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FHB Hormone/Repro > 81 - Metabolic homeostasis > Flashcards

81 - Metabolic homeostasis Flashcards

1
Q

Name some of the wasting states (stressors to the body).

A

Starvation, cancer, burns, trauma, severe infection, psychological, drug abuse

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2
Q

What are some of the consequences of the wasting states?

A
  • Proinflammatory cytokines
  • Activation of HPA axis
  • Dysregulation of growth hormone and IGF-I
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3
Q

How much glucose does the brain need per day?

A

180g

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4
Q

What state does starvation resemble?

A

Exercise

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5
Q

W/o starvation, how much protein is typically broken down per day?

A

About 300g

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6
Q

Describe energy sources during the initial stages of starvation vs. the late stages/prolonged fast.

A
  • Initial energy sources: 80% from fat stores, release of FFAs, breakdown of liver glycogen, breakdown of proteins.
  • Late stage energy sources: Metabolic switch- ketone bodies used as energy source for brain. Reduced reliance on glucose as fuel source. Protein breakdown continues (decrease to ~20g/day)
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7
Q

What hormone is responsible for the decrease in protein breakdown during prolonged fast, from 300g/day to 20g/day?

A

GH

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8
Q

How long can liver glycogen stores last?

A

2.5 days

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9
Q

For obesity, BMI =

A

More than 30

waist-hip ratio more important

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10
Q

For obesity, what’s the diagnostic waist/hip ratio for men and women?
What risk does it indicate?

A

Greater than 0.95 (men) or 0.85 (women)

- Indicates significant risk for cardiovascular disease and diabetes

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11
Q

What conditions must be present to be diagnosed w/metabolic syndrome?
(give the requirements for each of the 4)

A
  1. Visceral obesity – waist over 40” men, 35” women
  2. Insulin resistance – fasting glucose over 100 mg/dl
  3. Dyslipidemia – TGs over 150 mg/dl, HDL under 40 mg/dl
  4. Hypertension (BP over 135/80)
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12
Q

How does metabolic syndrome relate to DM dx?

A

Doesn’t mean you have T2DM, just increased risk

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13
Q

What is the primary hormone of white adipose tissue?

A

Leptin (of adipocytes)

“satiety hormone,” opposite of ghrelin

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14
Q

What 2 important things are produced by leptin?

A
  • Sterol regulatory binding protein 1C (SREBP-1C)

- PPARγ

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15
Q

What is SCREBP-1C activated by?

What are the 2 actions of SREBP-1C?

A

Lipids and insulin activate SREBP-1C

  • Promotes TG synthesis
  • Increases glucokinase “trapping” of glucose inside cells
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16
Q

What is PPARγ?

What does it regulate?

A
  • Nuclear steroid receptor (produced by leptin)
  • Regulates lipid uptake, TG storage and adipocyte differentiation (increases peripheral glucose uptake)
  • Induces differentiation of adipocytes (makes more fat cells, bad side effect)
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17
Q

How could PPARγ be taken advantage of clinically?

What are the names of these drugs?

A

PPARγ agonists used to treat insulin resistance and Type 2 diabetes mellitus
- Thiazolidinediones (TZD), (“Rosiglitazone = Avandia”)

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18
Q

What is an unwanted side effect of TZDs (PPARγ agonists)?

A

Weight gain (due to increased adipocyte differentiation and subsequent fat storage)

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19
Q

What is the relationship b/w leptin and total fat?

A

Linear (more leptin, more fat)

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20
Q

What 2 things does leptin inhibit to cause satiety?

A
  • Neuropeptide Y

- Agouti-Related Peptide (AGRP)

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21
Q

What 2 things does leptin stimulate to cause satiety?

A
  • αMSH – cleaved from POMC

- Cocaine-amphetamine regulated transcript (CART)

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22
Q

What happens to leptin KO mice?

In humans, does increasing leptin inhibit appetite?

A
  • Morbid obesity

- No (possible obesity-induced leptin resistance)

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23
Q

What is insulin resistance?
What happens to plasma glucose levels?
What happens to plasma insulin levels?
What happens to insulin receptors?

A
  • Insulin does not efficiently transport glucose into cells
  • Plasma glucose levels are high: saturating
  • Insulin levels are high
  • Hyperinsulinemia down-regulates insulin receptors
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24
Q

How long does DM take to develop? (read)

A

Gradual process: can take decades to develop into diabetes

- Over time pancreas reduces insulin output, leading to DM

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25
Q

What is T1DM?

What is T2DM?

A

In kids, autoimmune destruction of beta cells

Characterized by impaired beta cell function and insulin-resistance

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26
Q

What could cause conversion of T2DM to T1DM?

A

Beta cell depletion or “exhaustion” (over long period of time) will cause conversion from Type 2 to Type 1 diabetes.

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27
Q

Which type of DM is insulin-dependent?

A

Type 1

28
Q

In which state are the effects of high blood sugar reversible?

A

Pre-DM

- Once DM, irreversible due to beta cell disfunction and cell death

29
Q

What 2 proteins would be elevated in the blood w/obesity? (graphs)

A

Insulin + C peptide

30
Q

What are the 3 blood sugar tests for DM?

A
  1. HbA1C
  2. Fasting blood glucose (FPG)
  3. Oral glucose tolerance test (OGTT)
31
Q

What are the threshold levels for HbA1C, FPG, and OGTT?

A
  1. HbA1C greater than 48mMol/L or 6.5% (5.7-6.4% is pre-DM)
  2. FPG greater than 126mg/dL (100-125 is pre-DM)
  3. OGTT grater than 200 mg/dL (140-199 is pre-DM)
32
Q

Why is HbA1C the most preferable test and how does it work?

A
  • Measures average blood glucose concentrations over a longer period of time.
  • Avg. WBC life span = 120 days. Glucose increases the number of glycosylated RBCs.
  • Above 6.5% is DM (5.7-6.4% is pre-DM)
33
Q

How does the oral glucose tolerance test work?

A

8 hour fast; glucose measured before and 2h post consumption of 75g glucose.

  • Sometimes inacurate because people diet for week leading up to it
  • 140-199 mg/dL (pre-diabetes), 200+ T2DM
34
Q

What are the sx of T2DM? (3) (explain how each occurs)

A
  1. Polyphagia – excessive hunger due to inability of cells to utilize glucose: “cellular starvation”
  2. Polyuria – excess glucose in blood leads to increased plasma osmolarity, excessive water and sodium loss
  3. Polydipsia – excessive thirst due severe dehydration
35
Q

Which sx of T2DM occurs in DM but not diabetes insipidus?

A

Polyphagia

36
Q

What is the goal of treating T2DM?

A

Tight glycemic control

37
Q

What are the 3 classes of drugs you can use to treat T2DM?

A
  1. Sulfonylureas
  2. Biguanides
  3. Alpha-glucosidase inhibitors
38
Q

What are eg’s of sulfonylureas?

How do they work (1)?

A

“Glyburide,” “Glipizide”

- Close ATP-dependent K+ channels in beta cells causing insulin release

39
Q

What’s the eg of a biguanide?

How do they work (2)?

A

Metformin

  • Inhibits hepatic gluconeogenesis
  • Increases insulin receptor activity making cells more sensitive to insulin, increased glucose uptake
40
Q

What are eg’s of alpha-glucosidase inhibitors?

How do they work (1)?

A

“Precose,” “Glyset”

- Delays intestinal absorption of carbohydrates

41
Q

What are some proposed mechs of beta cell dysfunction? (just read)

A
  • Islet amyloid buildup
  • ER stress
  • Lipotoxicity
  • Oxidative stress
  • Glucose toxicity
  • Beta cell differentiation: reduced expression of key beta cell genes
  • Incretin hormone dysregulation
  • Islet inflammation
42
Q

What characterizes T1DM?

Onset?

A

Characterized by development of ketoacidosis in the absence of insulin therapy

  • Juvenile onset
  • Approx. 2-5% of all diabetes cases
43
Q

What is occurring during T1DM?

Is it insulin-dependent or not?

A

Destruction of pancreatic beta cells: insulin dependent

44
Q

How do you treat T1DM?

A

Insulin injections, close monitoring of blood glucose levels, diet

45
Q

How does DKA come about?

4 steps

A
  1. Decreased Insulin + increased counterregulatory hormones
  2. FFA release – hepatic precursor for ketone acids
  3. Metabolism of ketone bodies for energy results in increased blood acidity (H+)
  4. Diabetic coma: severe dehydration and acidosis
46
Q

While T1DM has an absolute insulin deficiency, T2DM has a ________ insulin deficiency.

A

Relative

- Therefore absent or minimal ketogenesis, in the presence of some insulin (T2DM)

47
Q

Both T1DM and T2DM stimulate the release of what counter-regulatory hormones to insulin?

A

Glucagon, GH, cortisol, catecholamines

48
Q

Increased counter-regulatory hormones, in the absence of insulin antagonism mobilizes energy stores and results in ______________.

A

Hyperglycemia

49
Q

How does mental status change w/increasing blood osmolality during DM?

A

Altert to drowsy to stupor to coma

50
Q

(just read, again)

When insulin is present:

A
  1. AA from protein stimulate GH which stimulates IGF-I (liver).
  2. IGF-I stimulates glucose uptake in muscle, proliferation of visceral organ tissues; inhibits proteolysis.
  3. GH opposes insulin lipogenesis.
51
Q

Describe the effects of metabolic hormones during the starvation state (read for now)

A
  1. Starvation
  2. No (undetectable) insulin
  3. Low glucose
  4. Catecholamines stimulate glucagon – nothing inhibits
  5. GH increases due to increased AA (proteolysis)
  6. No IGF-I (needs insulin), so no neg. feedback on GH
  7. Cortisol – stress: permissive effects on lipolysis, glycogenolysis
52
Q

Describe the effects of metabolic hormones during T1DM (read for now, contrast to other states)

A
  1. Type 1 DM
  2. No insulin
  3. HIGH glucose
  4. Catecholamines stimulate glucagon – nothing inhibits
  5. GH increases due to increased AA (proteolysis)
  6. No IGF-I (needs insulin), so no neg. feedback on GH
  7. Cortisol – stress: permissive effects on lipolysis, glycogenolysis
53
Q

Describe the effects of metabolic hormones during T2DM (read for now, contrast to other states)

A
  1. Type 2 DM
  2. RELATIVE insulin deficiency - some insulin, may not be effective
  3. HIGH glucose
  4. Catecholamines stimulate glucagon, insulin inhibits
  5. Cortisol – stress: permissive effects on lipolysis, glycogenolysis
  6. Insulin inhibits ketogenesis
54
Q

How do insulin levels vary b/w starvation, T1DM, and T2DM?

A
  • Starvation: no (detectable) insulin
  • T1DM: No insulin
  • T2DM: RELATIVE insulin deficiency
55
Q

Which of the following is GH not elevated in? Starvation, T1DM, or T2DM?
Explain.

A

T2DM (since some glucose is present, GH makes IGF-1, which can feed back to inhibit GH release)

56
Q

How do glucose levels vary b/w starvation, T1DM, and T2DM?

A
  • Starvation: low glucose
  • T1DM: high glucose
  • T2DM: high glucose
57
Q

Based on GWAS (genome-wide association studies), most genes affecting T2DM affect what cells?

A 
Beta cells (development, proliferation, survival, function)
- Some are linked to insulin signaling, glucose transport, or obesity.
58
Q

Most highly associated genetic polymorphism is in T2DM is what TS factor?
What pw’s is it associated w/?

A

Transcription factor 7-like 2 (TCF72)

- Wnt signaling pathway; coactivator of beta-catenin

59
Q

Islet neogenesis occurs during embryonic development. Beta cell replication continues during childhood/adolescence but is stable in adults.
What 3 important genes are associated w/T2DM?

A
  1. PDX-1
  2. TCF72
  3. Neurogenin 3
60
Q

In islet cell devo, what is PDX-1 important for?

A

Important for both islet neogenesis and beta cell proliferation.

61
Q

In islet cell devo, what is neurogenin 3 (NEUROG3) important for?

A

Key for endocrine cell development

62
Q

In T2DM, what are 2 possible causes of impaired beta cell differentiation during childhood?

A
  • Malnutrition

- Maternal factors during pregnancy

63
Q

In T2DM, what are two behaviors that are linked to increased propensity for insulin resistance?

A
  • High caloric diet

- Lack of physical activity

64
Q

In T2DM, is acquired organ dysfunction for glucose homeostasis reversible?

A

Yes

65
Q

In T2DM, hyperglycemic conditions result in disfunction of what organs?

A

Liver, adipose, pancreas

66
Q

In DM, what phase of insulin secretion is impaired?

A

Phase 1

67
Q

What type of drug is the new drug exenatide?

What is a dangerous side-effect?

A
  • GLP-1 agonist (incretin mimetics, ^ insulin)

- May cause pancreatic toxicity

FHB Hormone/Repro (16 decks)

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