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Phy Sci 111B > M3 L5 > Flashcards

M3 L5 Flashcards

(93 cards)

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1
Q

How would a glucose curve look for a diabetic who had been fasting but is now doing a glucose tolerance test?

A
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2
Q

What is type 1 diabetes?

A

Autoimmune mediated where destruction of the pancreatic β-cells leads to loss of insulin production

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3
Q

What is type 2 diabetes

A

Increased insulin resistance in cells (muscle, fat, liver)

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4
Q

What is insulin therapy?

A

insulin is administered externally to help manage blood glucose levels.

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5
Q

Why is insulin therapy effective in type 1 diabetes?

A

because it replaces the insulin their bodies canʼt produce.

their insulin receptors are not resistant—the problem lies in insulin deficiency

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6
Q

Why does insulin therapy alone not benefit type 2 diabetes?

A

bc they dont need more insulin - the issue is their insulin is ineffective

they need:
* Lifestyle changes such as regular exercise and a healthy diet are essential for improving insulin sensitivity.

  • Additionally, some medications can
    enhance the bodyʼs response to insulin and help regulate blood glucose levels more effectively.
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7
Q

Why does plasma glucose not decrease in diabetic subjects?

A

1) insulin uptake in muscles
2) insulin helps inhibit gluconeogensis and glycolysis

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8
Q

What does postprandial mean?

A

after eating

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9
Q

What is the criteria for diabetes?

A

not differentiating between type 1/2:

  • hemoglobin a1c greater than 6.5
  • fasting glucose greater than 126 mg/dL
  • glucose greater than 200 two hours postprandial during test or random plasma glucose test
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10
Q

What carries oxygen in your blood?

A

Hemoglobin A

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11
Q

Why is hemoglobin a diagnostic to detect diabetes?

A

When glucose levels are high, hemoglobin becomes coated with glucose (glycated) molecules.

Once the glucose sticks to the hemoglobin, it remains for the lifespan of the red blood cells, which is typically 3 months (which is an a1c test)

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12
Q

What does HbA1c measure?

A

how much glucose is stuck to hemoglobin. Gives you a long term assessment of glucose control.

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13
Q

What hemoglobin value indicates what type of diabetes?

A

A hemoglobin of 6.5% or more indicates type 2 diabetes.

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14
Q

what can increase the risk of type 1 diabetes?

A

2 or more autoantibodies

  • Most patients with 2 autoantibodies will develop type 1 diabetes before turning 18
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15
Q

Why do autoantibodies lead to type 1 diabetes?

A

These T cells will attack the Beta cells and essentially destroy them which means we cant make anymore insulin which leads to diabetes

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16
Q

What do adipose tissues store

A

triglycerides

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17
Q

What happens to adipose tissues when insulin is low?
* via what process?

A

When insulin is low (as in Type 1 Diabetes) and glucagon is high, the triglycerides in adipose tissues are broken down into free fatty acids (FFAs) via lipolysis.

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18
Q

What is lipolysis

A

the metabolic process by which triglycerides (fat molecules) stored in adipose tissue (fat cells) are broken down into:

Free fatty acids (FFAs)
Glycerol

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19
Q

What does the lack of insulin in type 1 diabetes lead to?
(in terms of lipolysis)

A

Insulin normally inhibits lipolysis and promotes fat storage. Bc it is low in Type 1 Diabetes, fat breakdown is uncontrolled.

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20
Q

What does glucagon do in type 1 diabetes?

A

Glucagon: Stimulates lipolysis. High in Type 1 Diabetes, so it drives fatty acid release from fat stores.

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21
Q

What are free fatty acids?

A

Travel to the liver, where they are converted into ketone bodies through a process called ketogenesis.

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22
Q

Name one important hormone in ketogenesis and why its important

A

HMGCS: HMG-CoA Synthase

this is the rate limiting step in ketogenesis

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23
Q

β-Hydroxybutyrate (β-OHB) is one of the ketone bodies produced for ketogenesis. what does it do?

A

sed as fuel for tissues:

  • Muscle (converted back to acetyl-CoA → enters TCA cycle to make ATP).
  • Brain (especially important when glucose is low, such as Type 1 Diabetes).
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24
Q

What happens when insulin is absent so lipolysis is not regulated? (what lead to?)

A

lipolysis is unchecked → massive FFA release.
FFAs → Excessive ketone production → ketones build up in blood.

Can lead to diabetic ketoacidosis (DKA): dangerously low pH due to excess acidic ketones.

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25
What is diabetic ketoacidosis (DKA)?
A condition caused by excessive ketone accumulation in the blood, leading to acidosis.
26
Why does the liver produce ketones during fasting or diabetes?
To provide an alternative energy source when glucose is low or unavailable.
27
What is the usual role of insulin in ketogenesis?
Insulin inhibits ketogenesis by blocking lipolysis, suppressing liver ketone production enzymes, and promoting glucose use instead of fat as fuel.
28
What is Ketogenesis
Ketogenesis is the metabolic process in which the liver converts fatty acids into ketone bodies to be used as an alternative energy source—especially when glucose is low.
29
What is a major symptom of ketogenesis?
Dehydration When ketone levels rise in the blood, they spill into the urine. Ketones pull water with them bc osmosis → increased urination (polyuria) → fluid loss. they keep peeing due to to the excess ketones in urine - need to get it out but it leads to dehydration
30
What is the Fatty Acid–Carnitine Shuttle
The Fatty Acid–Carnitine Shuttle is the system your body uses to transport long-chain fatty acids into the mitochondria so they can be broken down for energy (via β-oxidation).
31
Why Do We Need a fatty acid shuttle?
Long-chain fatty acids cannot cross the inner mitochondrial membrane on their own. So, the body uses carnitine as a “shuttle bus” to carry them in.
32
What is Diabetic Ketoacidosis (DKA)
complication of Type 1 Diabetes caused by severe insulin deficiency and overproduction of ketone bodies
33
What causes diabetic ketoacidosis?
The liver makes too many ketones due to lack of insulin, causing ketogenesis to spiral out of control. But without insulin, glucose stays in the blood → hyperglycemia.
34
Which ketone bodies contribute to acidosis in DKA?
β-hydroxybutyrate and acetoacetate lower blood pH due to their acidic nature → metabolic acidosis.
35
How does the liver increase glucose output during lack of insulin emergency?
via: Gluconeogenesis Glycogenolysis
36
What is metabolic acidosis
A condition where your blood becomes too acidic due to a buildup of acid
37
Why are patients with DKA dehydrated?
High glucose and ketones cause osmotic diuresis, leading to significant water loss in urine.
38
What are Kussmaul respirations and why do they occur in DKA?
Deep, rapid breathing to eliminate CO₂ and compensate for metabolic acidosis --> causes respiratory alkalosis
39
What is respiratory alkalosis
A condition where your blood becomes too alkaline (basic) because of low carbon dioxide (CO₂) levels. Usually caused by hyperventilation — breathing too fast or deep, which blows off (removes) CO₂ faster than the body produces it.
40
How does insulin help resolve DKA?
Insulin stops lipolysis and ketogenesis, lowers blood glucose, and corrects acidosis.
41
What symptoms are commonly seen in DKA?
Confusion, nausea, vomiting, abdominal pain, and signs of dehydration.
42
Where is SGLT1 found and what is its role?
In the small intestine and kidney (apical side) ; absorbs glucose from diet and reabsorbs ~10% glucose in kidneys.
43
Where is SGLT2 found and what does it do?
Located in the early proximal tubule; reabsorbs ~90% of filtered glucose in the kidney.
44
What type of transporter is GLUT2? where found
Facilitated glucose transporter with low affinity and high capacity, found in liver and pancreatic β-cells. * basolateral side
45
Where is GLUT4 primarily located and what triggers its action?
In muscle and fat cells; insulin triggers its movement to the cell membrane for glucose uptake.
46
What distinguishes SGLT transporters from GLUT transporters?
SGLTs use sodium gradient for active transport of glucose against its concentration gradient, unlike passive GLUTs.
47
What is the main function of GLUT4?
To increase glucose uptake in muscle and fat cells in response to insulin.
48
Glucose infusion rate:
the amount of glucose that is pumped into the blood to maintain a set glucose level.
49
Rapid acting insulin * role? * examples?
Used before meals to control post-meal (postprandial) glucose spikes Lispro, Aspart, Glulisine
50
Rapid acting insulin * onset? * peak? * duration of action?
Onset: 5–15 minutes Peak: 1–2 hours Duration: 4–6 hours
51
Regular (Short-Acting) Insulin * role?
Used around meal times but not as fast as rapid-acting
52
Regular (Short-Acting) Insulin * onset? * peak? * duration of action?
Onset: 30–60 minutes Peak: 2–4 hours Duration: 6–8 hours
53
Long-Acting Insulin * role * ex
Used to provide steady basal insulin throughout the day Detemir, Glargine
54
Long-Acting Insulin * onset? * peak? * duration of action? (diff for the two ex)
Onset: 1–2 hours Peak: Flat (no real peak) Duration: * Detemir: 12–24 hours * Glargine: 24 hours
55
Insulin Pump Therapy
have an insulin pump that controls insulin release directly into circulation.
56
what is basal insulin
the background insulin your body needs all day and night, even when you're not eating. It helps keep your blood glucose stable between meals and overnight.
57
What is Metformin
Medication that reduces sugar production from the liver
58
What is Insulin releasing pills (secretagogues):
Medication that increase insulin release from the pancreas. These include a large class of drugs called sulfonylureas
59
What is SGLT2 Inhibitors: * how work?
Meds that promote glucose excretion in the urine by blocking the SGLT2 * they block the reabsorption of glucose in the proximal convoluted tubule. Leading to a drop in blood glucose levels.
60
Name for SGLT2 inhibitors?
Glifozins
61
What medication are Glifozins commonly used in combination with?
Metformin
62
Side effects of SGLT2?
genital infections (bc more glucose in urine) and DKA (bc less glucose absorbs may trigger the body to make ketones instead).
63
What is Incretin based therapies:
Medication that reduces sugar production in the liver and slow the absorption of food
64
What are Amylin analogs:
Injections that reduce sugar production in the liver (glucagon production) and slow the absorption of food
65
How does metformin work?
Metformin promotes insulin sensitivity. * if you inc sensitivity this lowers the amount of insulin that's necessary to lower blood glucose
66
What does metformin target?
It targets the mitochondria and lowers ATP production.
67
What does metformin block?
blocks glucagon signaling, leading to reduced glucose production by the liver.
68
What happens when metformin activates AMPK? (also what is)
AMPK is an energy sensor that: * promotes insulin receptor function * increases glucose transport (more taken up) * reduces fatty acid synthesis.
69
Why is the med Insulin Secretagogues helpful?
These drugs are useful when beta cells are no longer able to adapt to hyperglycemia. It gives beta cells a stimulus to promote insulin secretion.
70
Sulfonylureas (most common insulin secretagogues ) have what risk?
risk leading to hyperinsulinemia, increasing the risk of hypoglycemia.
71
What are Incretins
class of hormones released by the gut that stimulate insulin secretion. * also reduces food intake and drives weight loss
72
What is Glucagon-like peptide 1 (GLP1)
a 30 amino acid peptide that is produced by L-cells in the ileum and colon in response to ingestion of nutrients.
73
What limits GLP-1’s activity naturally?
It is rapidly degraded by the enzyme DPP-4, giving it a half-life <2 minutes.
74
How do DPP-4 inhibitors help in diabetes?
They inhibit the breakdown of GLP-1, increasing its half-life and insulin-promoting effects.
75
What effect does GLP-1 have on the pancreas?
stimulates insulin secretion in beta cells, lowers glucagon secretion in alpha cells, and increases the number of beta cells.
76
How does GLP-1 affect the liver?
It reduces hepatic glucose production.
77
How does GLP-1 affect the GI tract and digestion?
It slows gastric emptying, which slows glucose absorption.
78
What central nervous system effect does GLP-1 have?
It reduces appetite and supports weight loss.
79
How does amylin affect gastric emptying?
It slows gastric emptying, delaying glucose absorption into the bloodstream.
80
What does amylin do to glucagon secretion post-meal?
It suppresses postprandial glucagon release.
81
How does amylin affect appetite?
It promotes satiety, helping reduce food intake and control blood glucose.
82
Name 3 islet antigens detected by autoantibodies
Insulin, glutamine decarboxylase, islet antigen 2
83
What is the probability of diabetes for patients that have 2 autoantibodies at the age of 10?
Approximately 40%
84
What is the cell type that makes autoantibodies?
B-lymphocytes, also known as B-cells
85
Describe how insulin regulates ketones in the blood.
Insulin signals through the insulin receptor in adipocytes to inhibit the enzyme ATGL (adipose triglyceride lipase). This reduces the amount of free fatty acids that are released from adipocytes. Lowering free fatty acids reduces the substrate for ketogenesis in the liver. Therefore, reducing ketone levels.
86
What are the functional cells in the liver that make ketones?
hepatocytes
87
Name the ketone bodies that are made by the liver.
Acetoacetate, b-hydroxybutyrate, acetone
88
Explain how glucagon promotes lipolysis?
Glucagon signals through the glucagon receptor that is found on the plasma membrane. This leads to activation of a G-protein that stimulates adenylate cyclase, an enzyme that utilizes ATP to generate cAMP. The production of intracellular cAMP stimulates PKA and that will activate the enzyme ATGL, which hydrolyzes triglycerides to generate free fatty acids and glycerol.
89
What is the mitochondrial enzyme that initiates fatty acid oxidation?
CPT1-carnitine palmitoyl transferase 1
90
How does lack of insulin lead to polyurea?
The lack of insulin raises glucose levels that cannot be reclaimed by the kidneys. The rise in glucose in the proximal tubule increases and affects the osmolarity of urine, reducing the amount of water that is reclaimed, increasing the volume of urine generated. This will lead to polyurea.
91
Why do diabetic patients develop polydipsia?
The increase loss of water through the urine, leads to compensatory increase in thirst.
92
How is diabetes managed in type 1 diabetics? Discuss the use of fast acting and long acting insulin.
Type 1 diabetics have to administer insulin 4-5 times per day. Patients typically are treated with long-acting insulin that maintains basal insulin levels. Prior to eating meals they will administer a dose of insulin subcutaneously to prevent the high rise in glucose that is seen in type 1 diabetics. If there are three meal a day, then there will be administration of fast acting insulin three times.
93
Name three ways that type 2 diabetes drugs help to improve glucose levels?
They stimulate insulin secretion or improve insulin sensitivity or block reabsorption of glucose in the proximal tubule

Phy Sci 111B (15 decks)

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