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Joeli Unit 5 > T2DM (Pancreas as endocrine organ and T2DM) > Flashcards

T2DM (Pancreas as endocrine organ and T2DM) Flashcards

1
Q

T2DM is a complex interplay between

A

impaired insulin secretion
insulin resistance

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2
Q

genetic factors that may contribute to T2DM

A

MODY
GLUT transporter defects
Mitochondrial defects –> abnormal fatty acid metabolism –> insulin resistance

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3
Q

environmental factors that may contribute to T2DM

A

Obesity –> dysfunctional adipokine release –> insulin resistance
High fat diet
Excess nutrient intake

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4
Q

increased amylin release leading to T2DM

A

increased amylin release –> amylin deposition –> beta cell damage

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5
Q

inability to fully synthesize mature insulin leading to T2DM

A

inability to fully synthesize mature insulin –> release of proinsulin (immunoreactive) –> beta cell damage

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6
Q

insulin receptor down regulation leading to T2DM

A

insulin receptor downregulation due to overstimulation –> further resistance

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7
Q

in people without T2DM, the maximum response is released when what percent of receptors are occupied by insulin

A

5%

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8
Q

obesity and endocannabinoid system

A

obesity –> increased ECS tone –> increased appetite and decreased energy expenditure –> further nutrient excess –> vicious cycle

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9
Q

overactive ECS and insulin

A

Overative ECS increases insulin sensitivity in peripheral tissue independent of obesity

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10
Q

ECS and dysfunction metabolism

A

ECS contributes to dysfunctional metabolism of adipose tissue, skeletal muscle, liver

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11
Q

ECS and inflammation effects on beta cells

A

ECS activation inflammatory cytokines and activates macrophages –> infiltration and inflammation of beta cells –> apoptosis of beta cells

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12
Q

Obesity up regulates

A

CB1 receptors and ECS expression

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13
Q

CB1 receptor in the brain

A

increases food intake by modulating hypothalamic neurons
activates mesolimbic system to activate reward and reinforcement pathways –> preference for palatable food

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14
Q

CB1 receptor in peripheral tissue

A

activation of anabolic pathway favoring energy storage

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15
Q

CB1 receptor in adipocytes

A

increases de novo fatty acid synthesis, TG accumulation, decreases lipolysis, down regulates adiponectin

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16
Q

CB1 receptor on liver

A

increases lipogenesis

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17
Q

CB1 receptor on skeletal muscle

A

promotes oxidate metabolism through dysfunctional mitochondrial oxidative phosphorylation –> ROS production

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18
Q

CB2 receptors

A

increase obesity associated inflammation, insulin resistance, and hepatic steatosis

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19
Q

hyperglycemia and HK

A

HK is saturation and is shunted to alternative pathways

20
Q

alternative pathway complications due to HK saturation

A

over utilization of NADPH and NAD+
oxidative stress
osmotic stress
glycosylation of proteins and lipids by end products
mitochondrial dysfunction

21
Q

what does the polyol pathway require

A

NADPH and NAD+ for enzymatic activity and oxidation

22
Q

polyol pathway converts

A

glucose to fructose

23
Q

from the polyol pathway, fructose can be—

A

can be recycled into energy pathway
can increase ROS and glycation (AGEs)

24
Q

NADPH and NAD+ would normally be used for redox reactions to create

A

NO
Glutathione
Myo-inositol

25
Q

NO is needed for

A

endothelial function

26
Q

Glutathione deficiencies

A

can lead to oxidative stress and ROS

27
Q

Myo-inositol is needed for

A

normal nerve function

28
Q

overload of both HK and polyol favors

A

sorbitol production

29
Q

excess sorbitol can lead to

A

osmotic influx

30
Q

under normal conditions, 1-3% of glucose goes through what pathway

A

hexosamine pathway

31
Q

end product of hexosamine pathway

A

UDP-C1cNAc –> protein glycosylation (think about hemoglobin)

32
Q

UDP contributes to

A

increase in ROS and mitochondrial dysfunction

33
Q

Other products from hexosamine pathway (O-GlcNAcylation) causes

A

hypertrophic growth factors, particularly in myocytes –> heart failure

34
Q

hexosamine pathways and nephrons

A

flux into hexosamine pathway contributes to nephrons damage in hyperglycemic patients

35
Q

Glycation

A

process of glucose/fructose attaching to proteins or lipids

36
Q

Effect of AGE binding to RAGE

A

gene transcription alteration –> induces ROS generation and inflammatory cytokines –> dysfunctional signaling

37
Q

AGEs lead to

A

protein/collagen cross linking

38
Q

Effects of protein/collage cross linking

A

vascular stiffening and trapping of LDL in arterial walls –> stiff arteries with atherosclerosis

protein degradation –> glomerular filtration barrier damaged and mesangial cells hypertrophy –> fibrosis and glomerulosclerosis

39
Q

Other pathologic effects of AGE

A

LDL oxidation (increases risk of atherosclerosis)
Interferes w NO release (decreased vasodilation)
Increases vascular permeability

40
Q

Protein kinase C (PKC) pathway is activated by

A

DAG

41
Q

what is DAG

A

glycerol + 2 fatty acids

42
Q

hyperglycemia and DAG

A

hyperglycemia causes overproduction of DAG –> activation of PKC

43
Q

Effects of PKC

A

collagen, fibronectin (mesangial expansion, glomerular hyperfiltration)
Profibrotic gene expression
Decrease fibrinolysis
Increase ROS
Angiogenesis

44
Q

How does polyuria occur in T2DM

A

hyperglycemia –> high renal filtered glucose > 180 ng/dL –> glucose exceeds reabsorption capacity –> glucose pulls water through osmotic pressure –> increased urinary output

45
Q

How does polydipsia occur in T2DM

A

hyperglycemia –> polyuria –> dehydration –> increased serum osmolality –> osmoreceptors in supraoptic and supra ventricular nuclei in hypothalamus recognize —> thirst

46
Q

How does polyphasic occur in T2DM

A

impaired insulin sensitivity –> decreased glucose utilization in cells –> dysfunctional signaling that body does not have glucose for metabolism –> increased hunger

47
Q

How do cataracts occur in T2DM

A

hyperglycemia –> shunting to alternative pathways (Polyol) –> increased concentration of sorbitol –> generation of fructose and ROS

AND

increased concentration of sorbitol with decreased sorbitol dehydrogenase –> increased sorbitol levels –> potent osmotic factor –> increased fluid accumulation in lens

Joeli Unit 5 (10 decks)

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