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81 - Metabolic homeostasis Flashcards

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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
What is T1DM? What is T2DM?
In kids, autoimmune destruction of beta cells Characterized by impaired beta cell function and insulin-resistance
26
What could cause conversion of T2DM to T1DM?
Beta cell depletion or “exhaustion” (over long period of time) will cause conversion from Type 2 to Type 1 diabetes.
27
Which type of DM is insulin-dependent?
Type 1
28
In which state are the effects of high blood sugar reversible?
Pre-DM | - Once DM, irreversible due to beta cell disfunction and cell death
29
What 2 proteins would be elevated in the blood w/obesity? (graphs)
Insulin + C peptide
30
What are the 3 blood sugar tests for DM?
1. HbA1C 2. Fasting blood glucose (FPG) 3. Oral glucose tolerance test (OGTT)
31
What are the threshold levels for HbA1C, FPG, and OGTT?
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
Why is HbA1C the most preferable test and how does it work?
- 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
How does the oral glucose tolerance test work?
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
What are the sx of T2DM? (3) (explain how each occurs)
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
Which sx of T2DM occurs in DM but not diabetes insipidus?
Polyphagia
36
What is the goal of treating T2DM?
Tight glycemic control
37
What are the 3 classes of drugs you can use to treat T2DM?
1. Sulfonylureas 2. Biguanides 3. Alpha-glucosidase inhibitors
38
What are eg's of sulfonylureas? | How do they work (1)?
“Glyburide,” “Glipizide” | - Close ATP-dependent K+ channels in beta cells causing insulin release
39
What's the eg of a biguanide? | How do they work (2)?
Metformin - Inhibits hepatic gluconeogenesis - Increases insulin receptor activity making cells more sensitive to insulin, increased glucose uptake
40
What are eg's of alpha-glucosidase inhibitors? | How do they work (1)?
“Precose,” “Glyset” | - Delays intestinal absorption of carbohydrates
41
What are some proposed mechs of beta cell dysfunction? (just read)
- 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
What characterizes T1DM? | Onset?
Characterized by development of ketoacidosis in the absence of insulin therapy - Juvenile onset - Approx. 2-5% of all diabetes cases
43
What is occurring during T1DM? | Is it insulin-dependent or not?
Destruction of pancreatic beta cells: insulin dependent
44
How do you treat T1DM?
Insulin injections, close monitoring of blood glucose levels, diet
45
How does DKA come about? | 4 steps
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
While T1DM has an absolute insulin deficiency, T2DM has a ________ insulin deficiency.
Relative | - Therefore absent or minimal ketogenesis, in the presence of some insulin (T2DM)
47
Both T1DM and T2DM stimulate the release of what counter-regulatory hormones to insulin?
Glucagon, GH, cortisol, catecholamines
48
Increased counter-regulatory hormones, in the absence of insulin antagonism mobilizes energy stores and results in ______________.
Hyperglycemia
49
How does mental status change w/increasing blood osmolality during DM?
Altert to drowsy to stupor to coma
50
(just read, again) | When insulin is present:
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
Describe the effects of metabolic hormones during the starvation state (read for now)
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
Describe the effects of metabolic hormones during T1DM (read for now, contrast to other states)
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
Describe the effects of metabolic hormones during T2DM (read for now, contrast to other states)
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
How do insulin levels vary b/w starvation, T1DM, and T2DM?
- Starvation: no (detectable) insulin - T1DM: No insulin - T2DM: RELATIVE insulin deficiency
55
Which of the following is GH not elevated in? Starvation, T1DM, or T2DM? Explain.
T2DM (since some glucose is present, GH makes IGF-1, which can feed back to inhibit GH release)
56
How do glucose levels vary b/w starvation, T1DM, and T2DM?
- Starvation: low glucose - T1DM: high glucose - T2DM: high glucose
57
Based on GWAS (genome-wide association studies), most genes affecting T2DM affect what cells?
``` Beta cells (development, proliferation, survival, function) - Some are linked to insulin signaling, glucose transport, or obesity. ```
58
Most highly associated genetic polymorphism is in T2DM is what TS factor? What pw's is it associated w/?
Transcription factor 7-like 2 (TCF72) | - Wnt signaling pathway; coactivator of beta-catenin
59
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?
1. PDX-1 2. TCF72 3. Neurogenin 3
60
In islet cell devo, what is PDX-1 important for?
Important for both islet neogenesis and beta cell proliferation.
61
In islet cell devo, what is neurogenin 3 (NEUROG3) important for?
Key for endocrine cell development
62
In T2DM, what are 2 possible causes of impaired beta cell differentiation during childhood?
- Malnutrition | - Maternal factors during pregnancy
63
In T2DM, what are two behaviors that are linked to increased propensity for insulin resistance?
- High caloric diet | - Lack of physical activity
64
In T2DM, is acquired organ dysfunction for glucose homeostasis reversible?
Yes
65
In T2DM, hyperglycemic conditions result in disfunction of what organs?
Liver, adipose, pancreas
66
In DM, what phase of insulin secretion is impaired?
Phase 1
67
What type of drug is the new drug exenatide? | What is a dangerous side-effect?
- GLP-1 agonist (incretin mimetics, ^ insulin) | - May cause pancreatic toxicity

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