Advances in Metabolism and Human Disease (E09F0A)

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General info

Metabolism, described as the intricate set of chemical reactions that occur in living organisms, is at the heart of any form of life. It provides cells and organisms with energy and substrates, essential to build structural components and to drive key biochemical processes. Wired to numerous sensors and control mechanisms it responds to a wide variety of environmental cues and continuously adjusts homeostatic processes to changing inputs. Defects or limitations in these circuits accompany or underlie the pathophysiology of a plethora of human diseases, including common life-style-associated disorders such as obesity, diabetes, cardiovascular disease and cancer, which collectively account for more than two thirds of all deaths in western countries.

This course aims to provide a state-of-the-art and in-dept analysis of the emerging links between metabolism and human disease. After this course, students should be able to appreciate the links between metabolism and human disease and understand how these links may provide novel opportunities to improve prevention, diagnosis and treatment.


Mode of examination

Written exam (outside normal exam period)

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Sjabloon:Advances in Metabolism and Human Disease (E09F0A)/bestanden

Exam questions

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1.Give the pathogenesis of type I and type II diabetes, focus on the differences. (Matieu)

2. a) What are primary and secondary mitochondrial disorders, give 2 examples for each. b) What is heteroplasmy? c) Which metabolites can be used to investigate the mitochondrial function? (Van den Heuvel) 3. How are metabolic changes in cancer cells used for medical imaging? (Swinnen)

4. What is a thrifty genotype. GOAT acetylates ghrelin. Is GOAT part of a thrifty genotype? (Depoortere)

5. Which are the major pathways in peroxisomes? What happens when they are defect? (Baes)

6. How are metabolic changes in cancer cells used for therapy? (Swinnen)

7. Give a title for this graph and explain. (Depoortere)

(graph of the synergistic inhibitory effect on food intake of GLP-1 and PYY)

8. On which sources of energy does your body relie on when you run out of glucose? Give them in the subsequent order they are used by your body and provide an example of a pathology (problems with usage of that source) for each. (Cassiman)

9.Discuss 5 mechanisms by which adiponectin protects against metabolic and cardiovascular diseases. (Holvoet)

10. Name 3 possible strategies for the treatment of inborn errors of metabolism, each time with an example of a specific disease. (Cassiman)

11. Speech of Otto Warburg is given with sentences that are underlined. Is that underlined text correct or not and why? Is there any proof? (Swinnen)

- "The primary cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar."

- "The key to the cancer problem is accordingly the energetics of life."

- "If it is true that the replacement of oxygen-respiration by fermentation is the prime cause of cancer, then all cancer cells without exception must ferment, and no normal growing cell ought to exist that ferments in the body."


Examenvragen '17-'18 =

1) Explain the difference between diabetic ketoacidosis in patients with type 1 diabetes and patients with type 2 diabetes treated with SGLT2-inhibitors. (Mertens)

2) Explain, using a graph, what the obesity paradox is and give an explanation for this paradox. (Scroyen)

3) Describe and explain the 4 characteristics for mass spectrometer analysers.

Which of these are the most critical in tracer metabolism and why?

Is researcher X has an analyte which he cannot ionize, can he use mass spectrometry? Why (not)?