Flashcards in 14. Control of Appetite Deck (18)
How many children under the age of five were overweight or obese in 2014?
Where is the appetite control centre?
In the hypothalamus.
Which nucleus processes neuronal, nutrient and hormonal signals?
The arcuate nucleus.
What are the two types of primary neurone in the arcuate nucleus?
The stimulators neurones that contain neuro peptide Y (NPY) and agouti-related peptide (AgRP). These promote hunger.
The inhibitory neurones that contain proopoimelanocortin (POMC) which yields several neurotransmitters including a-MSH and B-endorphin. These promote satiety.
Which hormonal signals come from the gut to the hypothalamus?
Ghrelin - released from stomach wall when empty, stimulates excitatory primary neurones in arcuate nucleus and this stimulates appetite.
PYY (peptide tyrosine tyrosine) - short peptide hormone released by cells in the ileum and colon in response to feeding. They inhibit the excitatory primary neurones of the arcuate nucleus and stimulate the inhibitory neurones so they suppress appetite.
Which hormones come from the body to the hypothalamus?
Leptin - released into blood by fat cells. It stimulates the POMC neurones and inhibits the AgRP and NPY so suppresses appetite.
insulin - same mechanism to suppress appetite.
Amylin - secreted from B cells in the pancreas. The mechanism is not known but they suppress appetite.
Which hormones affect the stimulatory primary neurone?
PYY from the small intestine and leptin from adipose tissue both inhibit it. Ghrelin from the stomach stimulates it.
What hormones affect the inhibitory primary neurones?
Insulin from the pancreas and leptin from adipose both stimulate it.
What is the effect of a loss of function and mutation in leptin gene?
Constant hunger, not able to stop eating so become obese.
A group or recognisable pattern of symptoms or abnormalities that indicate a particular trait or disease.
What are the risk factors associated with metabolic syndrome?
Abdominal obesity, high blood pressure, insulin resistance, raised fasting glucose and dyslipidaemia (low HDL and high TAGs).
How common is metabolic syndrome?
~20-25% of adults and 40% of adults over 40 years.
How is metabolic syndrome diagnosed?
Central obesity plus two of the following: raised TAGs, reduced HDL cholesterol, raised blood pressure or raised fasting plasma glucose.
What are the causes of metabolic syndrome?
Insulin resistance - cells are less sensitive to insulin so blood glucose levels raise and there is more insulin production. Eventually the B cells wear out so are less effective. This leads to hyperglycaemia and type II diabetes.
Central obesity - contributes to hypertension, high cholesterol and hyperglycaemia. Central obesity is a more useful indicator of metabolic syndrome than BMI.
How can metabolic syndrome be treated?
Primary intervention - promote a healthy lifestyle, reduce calorie intake to lose 5-10% body weight in a year, increase physical activity, and change to a healthy diet.
Secondary intervention - statins to reduce LDL cholesterol, anti hypertensive drugs to reduce blood pressure, anti diabetic drugs to treat hyperglycaemia.
What did the Dutch famine suggest?
That how you're treated in the womb has an effect on your appetite throughout life. If pregnant women were exposed to famine during early pregnancy then later in life they had a higher risk of diabetes, obesity and CVD.
What effects can epigenetics cause?
Histone modification or regulation of non coding RNA.