Module 6: Diabetes and Obesity Flashcards

1
Q

What is Type 1 diabetes

symptom, causes, diagnosis

A
  • 10% of diabetic cases
  • complete lack of insulin (body does not produce it)
  • Autoimmune disorder: immune system attacks and destroys pancreatic ß cells
  • Needs: environmental stimulus (infection) & genetic determinant (that allows ß cells to be targeted)
  • Symptoms appear when 80-90% of ß cells are destroyed (during childhood/puberty)
    3 main symptoms:
  • polyuria (frequent urination), polydipsia (excessive thirst), polyphagia (excessive hunger)
  • fatigue, weight loss, weakness
    Diagnosis
  • fasting blood glucose, FBG ≥ 126 mg/dl (normal is 70-99)
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2
Q

Describe the metabolic effect of type 1 diabetes: Hyperglycemia and ketoacidosis

A
  1. Hyperglycemia and ketoacidosis
    - liver increases glucose production, while muscle and adipose take up less glucose
    - Liver increases gluconeogenesis regardless if there’s glucose present
    - increased mobilization of FAs from adipose, increased oxidation of FAs in liver & increased ketone body synthesis
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3
Q

Describe the metabolic effect of type 1 diabetes: hypertriacylglyceridemia

A
  • high lvls of triacylglycerides in blood
  • liver cant dispose all FAs so they’re packaged as VLDL
  • chylomicrons and VLDL in plasma increase due to decrease in lipoprotein lipase activity
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4
Q

What is the treatment of type 1 diabetes?

A
  • patients rely on exogenous insulin (injections)
    Standard insulin treatment: 1-2 injections/ day
    Intensive insulin treatment: 1+ daily injections
  • frequent monitoring of blood glucose
  • decrease complications 60% but more difficult to monitor
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5
Q

How can hypoglycemia occur in type 1 diabetes?

A

When too much insulin is administired during insulin therapy

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6
Q

What is type 2 diabetes?

symptoms, causes, diagnosis

A
  • most common (90% of cases)
  • strong genetic contribution
  • results from:
    1. insulin resistance: insulin is present but cells (in liver, adipose, and muscles) aren’t responding to its presence (caused by obesity)
    2. Non-functional ß cells: inability to keep up with demand to produce insulin; if normal, ß-cells can increase amount of insulin
    Diagnosis & symptoms
  • develops gradually some experience polyuria, polydipsia, polyphagia
  • diagnosis based on hyperglycemia: blood glucose conc > 126 mg/dl
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7
Q

What is insulin resistance? What are the causes?

A
  • liver, adipose, and muscle cells can’t respond to normal insulin levels
  • signalling cascade not happening in response to insulin lvls
  • results uncontrolled production of glucose in liver and decreased glucose uptake by muscles and adipods
  • causes obesity
  • insulin resistance increases with weight gain
  • Changes in adipose secretions in obesity leads to insulin resistance
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8
Q

How is hyperglycemia associated with type 2 diabetes?

metabolic changes in type 2 causes….

A

increased production of liver glucose + decreased tissue usage of glucose
- ketosis is minimal: presence of insulin lowers ketogenesis

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9
Q

How is hypertriacylglycerolemia associated with type 2 diabetes?

metabolic changes in type 2 causes….

A

low lipoprotein breakdown in adipose due to low levels of lipoprotein lipase leads to elevated TAG in blood

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10
Q

Treatment for type 2 diabetes

A

modification of diet, weight loss, exercise, hypoglycemic drugs

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11
Q

What is the fed state?

A
  • 2-4 hours after a meal
  • anabolic period
  • insulin predominant hormone
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12
Q

What is the fasted state?

A
  • 4 hours after food has been injested
  • focus is maintaining blood glucose for brain
  • catabolic period
  • glucagon is predominant hormone
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13
Q

What is obesity? What is it caused by?

A

A complex disorder of body weight regulatory systems
(excess body fat)
- increase in cell size (hypertrophy) and cell number (hyperplasia)

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14
Q

What are the 2 types of body shapes/fat depots? Describe both.

A
  1. upper body obesity: apple-shaped
    - fat around central abdomen
    - higher risk of health defects
    - associated with high BP, insulin resistance, diabetes, heart disease
  2. Lower body: pear-shaped
    - 80-90% fat stores in subcutaneous depots in abdominal region
    - 10-20% stored in visceral depots within abdominal cavity
    - more biochemically active
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15
Q

True or False: Subcutaneous adipocytes in lower body are larger, very efficient TAG stores

A

True

more common in women

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16
Q

True or False: Abdominal fat cells have a higher rate of fat turnover and are more responsive to hormones

A

True

more common in men

17
Q

What signals regulate body weight?

A
  • Incoming (afferent) signals promote response from hypothalamus (efferent signals): influences appetite
  • leptin levels communicate with brain about body fat
  • Insulin acts on neurons to dampen appetite
18
Q

What role do the signals regulating body weight play in obesity development?

A
  • When leptin levels are increased, this means there’s an increase in fat so, appetite is supressed
  • leptin is synthesized in proportion to body fat levels
19
Q

What metabolic changes occur during obesity?

A

Increased mass of adipocytues results in:
1. metabolic syndrome: abdominal obesity associated with insulin resistance, dyslipidemia, and high BP
- increased risk of type 2 diabetes
2. Dyslipidemia: abnormal accumulation of lipids in the blood
- HDL cholesterol decreases
- TAG and LDL increases

20
Q

What is metabolic syndrome (MetS)?

A

cluster of conditions that lead to disease state.
- Requires lifestyle changes: weight loss, exercise, medication