Obesity and the metabolic syndrome

Question 1

Where are the ‘hunger’ and ‘satiety’ centres?

Answer 1

Hypothalamus

Question 2

Where is ghrelin produced?

Answer 2

Neuroendocrine cells in the stomach

Question 3

What is the signal for ghrelin release?

Answer 3

Empty stomach

Question 4

What is an orexigenic agent?

Answer 4

Appetite-inducing agent

Question 5

Which of the gut/pancreatic peptides are anorexigens?

Answer 5

CCK, insulin, GLP-1, peptide YY, oxyntomodulin and somatostatin.

Question 6

Which exogenous agents suppress hunger?

Answer 6

Foodstuffs, glucose, AAa and lipids.

Question 7

From where is leptin released?

Answer 7

Adipocytes

Question 8

What are the effects of leptin?

Answer 8

Central effects - potentiates insulin.

Question 9

What substances inhibit leptin?

Answer 9

TNF alpha and IL-6

Question 10

What structure in the brain collects central and peripheral messages concerning hunger?

Answer 10

Nucleus of the solitary tract (in medulla)

Question 11

Where is the satiety centre?

Answer 11

Ventromedial nucleus.

Question 12

Where is the hunger centre?

Answer 12

Lateral hypothalamic area

Question 13

What do anorexogenic neurons of the acruate nucleus secrete?

Answer 13

Proopiomelanocortin and cocaine-anphetamine-related transcript

Question 14

What do orexigenic neurones secrete?

Answer 14

Agouti-related peptide and neuropeptide Y

Question 15

How low must ones BMI be to be classed as anorexic?

Answer 15

More than 15% below standard (BMI < 17.5)

Question 16

What is the ‘metabolic syndrome’?

Answer 16

A combination of (3 out of 5) of:

Obesity, TIIDM, HTN, high plasma trigylcerides with low HDL cholesterol.

Question 17

What is the the lipid-overflow ectopic fat model?

Answer 17

Subcutaneous obesity is ‘healthy’ adipose tissue and visceral obesity is ‘dysfunctional adipose tissue’ (altered FFA metabolism and altered release of adipokines)

Question 18

Why is visceral fat different?

Answer 18

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.