, gluconeogensis decreases and conversion of glucose to fat is promoted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are adipokines

A

proteins produced and secreted from adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

adipokines production is increased in what condition? What can it cause?

A
  • production increased with obestiy
  • may contribute to a “low grade” inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the adipokines that may be involved in the pathophysiology of obesity linked disorders

A
  • Leptin
  • Adiponectin
17
Q

function of leptin

A
  • regulates energy intake, expenditure, and appetite
18
Q

where are leptin receptors located? what does binding signal?

A
  • satiety center of the hypothalamus
  • signals the brain that the body has had enough food to eat
  • *thus defect in gene or signal transduction -> overeating
19
Q

expansion of adipose stores increases what hormones which functions to decrease calorie intake by inhibiting hunger and stimulating satiety

20
Q

leptin stimulates thermogenesis which has what effect

A

restore fat mass to setpoint

21
Q

leptin circulates at levels proportional to

A
  • body fat content
    • in response to increases in adipose stores, higher leptin levels inhibit food intake
    • in response to decreases in adipose stores, lower leptin levels stimulate food intake
22
Q

obesity is associated with what level of leptin levels? what is the problem?

A
  • higher plasma leptin level
  • resistance to leptin
    • excess food intake not controlled by the anti-appetite effects of leptin
23
Q

Adiponectin is secreted primarly from what tissue

A

adipose tissue

24
Q

levels of Adiponectin are inversely correlated with

A
  • BMI
    • levels are decreased in obestiy
    • weight loss and caloric restriction all increase levels
25
in type I diabetics, Adiponectin levels are
lower, indepedent of age or BMI
26
Adiponectin effects
* metabolism * increases glucose uptake * increases insulin sensitivity * increases fatty acid oxidation and clearance * suppresses gluconeogenesis
27
type I diabetes have high or low pre-exercise glucose levels? why?
* **pre-exercise glucose is high** * remains the **preferred source of energy** * very little fatty acid oxidation * glucose use is greater than hepatic glucose production
28
type I diabetics don't typically have a plasma insulin drop during exercise. What effect does this have on glucagon and hepatic glucose production?
* elevated insulin levels prevent the release of glucagon (exogenous insulin refers to the insulin people inject or infuse via an insulin pump) * inhibits glycogenolysis and gluconeogenesis * hepatic glucose production is inhibited
29
therefore, type I diabetics have a greater risk of what occuring during exercise
* exercise induced hypoglycemia * work and high insulin levels enhance glucose uptake by the working muscle
30
describe insulin shock
* excessive insulin in blood -\> increased glucose uptake by cells -\> hypoglycemia and decreased CNS function -\> three things * if glucose intake, blood glucose returns to normal * clinical signs * no glucose intake, levels decrease further
31
exercise has what effect on insulin sensitivity in type II diabetics
* increases insulin sensitivity * increases GLUT-4 * increases glycogen synthase activity