HYPERLIPIDAEMIA

HYPERLIPIDAEMIA

abnormally elevated levels of lipids and cholesterol in the blood

PRIMARY CAUSE OF HYPERLIPIDAEMIA

genetic disorders in lipid metabolism

SECONDARY CAUSES OF HYPERLIPIDAEMIA

* diet/obesity
* diabetes
* obstructive lipid disease
* certain medications

MAJOR RISK FACTOR OF HYPERLIPIDAEMIA

coronary heart disease

WHERE IS CHOLESTEROL MADE?

liver

WHERE DOES CHOLESTEROL COME FROM?

comes from liver and diet

CHOLESTEROL

not water soluble and circulates in the blood as a lipoprotein

LOW DENSITY LIPOPROTEIN

* bad cholesterol
* higher risk of disease
* causes harm by the formation of deposits within the walls of the arteries

HIGH DENSITY LIPOPROTEIN

* good cholesterol
* lower risk of disease

ATHEROSCLEROTIC PLAQUE - DEPOSITS

* hardening and loss of elasticity of arteries
* narrowed arteries
* can rupture leading to an immediate blood clot at the site

TREATMENT OF HYPERLIPIDAEMIA - NON-PHARMACOLOGIC

diet and exercise

TREATMENT OF HYPERLIPIDAEMIA - PHARMACOLOGIC

* decrease production of lipoproteins
* increase breakdown of removal
* decrease of lipids

STATINS

lipid lowering medications

STATINS - HOW DO THEY WORK?

1. inhibit HMG CoA reductase, leading to a decreased concentration of cholesterol within the cell

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2. low intracellular cholesterol stimulates the synthesis of LDL receptors

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3. increased number of LDL receptors promotes uptake of LDL from blood

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4. low intracellular cholesterol decreases the secretion of VLDL

OBESITY

* disorder of body weight regulatory systems causing an accumulation of excess body fat
* underweight - increased mortality risk
* normal body weight - low mortality risk
* BMI>30 - increased mortality risk

APPLE SHAPED BODY

* excess fat deposited in the central abdominal region
* high risk of hypertension, diabetes

PEAR SHAPED BODY

* fat deposited around hips or gluteal regions (hips and thighs) - mainly in females
* risks are lower

ADIPOCYTES (FAT CELLS)

* they increase in size, expand and divide
* once gained, they are never lost
* in obesity, adipocytes increase in number and size
* reduction in weight causes adipocytes to decrease in size
* major energy source and endocrine functions

WHITE ADIPOCYTES

store energy as a single lipid droplet and have endocrine functions

BROWN ADIPOCYTES

store energy in multiple small lipid droplets - specifically used to generate heat

FACTORS CONTRIBUTING TO OBESITY

genetic: familial tendency
2 parents that are obese, high chance of children being obese

2 parents that are thin, lower chance of children being obese

environmental and behavioural
sex: women are more susceptible

activity: lack of physical activity

alcohol: problem drinking

smoking: sensation of smoking

drugs

LEPTIN

* increases metabolic rate and decreases appetite in humans
* resistance to leptin found in obese humans
* receptor for leptin is in the hypothalamus
* produced by the dp gene
* mutation in db gene causes leptin resistance in mice

ADIPONECTIN

* hormone secreted from adipocytes
* promotes the uptake and oxidation of fatty acids and glucose by muscle and liver
* blocks the synthesis of fatty acids and gluconeogenesis by hepatocytes

GHRELIN - THE HUNGER HORMONE

* peptide hormone secreted by the stomach
* stimulates appetite
* secretion increases just before meals and drops off after meals
* increases food intake
* the higher the weight loss, the higher the levels of ghrelin

ORLISTAT - ANTIOBESITY DRUGS

* prevents the absorption of fats from the intestine
* reduces calorific intake
* inhibits pancreatic lipase (breaks down triglycerides in the intestine)