Metabolism - Insulin Flashcards

1
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).
    Insulin is sometimes called the Fat Storage Hormone.
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2
Q

Insulin & energy storage: Metabolic Actions of Insulin

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Metabolic Actions of Insulin:
* 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.
Gluconeogenesis = the biosynthesis of glucose from non-glucose precursors.

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3
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.
  • Central adiposity (excessive belly fat) is a typical feature of insulin resistance.
  • This type of adipose tissue can produce inflammatory cytokines including TNF-αand 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.
    Visceral Fat = fat deposits around the internal organs in the main cavities of the body, especially those in the abdomen.
    Adiponectin = an adipose-specific protein hormone that increases the oxidation of fatty acids, promotes the clearance of excess fat in tissues, and improves insulin sensitivity.
    Adipose Tissue acts as an ‘Endocrine Organ’ and is capable of producing hormones and cytokines.
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4
Q

Visceral Fat

A
  • Visceral Fat = fat deposits around the internal organs in the main cavities of the body, especially those in the abdomen.
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5
Q

Adiponectin

A
  • Adiponectin = an adipose-specific protein hormone that increases the oxidation of fatty acids, promotes the clearance of excess fat in tissues, and improves insulin sensitivity.
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6
Q

Adipose Tissue

A
  • Adipose Tissue acts as an ‘Endocrine Organ’ and is capable of producing hormones and cytokines.
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7
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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8
Q

A word about Fructose

A
  • Dietary intake of fructose in the form of high-fructose corn syrup (HFCS) has dramatically increased in the US in recent decades.
  • It is used to sweeten soft drinks, jams, all manner of sauces, cakes, cookies, and even bread.
  • The liver metabolises fructose differently than glucose - when glycogen stores are full, fructose is converted directly to liver fat.
  • Excess fructose intake is associated with NAFLD, obesity, hypertension, excess uric acid levels (associated with gout), and elevated Advanced Glycation End products (AGEs) linked with accelerated ageing and diabetes complications
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