KINE 2P20 Lecture Notes - Lecture 7: Leucine, Transamination, Glutamine
9 May 2018
School
Department
Course
Professor
Nutrition 2P20
Low-density Lipoproteins (LDLs)
- Contain a lot of cholesterol and delivers it to the cells
- If amount LDL made exceeds amount used/taken up – high level blood LDL and
increased disease risk
▪ Atherosclerosis, heart disease, stroke, hypertension, cancer
Atherosclerosis
- Damage to artery increases inflammation (stress, rise in BP, smoking, toxins)
- Artery becomes permeable to LDL
- LDL enters the artery wall and becomes oxidized
- Local inflammatory response is mounted to clear ox-LDL-c and damage, recruitment of
macrophages (immune system)
- Macrophages take up ox-LDL-c, full, accumulate in arterial wall (cholesterol packed
macrophages = FOAM cells)
- Foam cells rupture, forming fatty streaks
- Streaks harden, plaque develops, process continues, plaque grows
- Fibrous cap forms over plaque
- Artery wall narrows as plaque grows, wall becomes hard, stiff, and non-elastic
- Fibrous cap ruptures overtime, content of plaque (lipid core) spills into lumen of artery
and cause blockage which blocks blood flow
- Heart attack, stroke
High-density Lipoproteins (HDLs)
- Rise in HDL help prevent too much cholesterol form depositing in artery walls and are
associated with a reduction in heart disease risk
- Exercise increases HDL
Fate of Lipids
Fatty Acids
- Storage (adipose tissue)
- Energy (acetyl-CoA; in the presence of CHO)
- Ketones (acetyl-CoA; without CHO)
▪ Excreted, energy, accumulated (ketoacidosis)
Glycerol
- Glucose (gluconeogenesis)
- Energy
Sports and Exercise Nutrition; Lipids/Fats
Fat as Fuel
- Goal: spare muscle glycogen and rely on fat as fuel
- High fat feeding increases fat oxidation during SUBMAXIMAL exercise
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Document Summary
Contain a lot of cholesterol and delivers it to the cells. If amount ldl made exceeds amount used/taken up high level blood ldl and increased disease risk: atherosclerosis, heart disease, stroke, hypertension, cancer. Damage to artery increases inflammation (stress, rise in bp, smoking, toxins) Ldl enters the artery wall and becomes oxidized. Local inflammatory response is mounted to clear ox-ldl-c and damage, recruitment of macrophages (immune system) Macrophages take up ox-ldl-c, full, accumulate in arterial wall (cholesterol packed macrophages = foam cells) Streaks harden, plaque develops, process continues, plaque grows. Artery wall narrows as plaque grows, wall becomes hard, stiff, and non-elastic. Fibrous cap ruptures overtime, content of plaque (lipid core) spills into lumen of artery and cause blockage which blocks blood flow. Rise in hdl help prevent too much cholesterol form depositing in artery walls and are associated with a reduction in heart disease risk. Energy (acetyl-coa; in the presence of cho)
