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Summary Behavioral Endocrinology

Course
- Behavioral Endocrinology
- Katja Teerds
- 2015 - 2016
- Wageningen University (Wageningen University, Wageningen)
- Dierwetenschappen
100 Flashcards & Notes
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A snapshot of the summary - Behavioral Endocrinology

  • College 10 deel 2

  • Explain the function of the pancreas in the short term regulation of energy expenditure.
    Pancreas
    • Exocrine function: produces digestive enzymes that are released in the small intestine
    • Endocrine function: produces hormones in Islets of Langerhans 

    Islets of Langerhans
    • Synthesis of e.g. insulin (b-cells) and glucagon (a-cells)
    • Storage of insulin/glucagon in granules
    • Released in blood via exocytosis
  • Explain the role of adipose tissue in the long term regulation of energy expenditure.
    Adipose tissue
    • Storage site for excessive energy (triglycerides)
    • Endocrine organ (e.g. leptin, adiponectin)


    BMI < 18 --> high insulin levels to convert all available glucose because cells 'cry' for glucose and energy. Therefore increased risk of insulin resistance, diabetes type 2 and cardiovascular disease. Same for BMI>25. Too much insulin enz...
  • Explain the effects of leptin in the long term regulation.
    Leptin
    • Produced by adipocytes
    • Levels are directly proportional to body fat mass
    • Binds to specific receptors (Ob Rb)
    • Transported into brain by active transport mechanism


    Effects
    :

    • Inhibits food intake, stimulates energy expenditure (via direct effect on hypothalamus)
    • Stimulates angiogenesis (formation of new blood vessels from pre-existing vessels), increases insulin sensitivity
    • Influences GnRH and LH/FSH secretion: very important role in onset of puberty especialy in females!!
    • In metabolic disorders --> leptin resistance
  • Explain the effects of adiponectin on the regulation of energy balance
    Adiponectin
    • Secreted by adipose tissue
    • Acts via specific receptors (AdipoR1/2)
    • Can cross the BBB to act in he brain
    Effects
    • Increases fatty acid oxidation and energy expenditure
    • Stimulates glucose uptake; inhibits glucose production
    • Levels are decreased in case of obesity and insulin resistance 
  • Explain how obesity causes insulin resistance
    Adiponectin:
    • Improves insulin sensitivity
    • Increases energy expenditure and inhibits food intake

    1. Obesity causes decreased adiponectin levels and effects, which decreases insulin sensitivity and thus increased insulin resistance.
    2. Insulin resistance causes hyperinsulinemia (excess insulin in the blood), which causes decreased adiponectin receptor expression, which causes adiponectin resistance and decreased adiponectin effects, which then again causes insulin resistance.
  • Explain the effects of insulin resistance
    Insulin resistance means that the cells no longer respond normally to insulin. They do not take up enough glucose.
    1. The liver produces glucose from glycogen stores and is slow to replenish glycogen
    2. In skeletal muscle there is a decrease in glycogen storage and use of glucose
    • Glucose remains in the blood and blood glucose levels rise
    1. In adipose tissue, fat is broken down to be used as an energy source
    • Increase in fatty acids; because some insulin is present, normal fatty acid metabolism can occur and no ketones are produced
  • What mechanisms have an effect on the short term energy regulation?
    • Initiation and termination of meals: GI hormones like CCK, GLP-1, ghrelin
    • Acute handling of nutrients: pancreas hormones insulin, glucagon
  • What mechanisms have an effect on the long term energy regulation?
    • Status of energy stores: adipose tissue hormones leptin and adiponectin
    • Thyroid hormones T3/T4
  • Explain glucose and insulin levels of the different stages of diabetes (II).
    Glucose:
    • Normal: low with a slight arch in the first 30 minutes
    • Prediabetic: arch is higher, but in the end it comes down to about the same level as normal
    • Type 2 less severe: arch is even higher, end value also higher than normal
    • Type 2 more severe: highest arch, doesn't recover, stays high.

    Insulin:
    • Normal: steep increase followed by gradual decrease to starting levels
    • Prediabetic: MUCH higher increase followed by steep decrease.
    • Type 2 less severe: increase is more gradual and slower. stays higher than initial value
    • Type 2 more severe: no increase in insulin
  • Explain the effects of insulin resistance in muscle, liver and adipose tissue
    1. Muscle - reduced glucose uptake --> reduced energy availability
    2. Liver - reduced glucose uptake -->
      . reduced energy storage (glycogenesis)
      . reduced suppression glucose production
    3. Adipose tissue - reduced glucose and free fatty acid uptake --> reduced suppression of lipolysis


    !! 1 and 2 happen first, therefore all glucose is initially diverted to 3 ==> obesity.
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