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Block 3: GI, Endocrine, Reproductive > Diabetes and Metabolism (Week 3) > Flashcards

Diabetes and Metabolism (Week 3) Flashcards

1
Q

Why is glucose so essential and what happens if we don’t have enough?

A

Brain uses primarily glucose

Brain cannot use fatty acids, but liver can oxidize free fatty acids to ketones, and brain can use ketones for energy

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2
Q

What is the “fed state”

A

Anabolic

Hormone released: insulin, which causes anabolism to build up body’s resources

Nutrients absorbed from small intestine

Increased glucose, branched chain AAs and triglycerides in plasma

Decreased ketones and FFAs

Have glycogen synthesis/storage, AA uptake, protein synthesis and triglyceride formation

Liver uptakes glucose

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3
Q

What is the “fasting state”

A

Catabolic

Hormone released: glucagon, which breaks down glucose etc

Nutrients must be taken out of storage sites (liver, adipose tissue, muscle) once glycogen runs out

Glycogenolysis (breaking down glycogen to glucose) happens for 8-10 hours, but then get protolysis and gluconeogenesis (form glucose from AAs), and lipolysis and ketogenesis (oxidize fatty acids in liver to make ketones for brain to use)

Decrease in glucose, triglycerides

Increase in AA, FFAs, ketones

Liver releases glucose

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4
Q

If a diabetic has low blood sugar (vomiting, bowel obstruction, etc), should you stop giving insulin?

A

No, never stop giving insulin!

If you stop insulin, person will get lipolysis which will increase FFAs which will increase ketogenesis (via glucagon excess), which will cause ketoacidosis and electrolyte abnormalities. That can lead to cerebral edema, vascular thrombosis, infection, MI, cardiac arrythmia, death

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5
Q

Insulin causing glucose uptake in muscle and adipose tissue

A

Insulin in the bloodstream binds insulin receptor on cell surface –> cascade of events –> GLUT4 in vesicles translocated to membrane –> GLUT4 channels let glucose into cell via facilitated diffusion

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6
Q

How is it that any food we eat (carbs, proteins) can be stored as fat?

A

During the breakdown of amino acids, get alpha-ketoacids which go to fatty acids then triglycerides

During the breakdown of glucose, get fatty acids and alpha-glycerol phosphate, which go to to triglycerides

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7
Q

Glycogen

A

9 carbon rings?

When we have too much glucose, we store it as glycogen

Have glycogen reserves in cells, and this makes up 10% of the weight in the liver

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8
Q

Big picture of glucose and glycogen

A

Cell takes in glucose and turns it to pyruvate to make ATP (does GLYCOLYSIS!)

If enough ATP around, won’t do glycolysis (ATP inhibits glycolysis), and instead will store glucose as glycogen

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9
Q

Glycogenolysis

A

Glycogen –> glucose-6-phosphate (G6P)

(later G6P –> glucose)

(opposite of glycogen synthesis)

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10
Q

Anaerobic metabolism

A

People do this when not enough O2 (because low BP so no perfusion, and/or hemoglobin so low that O2 carrying capacity compromised, and/or burst of intense activity)

Pyruvate turns to lactate and get buildup of lactate then metabolic acidosis

If serum pH below 6.9 you’ll die because cellular processes won’t work (also can get cardiac arrhythmia)

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11
Q

GLUT transporters in which locations of the body have high and low affinity for glucose?

A

GLUT in brain has high affinity because always want glucose in the brain

GLUT in liver changes affinity (?) because only want to store glucose if you have extra glucose around

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12
Q

Are all glucose transporters dependent on insulin?

A

No!

Insulin independent: liver, pancreatic beta cell, brain

Insulin dependent: muscle (GLUT4)

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13
Q

Gluconeogenesis

A

Oxaloacetate –> glucose

Happens in liver during first part of fast

If person fasted many days cells in kidney would do this too, but still liver also

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14
Q

What happens right after you eat?

A

Glucose in lumen of intestine is transported (active transport) into intestinal cells and into blood –> glucose stimulates beta cells in pancreas to secrete insulin –> insulin causes liver to stop releasing glucose into blood AND causes muscles to take up glucose from blood (via GLUT4)

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15
Q

What happens when you’re fasting?

A

Low glucose in blood and high glucagon (how?) –> glucagon stimulates liver to release glucose into blood –> now tissues have source of energy?

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16
Q

Where do we store our energy?

A

Liver: 70g of glycogen (24 hour supply)

Muscle: 120g of glycogen (not available for export as glucose)

Adipose: 15,000g fat (MAJOR store)

Muscle: 6,000g protein (not preferred to use though)

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17
Q

Energy consumption of brain

A

Major consumer of energy (uses 20% of body’s energy at rest)

Requires continuous supply of glucose

Can use ketone bodies in prolonged fast and when newborn baby

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18
Q

Energy consumption/storage of muscle

A

Needs to generate energy for contraction

Can use glucose of fatty acids

Stores glycogen

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19
Q

Energy storage of adipose tissue

A

Stores energy as fat (triglycerides) in fed state

Releases glycerol and fatty acids in fasting state

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20
Q

Energy consumption/storage of liver

A

“Altruistic organ” attends to own needs when glucose high (fed state)

Releases glucose into blood so other organs can get it when glucose is low (fasting state)

Note: kidney does similar thing as liver

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21
Q

What does the pancreas secrete?

A

Insulin and glucagon

(key regulators of metabolism)

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22
Q

Glycolysis

A

G6P –> pyruvate

8 steps, and 2 irreversible steps are regulated

Produces 2 molecules ATP per glucose oxidized

Anaerobic

Occurs in cytosol (then pyruvate transported to mitochondria for TCA cycle)

Regulation by allosteric effects and hormone signaling

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23
Q

Glycogen synthesis

A

G6P –> glycogen

(opposite of glycogenolysis)

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24
Q

Fast mechanisms to regulate glucose metabolism (immediate changes)

A

Substrate concentration

Allosteric regulation (feedback or feed forward)

Signals originating from hormone action (phorphorylation or translocation within cell)

Several of these mechanisms acting together

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25
Q

Slow mechanisms to regulate metabolism (long-term changes)

A

Genetic regulation

Response to diet and other environmental factors

Hormonal effects on gene expression

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26
Q

Km

A

Substrate concentration at which the reaction rate is half of Vmax

(lower Km means higher affinity; lower Km means slower rate of reaction)

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27
Q

Km’s of different glucose transporters

A

GLUT2: in the liver and pancreas beta cells, highest Km (lowest affinity); linear concentration in physiological range means will take up glucose proportional to how much in blood

GLUT1: mid-range Km

GLUT3: in the brain; lower Km (higher affinity) and flatter curve in physiological range means uptake in brain independent of plasma concentration (constant, steady supply of glucose to brain)

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28
Q

GLUT4 regulation by insulin

A

Insulin binds its receptor on cell surface –> signals through PI3 kinase, etc –> GLUT4 that exists in vesicles translocates to cell membrane –> lets glucose in

Whenno insulin (fasting state), GLUT4 transporters internalized again

(this happens in muscle and adipose tissue)

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29
Q

Once you get glucose into the cell, you have to phosphorylate it–how do you do this?

A

Glucokinase: high Km, glucose sensor, present in liver and pancreatic beta cells

Hexokinase: low Km, saturated at low glucose concentration, present in most cells

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30
Q

GK (glucokinase) lives in the nucleus, bound to GKRP (glucokinase regulatory protein), when does it come out of the nucleus?

A

When lots of glucose in cytoplasm (let in by GLUT2), GK comes out to phosphorylate it to G6P –> as glucose converted to G6P, MORE glucose enters cell –> as G6P then F6P builds up, F6P tells GK to go back to nucleus (negative feedback)

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31
Q

Can you regulate a step of a process (a reaction) that is reversible?

A

Apparently not…

Ex: 6 steps of glycolysis are reversible so are not regulated

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32
Q

Regulation/control points in glycolysis

A

1) Phosphofructokinase (PFK-1) (turns F6P –> F1,6BP); Stimulated by F2,6BP and AMP; Inhibited by ATP, citrate, H+
2) Pyruvate kinase (turns phosphoenolpyruvate (PEP)–> pyruvate); Stimulated by F1,6BP; Inhibited by ATP, alanine; last step in glycolysis

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33
Q

Why isn’t the “first” step of glycolysis, using hexokinase or glucokinase a control point of glycolysis?

A

Because end product G6P has many functions! Starts glycolysis but also glycogen synthesis, pentose phosphate pathway

PFK-1 (phosphofructokinase-1) catalyzes first unique and irreversible reaction in glycolysis so that is the first regulated step

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34
Q

What molecule regulates PFK-1?

A

F2,6BP activates PFK-1

F2,6BP is made by taking a little F6P from the chain and using PFK-2 (kinase activity) to phosphorylate it to F2,6BP

F2,6BP is not part of the pathway, it is created solely to be a regulating molecule

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35
Q

PFK-2/FBPase-2

A

Bifunctional enzyme that can be kinase (PFK2) or phosphatase (FBPase-2)

Kinase PFK2: F6P –> F2,6BP; when NOT phosphorylated; during fed state; increased insulin; stimulates PFK1 to do glycolysis

Phosphatase FBPase-2: F2,6BP –> F6P; when phosphorylated; during fasting state; increased glucagon; does NOT stimulate PFK1 so does gluconeogenesis

Want PFK2 NOT phosphorylated so it WILL phosphorylate F6P to make F2,6P to activate PFK1 to do glycolysis

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36
Q

How insulin stimulates glycolysis in the liver

A

Complicated pathway –> dephosphorylates PFK-2 –> high levels of F2,6BP –> activate PFK-1 to continue glycolysis –> more glycolysis!

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37
Q

How glucagon inhibits glycolysis in the liver

A

Glucagon binds cell surface glucagon receptor –> G-protein coupled response –> increased cAMP –> PKA –> PKA phosphorylates PFK-2 –> phosphatase activity increases –> lower levels of F2,6BP (so won’t stimlate PFK-1) –> inhibit glycolysis

38
Q

Epinephrine stimulates the heart via beta receptors and PKA, so what does this do to glycolysis?

A

Increased PKA phosphorylates an ISOFORM of the PFK-2 enzyme –> in this case, phosphorylation actually increases kinase activity of this bifunctional enzyme –> increased level of F2,6BP –> stimulate PFK-1 –> increased glycolysis

This is good because when HR up, maybe running from a lion and want to have glycolysis in that case!

Remember, muscle bifunctional enzyme works opposite way of liver bifunctional enzyme (if it worked like liver’s bifunctional enzyme, we’d get decreased glycolysis when running from lion–would be bad news!)

39
Q

Does skeletal muscle use a bifunctional (“PFK-2-like”) enzyme?

A

Yes, has a bifunctional enzyme but it is not phosphorylated by PKA

Skeletal muscle’s bifunctional enzyme is regulated only by levels of substrate (F6P)

40
Q

Pyruvate kinase

A

Turns phosphoenolpyruvate (PEP) –> pyruvate

Last step in glycolysis!

Inactivated by glucagon in the liver: glucagon binds receptor on cell membrane –> increase cAMP –> PKA –> PKA phosphorylates and thus inactivates pyruvate kinase

41
Q

Anaerobic metabolism

A

Pyruvate –> lactate (by lactate dehydrogenase) instead of going through TCA cycle

Cool side note: cancer cells do glycolysis then to lactate instead of TCA cycle even when there is O2 around and this can be used as a target for therapy

42
Q

Aerobic metabolism and pyruvate dehydrogenase (PDH)

A

After glycolysis, pyruvate –> acetyl CoA (by pyruvate dehydrogenase (PDH))

PDH is a multi-enzyme complex that is inhibited by NADH, acetyl CoA and ATP

PDH active when NOT phosphorylated (Ca2+ during muscle contraction stimulates phosphatase)

When phosphorylated, PDH inactive

43
Q

Regulation/control points of TCA cycle

A

1) Pyruvate dehydrogenase (PDH): turns pyruvate –> acetyl CoA; Inhibited by ATP, acetyl CoA, NADH; first step in TCA cycle
2) Isocitrate dehydrogenase: turns isocitrate –> alpha ketoglutarate; Stimulated by ADP; Inhibitied by ATP and NADH
3) alpha-ketoglutarate dehydrogenase: turns alpha-ketoglutarate –> succinyl CoA; Inhibited by ATP, succinyl CoA, NADH

44
Q

Why is there no phosphorylation/dephosphorylation regulation of the TCA cycle?

A

TCA cycle takes place in mitochondria and phosphorylation signals (via hormones) start on cell surface and go to cytosol!

Instead, TCA cycle regulated by immediate (NADH) and eventual (ATP) end products

(allosteric regulation)

45
Q

Is gluconeogenesis the reverse of glycolysis?

A

NO! Uses unique enzymes, and must go from pyruvate through oxaloacetate to get back to phosphoenolpyruvate

Also, requires 6 ATP (whereas glucose makes 2 ATP)

46
Q

Regulation/control points of gluconeogenesis

A

1) Phosphoenol-pyruvate carboxykinase (PEPCK): turns oxaloacetate –> phosphoenolpyruvate; Regulated by transcription (has very complex promoter), so more slowly; Tx decreased (activity inhibited) by insulin; Tx increased (activity stimulated) by fasting, glucagon, glucocorticoids, thyroid hormone
2) Fructose 1,6-bisphosphatase: turns fructose 1,6-bisphosphate –> F6P; Stimulated by citrate; Inhibited by F2,6BP, AMP
3) Glucose-6-phosphatase: turns G-6P –> glucose

47
Q

What step is the same but reversed in gluconeogenesis and glycolysis?

A

Fructose-6-phosphate <–> Fructose-1,6-bisphosphate

Citrate stimulates fructose 1,6-bisphosphatsase (to make F6P) and inhibits PFK-1

AMP and F2,6BP inhibit fructose 1,6-bisphosphatsase and stimulate PFK-1 (to make F1,6BP)

48
Q

How and where is G6P dephosphorylated to make glucose?

A

This happens in the liver and kidney in order to provide glucose to other tissues (cannot happen anywhere else, this is why the liver has to be nice/altruistic and give glucose to everyone!)

G-6-P enters the ER through G-6-P transporter –> SP is a Ca-binding stabilizing protein that stabilizes glucose-6-phosphatase enzyme –> glucose-6-phosphatase enzyme turns G6P to glucose –> Pi is transported out Pi transporter and glucose is transported out glucose transporter back into cytoplasm

49
Q

Van Gierke disease

A

Liver can’t produce glucose for the rest of the body and get severe hypoglycemia during fasting

Glucose-6-phosphate deficiency; glycogen storage disease (can either have messed up G6P transporter or messed up G-6-Pase)

Treatment: IV glucose (necessary for nighttime) or just can eat uncooked starch!

50
Q

What are the substrates for gluconeogenesis and where do they come from?

A

Alanine, lactate, glycerol (more?)

Come from peripheral tissues (muscle, RBCs, renal medulla, adipose tissue)

51
Q

How are glycogen synthesis and breakdown regulated regarding phosphorylation?

A

Glycogen –> glucose-1-phosphate (by glycogen phosphorylase-P)

UDP-glucose –> glycogen (by glycogen synthase)

Glycogen phosphorylase is active when phosphorylated

Glycogen synthase is active when NOT phosphorylated

Phosphorylation stimulated by glucagon and epi (during fasting state)

Dephosphorylation catalyzed by protein phosphatase 1 and stimulated by insulin (during fed state)

52
Q

What factors stimulate the synthesis of glycogen and the breakdown of glycogen?

A

Synthesis of glycogen (glycogenesis): G6P, ATP, glucose (in liver)

Breakdown of glycogen (glycogenolysis): Ca2+, AMP (in muscle)

(Makes sense because you want glucose (do glycogenolysis) only when you need it, not when you have plenty of G6P, ATP and glucose!)

53
Q

What is the rate-limiting step of fatty acid synthesis?

A

Lipogenesis

Acetyl CoA –> Malonyl CoA (by Acetyl CoA carboxylase)

Allosteric regulation of ACC: Acetyl CoA carboxylase exists in inactive dimers –> citrate stimulates formation into acetyl CoA carboxylase polymers (OR –> long-chain fatty acyl CoA inhibits formation into active polymer (just negative feedback??))

Regulation of ACC by hormones and phos/dephosphorylation: Insulin stimulates protein phosphatase to dephosphorylate acetyl CoA carboxylate and activate it; Glucagon and epi stimulate cAMP-dependent protein kinase to phosphorylate acetyl CoA carboxylate and inactivate it

Want to make fatty acids (which then you make into triglycerides to store) when you’ve just eaten

54
Q

Hormone sensitive lipase (HSL)

A

First enzyme of lipolysis (breaking down TGs to free fatty acids + glycerol so you can oxidize them to ketones and acetyl CoA to get more energy when you can’t do glycolysis!)

Glucagon binds receptor –> cAMP activates protein kinase that phosphorylates and activates HSL –> HSL turns fat (triglycerides) into fatty acids and glycerol

When glucose is low, glycerol is released into circulation and can be sent to liver and made back into glucose

Fatty acids released, bind to albumin and are taken up by tissues for activation to acyl CoA and then beta-oxidation (“fatty acid degradation”)

HSL active during fasting

Want to break down fat (triglycerides) into fatty acids and glycerol when fasting to give you more energy!

55
Q

What do glucagon and epinephrine do in general?

A

Phosphorylate enzymes!

Via cAMP and PKA

56
Q

What does insulin do in general?

A

Dephosphorylate enzymes!

Via protein phosphatase?

57
Q

Enzymes active in phosphorylated form

A

Phosphatase domain of PFK-2 (actually called FBPase2)

Glycogen phosphorylase

Hormone sensitive lipase

These are all phosphorylated by glucagon or epi, and are active during fasting (want to decrease glycolysis, break down glycogen (give glucose to rest of body?) and break down fat when fasting)

58
Q

Enzymes active in dephosphorylated form

A

Kinase domain of PFK-2

Pyruvate kinase

Glycogen synthase

Acetyl CoA carboxylase

These are all dephosphorylated by insulin (want to break down glucose (do glycolysis), synthesize glycogen and synthesize fat when fed)

59
Q

Glycogen storage disease

A

Defect in glycogen synthesis or breakdown

If can’t break down glycogen stored in liver, it accumulates and damages cells, can get enlarged liver

If can’t get glucose out into blood, get low blood sugar

60
Q

Which tissues have glucose-6-phosphatase?

A

Glucose-6-phosphatase converts G6P –> glucose

Liver (and kidney) ONLY produce glucose to send out to other tissues

Muscle does NOT have this enzyme so they can’t create their own glucose!

61
Q

Why do patients with liver failure get hypoglycemia?

A

Because liver can no longer put glucose into blood

(remember muscles can’t put glucose into blood)

62
Q

What can and cannot be converted to glucose?

A

Converted to glucose: lactate, amino acids, glycerol

Cannot be converted to glucose: fatty acids (bc chopped into 2 carbon chains and need 3 carbon chains to do gluconeogenesis)

63
Q

In Type 1 Diabetes, do all your beta cells get destroyed?

A

Eventually (I think), but at the beginning of the disease, some beta cells destroyed and others still surviving

64
Q

What is one reason we see Type 1 diabetes during teenage years?

A

Body is getting bigger, growing a lot but not much beta cell growth so don’t have enough insulin?

65
Q

C peptide

A

Used to distinguish between Type 1 and Type 2 Diabetes

C peptide connects the A and B chains of proinsulin and gets cleaved when insulin is formed, so level of C peptide tells you how much insulin you yourself are producing

Type 1 diabetes: low C peptide because not secreting much insulin on your own

Type 2 diabetes: high C peptide because when you secrete insulin you secrete same amt C peptide

66
Q

To test for Type 1 diabetes

A

C peptide: will be low

Anti-GAD antibodies or insulin autoantibodies: positive

67
Q

What does the liver do when there is no insulin around (Type 1 Diabetes)?

A

Insulin usually signals the liver to stop glycogenolysis, to stop gluconeogenesis, and to inhibit the release of glucose from the liver, but now insulin not there so liver puts out a ton of glucose into blood!

Lots of glycogenolysis so glycogen stores depleted

Lots of gluconeogenesis so lots of glucose made and dumped out into circulation

Lots of proteolysis and lipolysis to get more glucose made for rest of the body

68
Q

What do muscle cells do when there is no insulin around (Type 1 Diabetes)?

A

Insulin usually tells muscle cells to take up glucose from blood, but now no insulin around

Glucose can’t get into muscle cells because GLUT4 transporters not on cell surface –> cell deprived of energy –> Na/K ATPase pump fails with no ATP around –> K+ leaks out into blood –> K+ excreted in urine –> hypokalemia (whole body K+ depletion)

Also, muscle is broken down for energy since muscle can’t uptake glucose –> AAs used to make glucose instead and get negative nitrogen balance

Remember: Type 1 Diabetes used to be a WASTING disease

69
Q

What happens with the kidney when you have too much glucose in the blood?

A

Renal threshold is 180, and after this point, glucose cannot all be reabsorbed and is passed through kidney tubules with the rest of filtrate

Glucose in filtrate in loop of henle causes water and other ions to be secreted to maintain osmotic pressure

Lose water (polyuria thus polydipsia, dehydration), lose salts (NaCl, K), lose energy because losing glucose

70
Q

What happens to the beta cells that are still left in the pancreas in a patient with Type 1 Diabetes and thus high blood glucose?

A

Beta cells don’t function well in high glucose environment

So even if you have beta cells left, they won’t be secreting insulin well because glucose toxicity caused them to not function well

71
Q

What happens to the brain in a patient with high blood glucose (Type 1 Diabetes)?

A

Brain downregulates (to 10% of normal) glucose transporters to prevent glucose toxicity

Important when treating patient, because when you decrease blood glucose, brain thinks there’s not enough glucose around since it now has fewer transporters

72
Q

What happens to fat when you have no insulin (Type 1 Diabetes)?

A

Usually, insulin inhibits breakdown of triglycerides to free fatty acid and glycerol (lipolysis and ketogenesis)

Fat is all broken down into FFA and glycerol (lipolysis) –> also have no insulin, so presenting liver with lots of FFAs –> liver converts FFAs to ketones if no insulin around –> diabetic ketoacidosis

73
Q

What happens if you don’t treat Type 1 Diabetes?

A

Polyuria and polydipsia

Volume depletion (postural hypertension, tachycardia)

Loss of body fat and muscle (weight loss and muscle weakness)

Deep shallow breathing, breath of acetone (DKA)

Unexplained abdominal pain

Labs: high blood glucose, low bicarb (DKA, buffering acids), low pH, normal or high K+ even though hypokalemia

74
Q

How do we treat Type 1 Diabetes?

A

Give insulin!!

Now have insulin pumps, or shots that don’t hurt

Must test glucose level ~6 times per day

75
Q

How many people in the US have Type 2 Diabetes?

A

30,000,000

76
Q

What are some problems Type 2 Diabetes causes?

A

Most common cause of early death (heart attack, stroke), blindness, kidney disease, leg amputation

Greatest cost to health care system in USA

77
Q

Risk factors for Type 2 Diabetes

A

Genetics (Asian, AA, Latina, Pacific Islander, Native American)

Obesity (or any other cause of insulin resistance)

Low birth weight/fetal malnutrition

Sleep disturbance

78
Q

Relationship between BMI and insulin required per day

A

The fatter you are (higher BMI), the more insulin you need per day

Because fat people not very sensitive to insulin, so need a lot of it to suppress hepatic glucose release

79
Q

Why are obese people insulin resistant?

A

Have lots of adipocytes and these recruit inflammatory cells that release cytokines

Cytokines contribute to insulin resistance. Interleukins (ILs) oppose action of insulin

Note: because of this, can measure C-reactive protein (increased in inflammation) to predict risk for type 2 diabetes

80
Q

Why do you become insulin resistant when you’re pregnant?

A

Want baby to grow more than mother

Placenta makes hormones to tell glucose not to go to mother but to go to baby instead (placental lactogen)

81
Q

What happens to 80% of people who becomes insulin resistant?

A

They just increase insulin secretion to ensure that glucose is not released from liver too much and is taken up by muscles enough (don’t get diabetes even if they’re really obese)

Other 20% of those who become insulin resistant actually decrease insulin secretion (get Type 2 Diabetes)

82
Q

What causes glucagon levels to change?

A

We have baseline of glucagon in our blood (probably), but glucose suppresses glucagon so after we eat, glucagon decreases

83
Q

What levels of glucose, insulin and glucagon do we see in a type 2 diabetic after a meal?

A

High glucose

Low insulin

No drop in glucagon

84
Q

How do genetics and obesity combine to bring about Type 2 Diabetes?

A

If you have a hereditary component you’ll start losing beta cells early in life so can create less insulin. Then as you get older and/or more obese, you become insulin resistant and need more insulin. But you can’t make any more! Get Type 2 Diabetes.

85
Q

Treatment for Type 2 Diabetes

A

Education

Lifestyle (diet and exercise)

Insulin and other medications

Prevent complications

86
Q

Drug treatments for Type 2 Diabetes

A

Metformin: makes liver more sensitive to insulin (enhances how insulin causes liver to inhibit gluconeogenesis and glycogenolysis); causes people to lose weight; decreases risk of cancer

Sulphonylurea: lower blood sugar by making beta cells secrete more insulin

GLP-1: also lower blood sugar by making beta cells secrete more insulin (secrete this naturally from bowel when you eat); increases risk of pancreatic cancer

Glitazones: act on muscle to enhance how insulin causes muscle to bring glucose into muscle cell

Insulin

87
Q

How many people in the US have Type 1 Diabetes?

A

1,500,000 people (half as many as Type 2)

Not as heritable as Type 2, but more in caucasians

88
Q

Microvascular complications of diabetes

A

Tiny blood vessels exposed to high sugar causes damage to endothelium (glycosylation)

Diabetic nephropathy (renal failure)

Diabetic retinopathy (blindness)

Diabetic neuropathy (amputations, impotence, severe hypoglycemia)

89
Q

Macrovascular complications of diabetes

A

Coronary artery disease (MI)

Cerebrovascular disease (CVA/stroke)

Peripheral vascular disease (amputations)

90
Q

What is important to control in diabetics to prevent death and other disease?

A

Most diabetics die of cardiovascular disease (80%)!

Control cholesterol (use statins)

Control triglycerides

Use anti-platelet drugs to prevent clots (aspirin)

Keep BP low to prevent athreosclerotic complications

Keep blood sugar normal/low to prevent micro- and macro-vascular disease

Type 2 must lose weight–might even not need medications this way

91
Q

When someone is in diabetic ketoacidosis, you give insulin and this allows K+ to enter the cell–how?

A

Roundabout way!

Glucose enters the cell because insulin is around now –> glucose does glycolysis and TCA and electron transport to create ATP –> now have ATP for Na/K ATPase that wasn’t working before –> pump works to bring K+ into the cell

Note that you should still give K+ IV too!

Block 3: GI, Endocrine, Reproductive (30 decks)

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