Appetite and Metabolic Syndrome Flashcards
What does the ‘satiety’ centre in the hypothalamus control?
Timing and amount of food intake
Generally, how is appetite controlled?
Control is complex, involving many hormones and sensing of energy sources in our blood
What is the name of the nucleus in the pituitary that plays a central role in appetite control and contains primary neurones that sense metabolite and hormone levels?
Arcuate nucleus
What is the role of secondary neurone in other areas of the hypothalamus in appetite?
They receive inputs from arcuate primary neurones and co-ordinate a response via the vagus nerve.
The primary neurones in the arcuate nucleus can be divided into excitatory and inhibitory types. What is the role of the excitatory types?
Excitatory (or orexigenic) neurones stimulate appetite by the release of two peptides:
- neuropeptide Y (NPY)
- agouti-related peptide (AgRP)
The primary neurones in the arcuate nucleus can be divided into excitatory and inhibitory types. What is the role of the inhibitory types?
Inhibitory (or anorexigenic) neurones suppress appetite by releasing pro-opiomelanocortin (POMC) - a precursor to may polypeptide hormones including alpha-MSH which is involved in suppressing appetite
Apart from the hypothalamus what other regions of the brain are involved in controlling appetite?
Regions of the brainstem
Why can you feel euphoria and tiredness after a meal?
POMC is released as a result of the stomach being full of food which suppresses appetite, but the beta-endorphin POMC releases also produces feelings of happiness and tiredness
Which hormone activates the stimulatory neurones in the arcuate nucleus, stimulating appetite? How is this hormone released?
Ghrelin - a peptide hormone released from the walls of the empty stomach.
Stretching of the stomach walls by food inhibits Ghrelin release
What is the role of the peptide hormone leptin?
Leptin is released into the blood from adipocytes and its concentration correlates with the amount of adipose tissue in the body.
Leptin inhibits stimulatory neurones and stimulates inhibitory neurones in the arcuate nucleus to suppress appetite.
It also induces the expression of uncoupling proteins in mitochondria, which leads to the production of heat rather than ATP
What has a lack of production or insensitivity to leptin been associated with?
obesity
Other than leptin, name some hormones that suppress appetite?
PYY - peptide released from walls of small intestine in response to feeding
Insulin - same mechanism as leptin but does not seem as important as leptin in this role
What is insulin resistance associated with?
Obesity and often leads to type-2 diabetes
Which cells secrete the peptide hormone amylin?
Beta-cells in the islets of Langerhan
What is the role of Amylin?
Its function is not well understood. It is known to suppress appetite, decrease glucagon secretion and slow gastric emptying
Apart from sensing hormones what can neurones in the arcuate nucleus sense?
Level of glucose and fatty acids in the blood
What is the effect of alpha-MSH - at synapse between primary and secondary arcuate neurones - (from POMC) acting at MC4 receptors?
Promotes satiety
What is the effect of AgRP and NPY neurotransmitters at the synapse of primary and secondary neurones in the arcuate nucleus?
Promotes hunger
Name a hormone from the stomach that promotes hunger. How does it do this?
Ghrelin - stimulates stimulatory primary neurones
Name a hormone from the small intestine that suppresses hunger. How does it do this?
PYY - inhibits stimulatory primary neurones
Name a hormone from adipose that suppresses hunger by inhibiting stimulatory primary neurones and stimulating inhibitory primary neurones
Leptin
Name a hormone that is secreted from the pancreas which suppresses appetite. How does it do this?
Insulin - stimulates inhibitory primary neurones
What percentage of obese adults have morbidity arising from their obesity?
Aproximately 80%
The causes of the obesity epidemic that is occurring are not fully understood. What are some explanation?
- Partly decreased exercise
- Partly increased consumption of highly calorific foods
- 60-84% genetic component
What is the “thrifty-phenotype” theory?
Individuals are genetically predisposed to store energy more efficiently during times of plenty to increase their odds of survival during subsequent times of famine. Now that human society has changes in the developed world and there is a constant supply of food this has led to chronic obesity.
A new concept to explain the obesity epidemic is that of Metabolic syndrome, which arose from the observation of a common pattern of symptoms in obese people. Which symptoms?
A cluster of the most dangerous risk factors associated with cardiovascular disease: Abdominal obesity Insulin resistance Dyslipidaemia (low HDL, raised TAGs) Raised fasting glucose Hypertension
What are the major factors that predispose to insulin resistance?
Obesity and a sedentary lifestyle
What is insulin resistance associated with?
the development of a dyslipidaemic profile (high VLDL and LDL, low HDL) that is highly atherogenic
What is the new International Diabetics Federation (IDF) definition of metabolic syndrome?
Central obesity, plus any two of the following factors:
- Raised TAGs
- Reduced HDL cholesterol
- Raised blood pressure
- Raised fasting plasma glucose
Name some chronic adult diseases that low birth weight and placental weight at birth increases the risk for
CHD
hypertension
Type 2 diabetes
Define an epigenetic trait
A stably inherited phenotype resulting from changes in a chromosome without alterations in the DNA sequence
Explain what DOHaD (developmental origins of health and disease) is
The idea that embryonic or neonatal nutritional imbalance causes hormonal, metabolic and altered cellular differentiation in the foetus, which by means of epigenetic regulation can long-term effects on gene expression that cause disease to the individual later on in life and be passed down generations.
How does epigenetic modifications alter chromosomes without affecting their DNA sequence?
By methylating DNA at specific nucleotides, modifying histones (e.g. methylation) and through use of ncRNAs
