Obesity and the metabolic syndrome Flashcards
Where are the ‘hunger’ and ‘satiety’ centres?
Hypothalamus
Where is ghrelin produced?
Neuroendocrine cells in the stomach
What is the signal for ghrelin release?
Empty stomach
What is an orexigenic agent?
Appetite-inducing agent
Which of the gut/pancreatic peptides are anorexigens?
CCK, insulin, GLP-1, peptide YY, oxyntomodulin and somatostatin.
Which exogenous agents suppress hunger?
Foodstuffs, glucose, AAa and lipids.
From where is leptin released?
Adipocytes
What are the effects of leptin?
Central effects - potentiates insulin.
What substances inhibit leptin?
TNF alpha and IL-6
What structure in the brain collects central and peripheral messages concerning hunger?
Nucleus of the solitary tract (in medulla)
Where is the satiety centre?
Ventromedial nucleus.
Where is the hunger centre?
Lateral hypothalamic area
What do anorexogenic neurons of the acruate nucleus secrete?
Proopiomelanocortin and cocaine-anphetamine-related transcript
What do orexigenic neurones secrete?
Agouti-related peptide and neuropeptide Y
How low must ones BMI be to be classed as anorexic?
More than 15% below standard (BMI < 17.5)
What is the ‘metabolic syndrome’?
A combination of (3 out of 5) of:
Obesity, TIIDM, HTN, high plasma trigylcerides with low HDL cholesterol.
What is the the lipid-overflow ectopic fat model?
Subcutaneous obesity is ‘healthy’ adipose tissue and visceral obesity is ‘dysfunctional adipose tissue’ (altered FFA metabolism and altered release of adipokines)
Why is visceral fat different?
Less responsive to insulin. Hyperlipolytic state - produces more non-esterified fatty acids. Produces more pro-inflammatory cytokines such as IL-1, IL-6 and TNF alpha. Non-esterified fatty acids makes liver less sensitive to insulin.
