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GI GU Repro > Blood Glucose Homeostasis & Concept of Glucose Tolerance > Flashcards

Blood Glucose Homeostasis & Concept of Glucose Tolerance Flashcards

1
Q

Incretins […] insulin’s effects

A

Augment

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2
Q

What effect does exercise have on skeletal muscle?

A

Insulin-dependent increase in # GLUT4 transporters –> increased glucose entry. The effect can persist for hours after exercise and if a person exercises regularly the result can be prolonged improvement in insulin sensitivity.

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3
Q

What advice do you have to give to diabetic patients who want to exercise?

A

Because insulin makes muscle more sensitive to its effects, exercise will cause muscle to respond more to insulin and take in more glucose from the blood. As a result, diabetics should to reduce their insulin levels or take in extra calories prior to exercise to prevent becoming hypoglycemic due to the increased response to insulin that will result with exercise.

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4
Q

Insulin […] hormone sensitive lipase in white fat.

A

Inhibits

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5
Q

What hormones stimulate HSL in white fat?

A

Glucagon

Catecholamines

GH

Cortisol

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6
Q

What are some of the bodily processes that white fat is involved in?

A
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7
Q

How is adiponectin related to fat mass?

A

Inversely proportional –> high adiponectin = low body fat

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8
Q

What factors reduce adiponectin?

A

Pro-inflammatory cytokines (TNF-alpha, secreted by fat)

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9
Q

Low adiponectin puts one at risk for what diseases?

A

T2DM, Metabolic syndrome, Insulin resistance, coronary artery disease

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10
Q

What does adiponectin do to glucose levels in blood and insulin?

A

Reduce blood glu

Increase insulin sensitivity via increased FA oxidation and inhibition of hepatic gluconeogenesis

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11
Q

What is a normal fasting plasma glucose range?

A

60 - 100 mg/dL

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12
Q

Plasma glucose must be > […] to see glycosuria

A

180mg / dL

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13
Q

Why is it bad for plasma glucose to be too low?

To be too high?

A
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14
Q

Oral Glucose Tolerance Test

  • What does this test measure?
  • What are the indications for doing the test?
  • How do you peform this test?
A
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15
Q

In a normal person, renal threshold for glucose is around 180 mg/dL. How does this change in someone who is:

  • Pregnant
  • Elderly
A
  • Lower in pregnant women
  • Higher in eldergy

RTG has to do with SGLT2 transporter. In elderly for example, transporter may be less efficient or may be less of them in membrane. This results in higher levels of glu needed in blood to see entry of glu into urine.

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16
Q

Insulin resistance is almost always associated with […]

A

Hyper-insulinemia

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17
Q

What is believed to be the mechanism of insulin receptor resistance?

A

Down regulation of insulin receptors in response to hyper-insulinemia

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18
Q

Describe how the plasma glucose and plasma insulin levels would look in:

  • Normal person
  • Pre-diabetic person
  • Type 2 diabetic person
A
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19
Q

What is pre-diabetes?

A

Prediabetes is the stage before the onset of T2D. It is usually 5 - 10 years before T2D onset and it is characterized as a mildly hyperglycemic state which serves as a marker of patients at risk for developing T2D. Patients who are prediabetic exhibit impaired glucose tolerance (increased glucose levels 2 hours after meal), impaired fasting plasma glucose (increased fasting glucose levels), increased HbA1c (indication of glucose levels over time).

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20
Q

What are the 3 predominant mechanisms underlying insulin resistance in type 2 diabetes suggested by research?

A

1) Lipid burden hypothesis that causes a dysfunction of adipose tissue 2) Inflammatory response that causes a dysfunction of adipose tissue 3) Dysfunction of mitochondria in liver and muscle

21
Q

What are the 3 predominant mechanisms underlying impaired insulin secretion in the pancreas / beta cell failure?

A

1) Pyruvate cycling 2) ER stress 3) Amyloid fibrils

22
Q

Describe the lipid burden hypothesis.

A

In obesity, the capacity of adipocytes to store TAGs is decreased and adipocytes become less sensitive to insulin which leads to adipocyte dysfunction. Expression of PPAR gamma is decreased in adipose tissue and increased in muscle and liver, which leads to increased storage of lipids in liver and muscle and decreased storage in adipose tissue.

23
Q

Describe the role that inflammation has in leading to adipose dysfunction.

A

In the overweight state, adipocytes increase in size due to increased TAG storage. This results in increased expression of TAG storage enzymes. Continual overloading of the adipose tissue results in increased burden on the adipose tissue. This results in release of MCP-1, which attracts macrophages which release TNF alpha and other cytokines that cause inflammation. This inflammation decreases insulin signaling and leads to impaired TAG storage, resulting in increased lipolysis and increased circulating FAs. This, combined with increased expression of PPAR gamma, leads to increased accumulation of lipid in the liver and muscle and this accumulation interferes with GLUT4 function leading to insulin resistance.

24
Q

What are the consequences of FA accumulation in the liver and how does this lead to insulin resistance?

A

Overnutrition leads to increased [FA] and increased [glucose] from the diet. Increased dietary FA results in increased uptake of FA in the liver. Increased glucose means that there is more glucose than is needed to meet cellular energy demands and so it is used for FA synthesis. This results in increased [malonyl coA] which inhibits beta oxidation in the liver resulting in increased TAG synthesis and increased accumulation of fatty acid metabolites such as diacylglyerol and ceremide. These metabolites activate stress induced kinases which inhibit insulin signaling and lead to insulin resistance.

25
Q

What are the consequences of FA accumulation in muscle and how does it lead to insulin resistance?

A

In muscle, over nutrition leads to increased FA being taken up in muscle from diet. Unlike the liver, this FA can be oxidized because the muscle cannot use the excess glucose to make FAs. So any increase in FAs results in increased FA oxidation. This increased demand for oxidation results in overload of the mitochondria such that the rate of beta oxidation surpasses that of the CAC and ETC. This high demand surpasses the capabilities of the mitochondria leading to incomplete oxidation products, such as acylcarnitines and reactive oxygen species. These byproducts activate stress induced kinases, which inhibit insulin signaling and decrease the [GLUT4] in the membrane of the cell leading to hyperglycemia.

26
Q

Describe the role that pyruvate cycling plays in a NORMAL BETA CELL.

A

Pyruvate can also be converted to OAA by pyruvate carboxylase (PC) in the mitochondria. Increased [OAA] produces increased intermediates of CAC. Some of these intermediates (malate, citrate) can exit the mitochondria into the cytosol via transporters. Once in cytosol, they can enter pathways that produce NADPH, alpha ketoglutarate, and GTP, which will result in amplification of insulin signaling, leading to increased insulin secretion.

27
Q

Describe the role that pyruvate cycling plays in a DYSFUNCTIONAL BETA CELL.

A

Overnutrition leads to increased FA uptake in beta cells as well as increased glucose uptake. Increased FA uptake results in increased FA oxidation producing lots of acetyl coA. Increased glucose uptake also results in increased glycolysis and production of acetyl coA. Build up of AcoA inhibits PDH and activates PC, converting pyruvate to OAA instead of AcoA. Increased [OAA] results in increased flux of pyruvate cycling, leading to hyper secretion of insulin that is independent of energy state (amount of ATP). Overtime, hyper secretion of insulin leads to decrease in responsiveness of beta cell to glucose and decrease in insulin release.

28
Q

Describe how ER stress plays a role in Beta cell dysfunction / reduced insulin secretion.

A

Insulin is a protein that folds in the ER. In over nutrition/T2D there is increased production of insulin. This means that the ER is overloaded with the amount of insulin protein it is processing. This chronic increase in workload due to increased demand leads to ER stress and protein misfiling, which stresses the cell and leads to apoptosis.

29
Q

IN NORMAL BETA CELLS, what is the role of amylin?

A

Amylin is co-secreted with insulin (in lower [conc.]). It slows gastric emptying (slows time nutrients and glucose are being absorbed by intestines to blood, keeping blood sugar levels from spiking), suppresses glucagon release, and suppresses appetite.

30
Q

IN DYSFUNCTIONAL BETA CELLS, what is the role of amylin?

A

In a state of insulin hyper secretion (early T2D), amylin is also co-secreted in elevated amounts. Amylin is a protein that tends to “clump” together into aggregates, so increased secretion of amylin increases amylin aggregate formation. Large clumps of amylin in the cell overload cellular machinery and lead to cell dysfunction and potential apoptosis.

31
Q

Weight Loss 1) Effect on adipose tissue? 2) Effect of treatment wrt lipid burden hypothesis? 3) Increases capacity for ___ ___ 4) Effect on insulin sensitivity

A

1) Decreased TAG content 2) Decreases lipid burden 3) TAG storage in adipose 4) Restores insulin sensitivity

32
Q

Exercise 1) What molecule is the target of exercise? 2) Effect on FA and cholesterol synthesis 3) ___ FA oxidation 4) ___ Glucose uptake 5) ___ gluconeogenesis

A

1) Activating AMPK (activated by increased [AMP]/[ATP], turns on catabolic pathways) 2) Decreases 3) Increases 4) Increases 5) Decreases

33
Q

How do sulfonylureas function to treat T2D? What are their limitations?

A

Sulfonylureas inhibit K+ channels that are ATP sensitive. This leads to accumulation of K+ inside the cell, leading to depolarization and insulin release. These drugs are more beneficial in late stage T2D when the patient has lost beta cell function and is lacking insulin secretion. They are completely ineffective if the patient is insulin resistant at the insulin receptor level.

34
Q

How do GLP-1 analogues function to treat T2D?

A

Endogenous GLP-1 is released from the intestines and it functions to increase insulin release. However endogenous GLP-1 has a very short half life, so it is quickly broken down. The analogue is able to resist degradation for a while longer to exert its effects.

35
Q

What effects does GLP-1 have on the brain?

A

Increased neuroprotection Decreased appetite

36
Q

What effects does GLP-1 have on the stomach?

A

Slows gastric emptying

37
Q

What effect does GLP-1 have on the pancreas?

A

Increases insulin secretion Increases beta cell neogenesis Decreases beta cell apoptosis Decreases glucagon secretion

38
Q

What effect does GLP-1 have on the muscle?

A

Increases glucose uptake

39
Q

What effect does GLP-1 have on the liver?

A

Decreases gluconeogenesis

40
Q

Biguanides (Metformin) 1) Through what protein does it work? 2) Effect on glucose metabolism in liver? 3) Effect on glucose uptake in muscle and adipose tissue? 4) Effect on lipid synthesis?

A

1) Metformin activates AMPK which in turn activates catabolic pathways and reduces flux through anabolic pathways. 2) Metformin also reduces hepatic glucose production by inhibiting gluconeogenesis. 3) It increases glucose uptake in skeletal muscle and adipocytes 4) It decreases lipid synthesis thus decreasing lipid burden.

41
Q

Thiazolidinediones 1) Through what protein does it work? 2) Effect on muscle and liver? 3) Effect on genes? 4) Effect of fat stores?

A

1) Activates PPAR gamme in adipose tissue 2) Increases insulin sensitivity 3) Effects transcription of genes involved in glucose/lipid metabolism and energy balance 4) Shifts fat storage from visceral to subcutaneous

42
Q

How do α-glucosidase inhibitors function to treat T2D?

A

In the small intestines, α-glucosidase is an enzyme that hydrolyzes polysaccharides into glucose monomers. Inhibitors of this enzyme reduce the digestion of polysaccharides from the diet and therefore reduce their absorption into circulation.

43
Q

Why is carrying a lot of fat around the waist (apple shape) particularly bad?

A

Associated with higher risk of CV related illnesses

44
Q

Metabolic Syndrome

  • Signs/symptoms
  • Consequences
  • When do you make dx?
A
  • See slide
  • See slide
  • Make dx when pt had 3 of following:
    • High abdominal waist circumference
    • Hyper-triglyceridemia
    • Low HDL
    • HTN
    • Hyperglycemia
45
Q

What is diabetes?

A

Disorder characterized by impaired CHO, fat and AA metabolism

46
Q

What are the clinical signs/symptoms of diabetes?

A

Polyuria

Polydipsia

Hyperglycemia

Ketonuria

Ketoacidosis

Weight loss (sudden, rapid)

Polyphagia

47
Q

What are the chronic macro and microvascular complications of diabetes?

A
48
Q

What is hypoglycemia?

Why is it so dangerous?

What can cause it?

How would a person present if they are hypoglycemic?

How do dx and treat?

A

GI GU Repro (58 decks)

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