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Cell > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

a broad term that refers to an abnormality in blood sugar stability

A

dysglycemia

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2
Q

Blood glucose is controlled by ___ and ___

A

Insulin and Glucagon

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3
Q

This biomolecule is not a fuel reservoir

A

Protein

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4
Q

body proteins can be degraded protein during ___ and ___ and provide AA substrate for gluconeogenesis

A

starvation and periods of stress

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5
Q

Most efficient form of energy storage in humans

A

triglycerides

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6
Q

Excess glucose can be stored as

A

glyceride

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7
Q

Largest reservoir of glycogen ____; Principal reservoir of glycogen ____

A

Skeletal muscles; liver

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8
Q

Where production of glucose occurs

A

Liver

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9
Q

Serves to spare the body’s use of protein as fuel source

A

Fatty acid oxidation and ketogenesis

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10
Q

The two principal circulating fuel in humans

A

Glucose and FFA

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11
Q

In the ___ state, nutrients are stored

A

Fed

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12
Q

What happens to nutriends in the fasting state

A

they are oxidized for energy production

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13
Q

Where will excess energy energy be deposited?

A

Liver, muscle, and fat

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14
Q

In fed state, body has a preference for ____ over _____.

A

Glucose oxidation; fat oxidation

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15
Q

Intermediary hormone in fed state

A

Insulin

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16
Q

This state is associated with the release at times of requirement

A

Fasting state

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17
Q

In fasting state, glycogen is transformed into ____ and triglycerides are transformed into ____

A

Glucose; FFA

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18
Q

Body has a preference for ____ over ____ in Fasting sate

A

fat oxidation; CHO oxidation

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19
Q

Intermediary hormone of Fasting state

A

Glucaon

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20
Q

Function of insulin

A

helps glucose in the blood get into the cells

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21
Q

Function of glucagon

A

works with insulin to control blood glucose levels

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22
Q

In the fasting state, the presence of glucagon will cause glucose levels to go down. (T/F)

A

False

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23
Q

Instead of causing the storage of energy, you will withdraw energy through ____ and ____ to produce ____. What state?

A

Gluconeogenesis; glycogenolysis; glucose; fasting state

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24
Q

If insulin goes decrease, what will glucagon do?

A

Elevate blood sugar

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25
Q

Capacity for skeletal muscle to acutely shift its reliance between lipids and glucose during fasting in response to insulin

A

Metabolic Felxibility

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26
Q

After eating (fed state), we use the _____ as our energy source, but when we’ve used this up and haven’t eaten (fasting state), we convert ____ into energy

A

carbohyrates; stored fat

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27
Q

○ Suppression of fatty acid oxidation
○ Preference for glucose uptake, oxidation, and storage

State and metabolic flexibility or inflexibility?

A

Fed state; flexibility

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28
Q

○ Preference for the use of fatty acid oxidation in muscle ○ Suppressed glucose oxidation

State and metabolic flexibility or inflexibility?

A

Fasting state; flexibility

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29
Q

● Decrease or loss of flexibility is hypothesized to play a role in various disease processes (Kelley et al., 2000)
● This is not the typical condition experienced by a healthy individua

A

Metabolic Inflexibility

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30
Q

○ Less suppression of fatty acid
○ Blunted preference for glucose oxidation

State and metabolic flexibility or inflexibility?

A

Fed State (Metabolic Inflexibility)

31
Q

Less suppression in beta oxidation
○ Blunted preference for fatty acid oxidation in muscle

State and metabolic flexibility or inflexibility?

A

Fasting state; inflexibility

32
Q

The 2 cycles depict the interplay between the use of glucose and FFA

A

Randle and Reverse Randle

33
Q

Aka the Glucose-Fatty Acid Cycle

A

Randle Cycle

34
Q

Three mechanisms of Randle Cycle

A

Glucose, FFA, Joint pathway (Acetyl-COA to Malonyl Coa)

35
Q

Similar to the Randle Cycle excpe thtat there is an increase in the ____ which will lead to the production of ____

A

Malonyl Coa Pathway; triglycerides

36
Q

Results from the autoimmune destruction of β-cells of the endocrine
pancreas in the Islets of Langerhans

A

Type 1 Diabetes

37
Q

How does Type 1 Diabetes occur?

A

The body’s immune system attacks and destroys the cells in the pancreas that make insulin which is needed to allow glucose to enter into the cells and produce energy

38
Q

Increased thirst and urination ○ Increased hunger
○ Blurred vision
○ Fatigue
○ Unexplained weight loss

are symptoms of ____

A

Type 1 Diabetes

39
Q

The body either fails to produce enough insulin to maintain normal glucose levels or resists the effects of insulin

A

Type 2 Diabetes

40
Q

Pathoegenesis of Type 2 diabetes involve the ______ folloed by _____

A

Development of insulin resitance; progressive B- cell impairment

41
Q

This disease occurs most often to those Aged 45 or older

○ With family history of diabetes ○ Who are overweight or obese

A

Type 2 Diabetes

42
Q

T/F: Lifestyle plays a role in the devt of Diabetes type 2

A

T (Physical inactivity and certain health problems (i.e. high blood pressure, gestational diabetes during pregnancy) affect chances of Type II DM as well)

43
Q

o Glucose increases insulin
o Entry of glucose in the skeletal muscle
o Hepatic glucose production is decreased o Thus, no elevation of blood glucose

Refer to the ___ postprandial response to insulin

A

Normal

44
Q

Glucose increases insulin but because of resistance, the skeletal muscle
will not recognize it
o Glucose will not be absorbed in the muscles
o Muscles will send signals to the brain, then the brain will think that thebody is in the tfasting state
Brain will then e liver that they don’t have enough glucose o The liver will keep breaking down glycogen to produce glucose thus hyperglycemia happens

Refer to the ____ postprandial response to insulin

A

Abnormal

45
Q

In insulin resistance (IR), insulin has no effect because?

A

IR prevents carbs from entering the cell and mitochondira

46
Q

3 Sources of insulin resitance

A

Skeletal muscles
▪ Hepatocytes - parenchymal
cells in liver ▪ Adipocytes

47
Q

caused by a decrease in mitochondrial biogenesis, reduced mitochondrial content, and/or decrease in the protein content and activity of oxidative proteins

A

Mitochondrial dysfunction

48
Q

What happens if there is a mitochondrial dysfuction

A

Greater decrease in energy production

49
Q

n effect of the dysfunction due to the oxidative stress

A

Reactive oxygen species

deteriorate -cell function and increase insulin resistance which leads to the aggravation of type 2 diabetes.

50
Q

T/F: diabetes mellitus is an accumulation of both excess glucose and lipids

A

True

51
Q

FFAs can have a dual impact on the liver and skeletal muscle (T/F_

A

True

● FFAs entering the skeletal muscle are converted to DAG due to mitochondria dysfunction
○ DAG and ROS from the mitochondria can activate PKCs
● This results in inhibition of the insulin receptor signaling and glucose uptake in the muscle cells
● In hepatocytes, DAG from FFA utilization can activate PKCs, leading to impairment of the insulin receptor signaling pathway
● In addition, less inhibition of the FOXO protein increases the production of gluconeogenic enzymes such as PEPCK and PC, leading to gluconeogenesis and elevation of blood glucose level

52
Q

Why are PUFAs better to consume than monounsaturated fats?

A

More difficult to solidify;many molecules stick out -» harder to stack

53
Q

Theory of Whole Body Insulin Resistance

A

● During the early phases of insulin resistance, excess intake of nutrients stimulates insulin secretion
● This extra insulin production results in the liver producing more VLDL that can build up in skeletal muscle and the adipocyte
● The adipocyte experiences hypertrophy and results in increased TAG lipolysis to increase plasma FFA levels that can then go back to the pancreas to stimulate even more insulin secretion
● In the later phases of insulin resistance, the liver maximizes its production of VLDL, and there are elevations of lipolysis in skeletal muscle and adipocytes
● At the same time, there is an increase of hepatic gluconeogenesis. This in combination with the excessive plasma FFAs leads to over stimulation of the pancreas
● On the other hand, an excess of plasma FFAs will cause insulin resistance in tissues and organs, which establishes a vicious cycle and will eventually lead to β-cell failure and development of overt NIDDM

54
Q

Social determinants of DM

A

Energy Balance, Individual Factors, Behavioral settings

55
Q

Impaired Glucose Tolerance and Impaired Fasting Gucose are two indicators of ____

A

Pre-diabetes

56
Q

Blood glucose level is higher than normal but is not high enough to be classified as diabetes

A

Impaired Glucose Tolerance

57
Q

Blood glucose level is escalated during the fasting state but has not reached the diabetic stage

A

Impaired Fasting Glucose

58
Q

Drugs tha help delay or prevent jabetis

A

Metformin, Acarbose, Pioglitazone, Orlistat

59
Q

Eye, Kidney, Nerves are ____ complications of DM

A

microvascular

60
Q

Brain, heart, extremities are _____ complicatios of DM

A

Macrovascular

61
Q

diabetic patients without prior MI (MYOCARDIAL INFARCTION) are not at risk of MI compared to nondiabetic patients with previous MI.

A

False

62
Q

Hyperglycemia leads to

A

Oxidative stress

Oxidative stress is an imbalance between free radicals and antioxidants in your body.

63
Q

Normal fasting blood sugar would always change t/f

A

truw

64
Q

With glucose buildup after meals, blood vessels will leak blood or fluid, distorting vision; treatment

A

Retinopathy; Anti- VEGF Injection Therapy

65
Q

End stage renal disease; treatment

A

Nephropathy; Dialysis

66
Q

LOPS (Loss of Protective Sensation)

▪ Not being able to feel pain from injury; treatment

A

Neuropathy; Amputation

67
Q

Diabetics are 2-4x more likely to suffer from ischemic stroke

A

Brain

68
Q

Mortality from coronary heart disease in subjects with
type 2 diabetes and in nondiabetic subjects with and without prior
myocardial infarction

A

Haffner Case

69
Q

Diabetics’ extremities are often dismembered in the wards ○ Have to check the pulse of the feet as well

A

Extremities

70
Q

TThe trend of escalating diabetes prevalence, with its impact on CVD, will no doubt lead to an immense financial burden in many countries, unless action is taken to prevent diabetes and its complications

A

true (pls read last page) :)

71
Q

Who discovered insulin

A

Insulin was discovered by Sir Frederick G Banting (pictured), Charles H Best and JJR Macleod

72
Q

He rediscovered the sweetness in urine and blood of patients; mellitues was added

A

Thomas Wellis

73
Q

When was insulin discovered

A

July 27 1921

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