Flashcards in Diet and Coronary Heart Disease Deck (9)
What is meant by 'the metabolic syndrome'
This is a syndrome which consists of insulin resistance/type 2 diabetes, abdominal obesity, dyslipidaemia and hypertension leading to an increase in CVD.
Outline the mechanism of atherosclerotic plaque formation
1) LDL carries cholesterol into the intimal layer of the artery wall
2) This oxidised LDL is treated like a pathogen and causes monocytes to adhere to the endothelium via adhesion molecules
3) The monocytes migrate into the intimate and become macrophages and engulf the oxidised LDL to become foam cells
4) These foam cells subsequently die and release the cholesterol leading to build up of cholesterol and plaque formation
What is the role of HDL?
To reverse cholesterol transport i.e. transport cholesterol out of the intimal wall of the blood vessel
What are the three main factors that mediate atherosclerosis?
Endothelial dysfunction, pro-inflammatory molecules an pro-atherosclerotic molecules
Name some anti-inflammatory and anti-atherosclerotic molecules which can aid in preventing atherosclerotic plaque formation
HDL (removes cholesterol), increased blood flow i.e. during exercise, nitrogenous vegetables (nitric oxide), flavonoids, anti-inflammatory mediators such as omega 3 fatty acids and statins
What may cause endothelial dysfunction leading to atherosclerosis?
Endothelial dysfunction can arise as a result f hyperlipidaemia, smoking, hyperglycaemia, diabetes, homocysteinaemia and atherosclerosis itself
What transporter on skeletal muscle is associated with fatty acid uptake?
How may hypertriglyceridaemia lead to insulin resistance?
Increased TG levels means more lipolysis; these fatty acids are taken up by the CD36 transporter on the muscle cell membrane which usually results in metabolism from the mitochondria, but when FAs are in excess, they accumulate and aren't completely utilised by the mitochondria but these saturated fatty acids are instead metabolised to toxic products such as ceramide which results in impeded insulin receptor signalling and resultant lack of GLUT4 translocation.