Metabolism Quiz

Energy Out

Mainly Basal Metabolic Rate, Some physical activity, some thermoregulation; Oxidation/Reduction

Energy In

Absorption

Arcuate Nucleus

Orexogenic Neurons and Anerexogenic Neurons

Orexeogenic Neurons

Respond to Gherlin and inhibit satiety (think oral- food)

Anerexogenic Neurons

Activation stimulates paraventricular nerves in the hypothalamus which promote satiety (think anorexic - no food)

Ghrelin

Secreted by the stomach; Suppresses leptin; Stimulates NPY (stress can also increase NPY)

Lipostatic Theory

Metabolism of the body is altered based on the amount of fat present (not true)

Leptin

Shuts off orexogenic nerves to promote satiety; Released from fat cells; People born without leptin are predisposed to obesity but can receive treatment (no effect if you already have leptin)

Glucostatic Theory

Metabolism adjusts based on the body’s glucose levels

Gluconeogenesis

Formation of glucose from non-carb sources

Fed State

Absorptive; Anabolic; Hyperglycemia; HSL in adipose tissue is activated and triglycerides are broken down into free fatty acids and glycerol; free fatty acids undergo beta oxidation; glycerol is picked up by the liver to undergo gluconeogenesis

Fasting State

Post-Absorptive; Catabolic; Hypoglycemia; Glucose drops and glycogen stores are accessed; Liver and skeletal muscle use glycogen phosphorylase to break down glucose; G-6 phosphate in the liver produces glucose

Energy Sources

Glycogen is easy to make and good source of short-term energy; Triglycerides need less water to be stored, but are harder to form/access

Too Much Glucose

Glycogen is formed and stored in skeletal muscle and liver (places with glycogen synthase)

Too Little Glucose

Glycogen broken down into Glycogen Phosphorylase; Glucose-6 Phosphatase removes phosphate in skeletal muscle to form Glucose

Protein Energy

Not stored (use it or lose it); Amino acids are either used to make proteins or are broken down for gluconeogenesis

Beta Oxidation

Using free fatty acids as fuel (most cells do this)

Fat Energy

Excess glucose in the body leads to lipogenesis which produces triglycerides; Triglycerides in the blood can be stored in adipose tissue; LPL digest triglycerides, the free fatty acids cross the membrane, triglycerides are stored, and broken down by HSL

HSL

Hormone Sensitive Lipase converts triglycerides to glycerol and fatty acids; Glycerol is converted to glucose by the liver; Fatty acids are beta oxidized

Chylomicrons

Absorbed in lymphatic system and travel through circulation before entering blood; Made up of cholesterol, triglycerides, protein components (Apoliproteins)

VLDL

Very Low Density Lipoprotein; Made in the liver; Supplies body with triglycerides; Apoliprotein B/C

LDL

Low Density Lipoprotein; Delivers cholesterol to tissues; Forms from VLDL in the blood; Apoliprotein B/C; All nucleated cells have LDL receptors

HDL

High Density Lipoprotein; Made in liver and small intestine; Accepts cholesterol and brings it back to the liver; Apoliprotein; Liver and cortical cells have HDL receptors (SCARBI)

Atherosclerosis

Accumulation of cholesterol can cause plaque to form in the blood vessels (ratio of HDL to LDL is the most predictive of problems)

Starvation

Glucose sparing to shift metabolism away from glucose and save it for neurons; Beta oxidation occurs until fat stores are depleted; Liver uses fatty acids which can form ketone bodies; Muscle proteins are also broken down to use amino acids for gluconeogenesis; Muscle atrophy can lead to death

Ketone Bodies

Only other substrate neurons can use to make ATP (can form keto acids which lead to ketoacidosis)

Pancreas Beta Cells

Produce insulin which is an energy storage hormone; Anabolic

Pancreas Alpha Cells

Produce glucagon which is an energy release hormone; Catabolic

Insulin

Released with hyperglycemia to promote glucose uptake; Affects muscle, liver, and adipose tissue; Glycogen synthesis and Lipogenesis; Released with amino acids

Glucagon

Produced with hypoglycemia; Affects liver; Glycogenolysis, lipolysis, gluconeogenesis; Released with amino acids

Intrinsic Insulin Regulation

Glucose causes ATP to be released; Potassium channels close in the presence of ATP; membrane depolarizes and calcium enters; Insulin is exocytosed into the blood

Extrinsic Insulin Regulation

Stretch receptors activate the PSNS; ACH is released onto beta cells; insulin is released; GIP can also cause insulin release with the endocrine system

GLUT-4

Presentin adipose tissue and skeletal muscle; Expression increases in the presence of insulin; brings in glucose which leads to glycogen synthesis in skeletal muscle and lipogenesis in adipose tissue; Inhibits HSL in adipose tissue and inhibits glycogen synthase in skeletal muscle/hepatocytes

No Insulin (Post-Absorptive) Effect on Hepatocytes

Glycogenolysis occurs and glycogen is broken down using GLUT-2; There is then a lot of glucose in the cell which moves into the blood

Insulin (Absorptive) Effect on Hepatocytes

Insulin binds and activates Hexokinase; Glucose is phosphorylated and incorporated into glycogen; There is less glucose in the cell which causes glucose to flow into the cell