Uploaded by Ja'Merica Dixon

Hormonal Regulation

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• Explain hormonal regulation of metabolic processes. (EOC 1.A, Level 1)
The 4 major tissues play a role in fuel metabolism. Those are the liver, adipose
tissue, muscles, and the brain. Insulin, glucagon, and catecholamines (E/NE) are
important for fuel metabolism. The hormones can be carried by the bloodsteam to
nearby cells or another organ. Insulin and glucagon are produced in the islet of
Langerhans of the pancreas.
Compare and contrast the roles of insulin and glucagon during the fed, basal, and
starvation states. (EOC 1.A, Level 1)
Insulin “ I just ate” – secreted in response to increased blood glucose levels,
promotes the storage of glucose, fat, and amino acids; stimulates the synthesis of
macromolecule breakdown
•
The actions of insulin and glucagon are opposing.
High blood glucose – insulin released – fat cells take in glucose – normal glucose level
Low blood glucose – glucagon – liver releases glucose to blood – normal glucose level
Fed State : Insulin dominates - increase of glycogen synthesis, fat synthesis, protein
synthesis, glucose oxidation
Insulin : Glucagon Ratio
Liver – High ; increases glucose uptake and glycolysis, increased glycogen synthesis,
increased fatty acid synthesis inhibits gluconeogenesis, glycogenolysis, ketogenesis,
lipolysis some G6P is used in the PPP to make NADPH , excess glucose and amino
acids are catabolized to acetyl coA
Muscle – High ; increase uptake of glucose by GLUT4, inhibits protein degradation
Muscles lack fatty acid synthase and G6Phophatase, excess G6P is used to replenish
glycogen stores
Adipose Tissue – Hight fuel needs for the brain are large and easily met during fed
state; depends on glucose as the main fuel during this state and enters through
GLUT1 that is insulin dependent the brain has no storage for glycogen or tag to be
used for energy and fatty acids cannot cross the blood brain barrier
2hrs post prandial , the blood glucose begins to drop this causes glucagon to be
secreted to switch from being anabolic to catabolic process ; gluconeogenesis is
stimulated and glycogenolysis is increased
4hrs postprandial more glucagon is released, more TAG is hydrolyzed and FA
become fuel for the muscle and liver
Fasted State : Glucagon dominates – increase glycogenolysis, gluconeogenesis,
ketogenesis
Insulin Glucagon Ratio Low
Liver - increases glycogenolysis , TAG breakdown, glycogen phosphorylase,
gluconeogenesis inhibits glycogen synthase
Muscle – responds to Epinephrine; muscle cells lack glucagon receptors cell get
energy from Boxidation of fatty acids from blood increased acetyl CoA inhibits
glycolysis lactate is released from the muscle and sent to the liver by
gluconeogenesis, glycogen stores are rapidly depleted
Adipose Tissue – glycerol is sent to the liver for gluconeogenesis , fatty acids are
released to the liver to under Boxidation to produce acetyl CoA needed for ketone
bodies HS lipase is activated to breakdown TAG
Brain – glucose is provided from the liver; ketone bodies can also be used as an
alternative source for fuel
•
Predict how alterations in metabolic processes can lead to disease.
Elevated levels of glycosylated proteins increase the risk of cardiovascular
disease, renal failure, and damage to small blood vessels and nerves. High
blood glucose levels is a warning sign for diabetes. Low fasting glucose levels
are warning signs for hypoglycemic conditions.
•
Compare and contrast the role of insulin and glucagon in the liver, muscle, adipose
tissue, and the brain.
Identify which hormone is predominant in fed, fasted, and starved state.
Insulin is predominant in the fed state, Glucagon is predominant in the fasted state
Describe the role of glucose transporters and identify which GLUT are insulin
dependent.
Glucose is taken into the cells and phosphorylated to trap it inside of the cells.
GLUT1 – brain, muscle, placenta, adipose tissue
GLUT2 – pancreatic b cells, liver, small intestine, renal proximal tubule
GLUT3 – neural small intestine
GLUT4 – muscle heart, adipose tissue insulin dependent
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Describe the metabolic alterations that occur in T1D and T2D.
Type I – fat breakdown is accelerated which leads to a high production of
ketone bodies. Some ketone bodies are acids which can lead to ketoacidosis.
Untreated diabetes leads to a dramatic weight loss. No insulin is produced
Glucagon has an unopposed action
Type II – 27% of population, high levels of free fatty acids, resistant to insulin
hyperglycemia increases glucose uptake
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