Nutrition 2: Starvation / Obesity

Question 1

Describe the feedback mechanisms controlling hunger and satiety.

Answer 1

• Hunger and satiety is controlled by the hunger and satiety centres of the hypothalamus. It is controlled by 3 mechanisms:

1 - Glucostatic theory. High blood glucose stimulates the pancreas to release insulin, which in turn stimulates the hypothalamus to decrease appetite.

2 - Adipostatic theory. Large amounts of adipose tissue produces leptin, which in turn stimulates the hypothalamus to decrease appetite.

3 - The presence of fats, proteins and carbohydrates in the GIT results in the release of hormones which modify appetite in different ways.

Question 2

Where is ghrelin released?

What is its function?

How is ghrelin release controlled?

Answer 2

• Ghrelin is released from the stomach.
• Ghrelin stimulates the hypothalamus to increase appetite.
• Ghrelin release is inhibited by ingestion of food.

Question 3

List 3 hormones released in the intestine that modify appetite.

How do these hormones modify appetite?

Answer 3

Hormones in the intestine that modify appetite include:

1 - PYY.

2 - CCK.

3 - GLP-1.

• All of these hormones stimulate the hypothalamus to decrease appetite.

Question 4

List 2 neurotransmitters that modify appetite.

How do these hormones modify appetite?

Answer 4

Neurotransmitters that modify appetite include:

1 - Serotonin.

2 - Dopamine.

These neurotransmitters stimulate the hypothalamus to increase appetite.

Question 5

What is the difference between enteral and parenteral nutrition?

Answer 5

• Enteral nutrition is any nutrition which uses the GIT (normal oral feeding, tube feeding etc.).
• Parenteral nutrition is any nutrition which bypasses the GIT and supplies nutrients directly to the blood.

Question 6

What is rickets?

Answer 6

• Rickets is a condition characterised by poor bone mineralisation, causing a significant effect on development, causing deformation of load-bearing bones.
• It is caused by a chronic deficiency in vitamin D.

Question 7

What is scurvy?

What causes it?

Answer 7

• Scurvy is a condition characterised by:

1 - Destruction of collagen.

2 - Damage to myelin.

3 - Bleeding gums.

4 - Sunken eye sockets.

• It is caused by a chronic deficiency in vitamin C.

Question 8

What is pernicious anaemia?

What causes it?

Answer 8

• Pernicious anaemia is a type of macrocytic normochromic anaemia.
• It is caused by an autoimmune response against intrinsic factor, which is required for absorption of vitamin B12. The vitamin B12 deficiency causes the anaemia.

Question 9

What is iron deficiency anaemia?

What causes it?

Answer 9

• Iron deficiency anaemia is a type of microcytic hypochromic anaemia.
• It is causes by iron malabsorption or inadequate iron intake from the diet.

Question 10

List 4 causes of obesity.

Answer 10

Inherited causes of obesity:

1 - Leptin mutation (monogenic).

2 - Prader-willi syndrome (polygenic - multiple genes on chromosome 15).

Acquired causes of obesity:

1 - Drugs, e.g. corticosteroids, antidepressants and the contraceptive pill.

2 - Stress.

Question 11

What are chylomicrons?

Answer 11

Chylomicrons are lipoproteins that transport exogenous fat from the GIT to the liver and adipose tissue.

Question 12

What are VLDLs?

Answer 12

VLDLs (very low-density lipoproteins) are lipoproteins that transport endogenous fat from the liver and adipose tissue to other structures.

Question 13

How do fats enter adipocytes?

What happens to the fat once it is inside the adipocyte?

Answer 13

• Lipoprotein lipase on the adipocyte cell surface converts circulating fats in the form of chylomicrons and VLDLs into free fatty acids and glycerol.
• Free fatty acids and glycerol are able to enter the adipocytes, where they are re-converted into triglycerides.
• The triglycerides are broken down again into fatty acids (as long as insulin is not present, as insulin inhibits triglyceride breakdown), which exit the cell for metabolism elsewhere in the body.
• Remember glucose can also enter the adipocyte (stimulated by insulin), undergo lipogenesis to form glycerol and contribute to triglyceride formation.

Question 14

What is the nutritional difference between glucose and fructose?

Answer 14

• Fructose contains the same amount of energy than glucose (but fructose tastes sweeter, meaning less has to be used to achieve the same sweetness in food).
• However, fructose doesn’t stimulate insulin secretion, meaning the hypothalamus is not stimulated to produce satiety.
• Furthermore, fructose is more lipogenic than glucose (can be converted into more triglycerides).

Question 15

What is the equation for BMI?

Answer 15

BMI = mass (kg) / height (m^2)

Question 16

List the BMI categories for normal weight, overweight and obese.

Answer 16

• Normal weight BMI is 18.5-25.
• Overweight BMI is 25-30.
• Obese BMI is >30.

Question 17

List 6 diseases that are common comorbidities of obesity.

Answer 17

1 - Diabetes.

2 - Hypertension.

3 - Cancer.

4 - Cardiovascular disease.

5 - Joint damage.

7 - PCOS.

Question 18

List 5 methods of estimating body fat.

Answer 18

1 - BMI.

2 - Bioelectric impedance.

3 - Dual-energy X-ray absorptiometry (DEXA).

4 - Waist-hip circumference ratio.

5 - Skin fold thickness.

Question 19

List 5 treatments for obesity.

Describe the mechanisms for each.

Answer 19

1 - Sibutramine (inhibits neurotransmitters of the endocannabinoid system, suppressing appetite). *This is what cannabis does.

2 - Orlistat (inhibits pancreatic lipase, reducing fat absorption at the GIT).

3 - Diet restriction.

4 - Bariatric surgery (gastric banding or resection).

5 - Gastric balloon (inflates to distend the stomach).

Question 20

List 2 metabolic processes that are upregulated during starvation.

Answer 20

Starvation causes upregulation of:

1 - Gluconeogenesis.

2 - Ketogenesis (production of ketone bodies from fat).

Question 21

List 2 organs that rely entirely on glucose for energy metabolism (rather than FFAs).

Answer 21

Organs that rely entirely on glucose for energy metabolism include:

1 - The brain.

2 - RBCs.

*All other organs can use a combination of glucose and FFAs.

Question 22

List the stages of starvation.

Which metabolic shifts accompany the beginning of each stage?

When does each stage occur?

Answer 22

• Early starvation follows the postabsorptive phase.
• Early starvation begins when glucose production from gluconeogenesis exceeds that of glycogenolysis (16 hours postprandial).
• The low glycogen levels in early starvation trigger an increase in gluconeogenesis, causing weight loss (fat) and muscle wasting (protein).
• Intermediate starvation begins when glycogenolysis stops as glycogen stores are depleted, and the body relies on endogenous sources of energy, including fats and proteins, for gluconeogenesis (30 hours postprandial).
• Later in the intermediate phase of starvation, gluconeogenesis decreases to safeguard muscle mass.
• Prolonged starvation begins when fat stores are depleted, and gluconeogenesis can only utilise proteins (24 days).
• Prolonged starvation causes significant muscle wasting, which can lead to death.
• Prolonged starvation decreases basal metabolic rate by 50%.

Question 23

Why does decreasing calorie intake decrease rate of absorption of nutrients?

Answer 23

• Decreasing calorie intake decreases rate of cell growth.
• This can lead to villous atrophy as they are rebuilt less quickly.
• This results in a decreased surface area for absorption in the GIT, resulting in malabsorption of nutrients and diarrhoea.

Question 24

Briefly describe the impacts of deficiency of vitamin D, E, K and A.

Answer 24

• Vitamin D deficiency affects bone density (rickets).
• Vitamin E deficiency affects immune function.
• Vitamin K deficiency affect blood clotting.
• Vitamin A deficiency affects cognitive function / development.