Food Hormones Flashcards

1
Q

Cholecystokinin (CCK)

A
  • CCK is secreted in response to the presence of food in the duodenum:
  • It stimulates the gall bladder to release bile
  • It stimulates the pancreas to release
    pancreatic juice (digestive enzymes)
  • It delays gastric emptying
  • It acts on CCK receptors throughout the central nervous system (CNS) and in the satiety centres in the brain stem.
  • Meals rich in protein and fat stimulate CCK more than meals that just contain carbohydrates.
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2
Q

Insulin & Energy Storage

A
  • Insulin is released by the beta cells of the pancreas in response to elevated blood glucose.
  • Its role is to lower blood glucose by facilitating its storage predominantly in muscle tissue and the liver as glycogen.
  • It is also responsible for controlling the storage and the release of fatty acids in and out of adipose tissue. In fact, fat cannot be stored without insulin.
  • This is achieved via:
    1. The regulation of several lipase enzymes.
    2. The activation of glucose transport into the fat cells via recruitment of glucose transport protein 4 (GLUT4).
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3
Q

Metabolic Actions of Insulin

A
  • Stimulates synthesis of triglycerides
    from free fatty acids.
  • Inhibits release of free fatty acids from triglycerides.
  • Increases synthesis of liver glycogen, thereby increasing glucose uptake and storage.
  • Inhibits gluconeogenesis
  • Stimulates glucose uptake in skeletal muscle.
  • Reduces hunger via the hypothalamus.
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4
Q

Insulin Resistance Adipocytes

A
  • Chronic excess energy intake (combined with a sedentary lifestyle) leads to the body producing excessive amounts of insulin.
  • Increased insulin levels inhibit lipolysis the breakdown of fat from adipose tissue.
  • With insulin resistance, lipolysis is not inhibited leading to visceral fat deposition (also referred as “Central Adiposity”)
  • As visceral fat increases, adiponectin production decreases.
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5
Q

Central Adiposity

A
  • Central adiposity (excessive belly fat) is a typical feature of insulin resistance.
  • This type of adipose tissue can
    produce inflammatory cytokines including TNF-α and
    interleukin-6, raising the levels of systemic inflammation. This promotes further hormone resistance, obesity and chronic diseases.
  • Visceral fat supplies a constant source of excess free fatty acids (FFA) because lipolysis is not working properly.
  • The additional FFAs pass into the blood and to the liver.
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6
Q

Insulin Resistance Liver

A
  • Insulin Resistance is a major feature in Non-Alcoholic Fatty Liver Disease (NAFLD).
  • Normally, insulin sends two signals to the liver
    1 Stop making glucose i.e. inhibit gluconeogenesis.
    2. Store the available blood glucose
    as glycogen i.e. glycogenesis
  • However, in insulin resistance both of these processes respond poorly to the insulin signal putting patients at risk of chronically elevated glucose levels
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7
Q

Ghrelin & Appetite

A
  • Ghrelin is produced by the stomach cells when the stomach is empty to stimulate feeding behaviour and
    its secretion is suppressed after a meal.
  • Obese subjects have been found to have reduced post prandial ghrelin suppression.
  • Studies show ghrelin levels increase after weight loss this might explain why it is harder to keep weight off once you have lost it.
  • Dysregulated sleep and elevated cortisol levels are associated with increased ghrelin secretion whereas exercise has been shown to decrease ghrelin concentrations.
  • High protein meals (35% of calories) with moderate carbohydrates (45%) have been shown to be better for suppressing
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8
Q

Leptin & Appetite

A
  • Leptin is an adipokine produced by
    white adipose cells in proportion to
    overall body fat (Adiposity).
  • Increased adiposity = Increased leptin = Suppressed appetite.
  • However, whilst leptin levels are often
    elevated in overweight people , obesity
    promotes a number of inflammatory
    cellular processes that weaken leptin
    signalling leading to leptin resistance
    and its failure to suppress appetite
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9
Q

Leptin Resistance

A
  • Excess Leptin can modify insulin sensitivity, tissue metabolism, stress responses, and reproductive function
    all mediated via the hypothalamic pituitary axis.
  • Over time, these changes in metabolism produce abdominal weight gain in both men and women, as well as thigh and hip weight gain in females, chronic fatigue sleep problems, cardiovascular distress, and a host of other changes.
  • Additional adipose tissue then
    contributes further to leptin resistance (becoming a vicious cycle)
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10
Q

Increasing Leptin Sensitivity

A

Go Gluten Free: Wheat gluten has been shown to stop leptin binding to the leptin receptor.

Reduce sugar consumption: Especially
fructose as this has been shown to
induce leptin resistance.

Support gut flora with prebiotics: Some evidence to show that prebiotics can
improve leptin sensitivity.

Reduce Inflammation: Following an
anti inflammatory diet can contribute
to restoring leptin sensitivity.

Regular exercise: Shown to increase leptin sensitivity

Sleep hygiene: Poor sleep can adversely affect leptin sensitivity.

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