Making it to Medical School

Many students wrote in to find out but I am not the right person to answer doubts and queries. Students and parents should write directly to the deans of the medical schools whether in Malaysia or overseas. If scholarship is a concern, parents/students can apply for PTPTN or MARA/JPA scholarships.

There are so many medical schools to choose from. Once students register they cannot simply hop from one school to another as there are many obstacles.

Where do you start searching for medical schools? It depends. If the student is from a poor family, I would suggest to seek advice directly from the dean of any public university that has a medical school. In my last care of students' database, I found that 60% of our local students were from poor families. In some families, the father had died and the mother had to work to earn an income to feed the family. Some of these jobs were harsh, like driving a school bus/van. Many poor students had trouble going home as they did not have money. But our medical school had set up a students' fund to assist these poor students during crisis.

Students usually score 4.0 (four flat) before applying to medical school. But nowadays, many medical schools have programs and remedies to help non 4-flat students once they register. Many medical schools today will accept students who are motivated, have passion, and are willing to give their all to study hard and obtain a medical degree. This gives hope to students and parents to approach the various medical school with an open heart, and try and ask around for seat in medical school.

Which are the good medical schools to try? This is my personal list and views:

1. USM medical school - limited to 180 students per year. Space is a major constraint. We don't have good facilities and we are already 30 years old. Only BPSP is new. We don't have corpses at all, so Anatomy is dry.
2. UniKL medical school in Ipoh - the Anatomy Dept is very good as they have corpses and the lecturers (all Burmese) are very dedicated. Their OSPE (exam) is also very good and well set-up. The MCQ format is different from that of USM medical school.
3. Cyberjaya Medical University - the lecturers are very good and students successfully complete their degrees. Students can transfer credits here and complete a medical degree.
4. Management & Science University (MSU) in Shah Alam - the medical program is 1 year in Shah Alam and 5 years overseas  in Bangalore. Students seem to enjoy the extra coaching and intensive teaching-learning activities, and good weather in Bangalore. The housing, teaching & learning facilities in Bangalore are modern and better than in Malaysia. 
5. USM KLE medical program in Belgaum, India - same program as USM but there is good coaching by the dedicated teachers. The place is new. Facilities are modern and better than in USM and elsewhere in Malaysia.
6. College Insaniah in Alor Star, Kedah - the program is good but sometimes they have problems as aired on TV and news recently.

A traditional Malay remedy for small gallstones

Caution:
This traditional remedy may ONLY work if your gallstone(s) is really SMALL (like a grain of rice) as detected by ultrasound of the abdomen. This traditional remedy will NOT EVER work on gallstones that are already large, as large as your thumb (1-2 cm long)! Only surgery to remove the entire gallbladder will help in advanced cases where the large gallstones are a cause of worry and colic as the gallstone(s) try to exit the gallbladder.

How do you dissolve gallstones (batu karang hempedu)?

This may work for some, and not work for others. For many whom this remedy has worked, they shared the formula with friends and now the formula has reached me. So I will share with you.

What you will need:

Take 33 pieces of belalai gajah leaves and 33 pieces of lidah jin leaves and 1-2 Granny Smith (green) apples. 

What to do?

Wash and place the leaves in a blender. Chop the green apples (with seeds) and add to blender. Add cold water (from the fridge). Blend till fine. It will fizzle at the top. Strain into drinking cups - the thicker the better taste. Add 1-2 plastic teaspoonful honey - the sweeter the better. Stir and drink cold, immediately. The drink is light green when freshly prepared, sweet and smells of green apples. If you let is stand long enough, it turns an ugly wooden color, but can still be taken.

What else is this remedy good for?

This same remedy works for those with diabetes and renal problems (renal stones/batu karang kencing). Can take it daily. I take it for buka puasa. I take 2 cups full and I feel ok. This is much better than commercial apple juice or fresh apple juice.

Lidah jin or Strobilanthes crispus.
Other known names: Pecah kaca, Pecah beling, Bayam karang, Keji beling, Panglima hitam, and Black-face general. 

Belalai gajah or Clinacanthus nutans.
Other known names: Dandang gendis, Daun kalingsir, Sabah snake grass, Drooping Clinacanthus, Phaya-Yor, and Snake Plant.

Add to blender

Juice for dissolving gallstones

Scientific names of the 2 plants as provided by the Medicinal Plants Interest Group in Facebook:

https://www.facebook.com/groups/100705113390880/

Ahmad Fuad Haji Morad: The "Lidah Jin", or rather the correct vernacular name, "Jin batu" (referring to its ability to act upon gallstones) is Strobilanthes crispus. Other names mentioned are - Pecah kaca, Pecah beling, Bayam karang, Keji beling, Panglima hitam, Black-face general. Whilst, the one labeled "Belalai gajah" is Clinacanthus nutans. Other names used for the species are - Dandang gendis, Daun kalingsir, Sabah snake grass, Drooping Clinacanthus, Phaya-Yor, Snake Plant. Both are in the same plant family, Acanthaceae.

External link:
http://www.healthline.com/health/gallstones#Overview1

Serotonin

Diet
Both serotonin and its precursor tryptophan are amino acids. Our diet cannot feed our brain the serotonin it needs because the blood-brain barrier (BBB) will block it from entering. Even tryptophan cannot cross BBB. Low serotonin is linked with depression.
http://bebrainfit.com/serotonin-foods-mood-brain/


Sources

1. Serotonin is released into the space between neurons, and diffuses over a relatively wide gap (>20 µm) to activate 5-HT receptors located on the dendrites, cell bodies and presynaptic terminals of adjacent neurons.
2. Serotonin in mammals is made by two different tryptophan hydroxylases: TPH1 produces serotonin in the pineal gland and the enterochromaffin cells, while TPH2 produces it in the raphe nuclei and in the myenteric plexus. 
3. Genetically altered mice lacking TPH1 develop progressive loss of heart strength early on. They have pale skin and breathing difficulties, are easily tired, and eventually die of heart failure. Genetically altered mice that lack TPH2 are normal when they are born. However, after three days, they appear to be smaller and weaker, and have softer skin than their siblings. In a purebred strain, 50% of the mutants died during the first four weeks, but in a mixed strain, 90% survived. Normally, the mother weans the litter after three weeks, but the mutant animals needed five weeks. After that, they caught up in growth and had normal mortality rates. Subtle changes in the autonomic nervous system are present, but the most obvious difference from normal mice is the increased aggressiveness and impairment in maternal care of young. Despite the blood–brain barrier, the loss of serotonin production in the brain is partially compensated by intestinal serotonin. The behavioural changes become greatly enhanced if one crosses TPH1- with TPH2-lacking mice and gets animals that lack TPH entirely.
4. Serotonin secreted from the enterochromaffin cells eventually finds its way out of tissues into the blood. There, it is actively taken up by blood platelets, which store it. When the platelets bind to a clot, they disgorge serotonin, where it serves as a vasoconstrictor and helps to regulate hemostasis and blood clotting. 
5. Serotonin also is a growth factor for some types of cells, which may give it a role in wound healing.
6. Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the alimentary canal (gut), where it is used to regulate intestinal movements. 
7. The remainder is synthesized in serotonergic neurons of the CNS, where it has various functions. These include the regulation of mood, appetite, and sleep. 
8. Modulation of serotonin at synapses is thought to be a major action of several classes of pharmacological antidepressants.

Actions

1. Serotonin is known to regulate aging, learning and memory. 
2. Serotonin also has some cognitive functions, including memory and learning. 
3. Serotonin or 5-hydroxytryptamine (5-HT) is a monoamine neurotransmitter. Biochemically derived from tryptophan, serotonin is primarily found in the gastrointestinal (GI) tract, platelets, and in the central nervous system (CNS) of animals and humans. It is popularly thought to be a contributor to feelings of well-being and happiness.
4. In humans, serotonin levels are affected by diet. An increase in the ratio of tryptophan to phenylalanine and leucine will increase serotonin levels. Fruits with a good ratio include dates, papayas and bananas. Research also suggests eating a diet rich in carbohydrates and low in protein will increase serotonin by secreting insulin, which helps in amino acid competition. However, increasing insulin for a long period may trigger the onset of insulin resistance, obesity, type 2 diabetes, and lower serotonin levels. Muscles use many of the amino acids except tryptophan, allowing more muscular individuals to produce more serotonin.
5. Serotonin functions as a neurotransmitter in the nervous systems of simple, as well as complex, animals.
6. Serotonin is a neurotransmitter and is found in all bilateral animals, where it mediates gut movements and the animals' perceptions of resource availability. 
7. Serotonin is found in animals, fungi and plants. Serotonin is present in insect venoms and plant spines and serves to cause pain, which is a side effect of serotonin injection. 
8. Serotonin is produced by pathogenic amoebae, and its effect on the gut causes diarrhea. 
9. Its widespread presence in many seeds and fruits may serve to stimulate the digestive tract into expelling the seeds.
10. Serotonin is mainly metabolized to 5-HIAA, chiefly by the liver. Metabolism involves first oxidation by monoamine oxidase to the corresponding aldehyde. This is followed by oxidation by aldehyde dehydrogenase to 5-HIAA, the indole acetic acid derivative. The latter is then excreted by the kidneys. 
11. One type of tumor, called carcinoid, sometimes secretes large amounts of serotonin into the blood, which causes various forms of the carcinoid syndrome of flushing, diarrhea, and heart problems. 
12. Because of serotonin's growth-promoting effect on cardiac myocytes, persons with serotonin-secreting carcinoid may suffer a right heart (tricuspid) valve disease syndrome, caused by proliferation of myocytes onto the valve.
13. Since serotonin is an indicator of bleeding, a sudden large increase in peripheral levels causes pain. The reason wasps and deathstalker scorpions have serotonin in their venom may be to increase the pain of their stings on large animals, and also to cause lethal vasoconstriction in smaller prey.
14. Some serotonergic agonist drugs also cause fibrosis anywhere in the body, particularly the syndrome of retroperitoneal fibrosis, as well as cardiac valve fibrosis. In the past, three groups of serotonergic drugs have been epidemiologically linked with these syndromes. They are the serotonergic vasoconstrictive antimigraine drugs (ergotamine and methysergide), the serotonergic appetite suppressant drugs (fenfluramine, chlorphentermine, and aminorex), and certain anti-Parkinsonian dopaminergic agonists, which also stimulate serotonergic 5-HT2B receptors. 
15. Serotonin, in addition, evokes endothelial nitric oxide synthase activation and stimulates, through a 5-HT1B receptor-mediated mechanism, the phosphorylation of p44/p42 mitogen-activated protein kinase activation in bovine aortic endothelial cell cultures. 
16. In blood, serotonin is collected from plasma by platelets, which store it. It is thus active wherever platelets bind in damaged tissue, as a vasoconstrictor to stop bleeding, and also as a fibrocyte mitotic (growth factor), to aid healing.
17. In humans, though insulin regulates blood sugar and IGF regulates growth, serotonin controls the release of both hormones, so serotonin suppresses insulin release from the beta-cells in the pancreas, and exposure to SSRIs reduces fetal growth. 
18. Human serotonin can also act as a growth factor directly. Liver damage increases cellular expression of 5-HT2A and 5-HT2B receptors. Serotonin present in the blood then stimulates cellular growth to repair liver damage. 5HT2B receptors also activate osteocytes, which build up bone. However, serotonin also inhibits osteoblasts, through 5-HT1B receptors.
19. In humans, increased blood serotonin levels have been shown to be significant negative predictor of low bone density. Serotonin can also be synthesized, albeit at very low levels, in the bone cells. It mediates its actions on bone cells using three different receptors. Through Htr1b receptors, it negatively regulates bone mass, while it does so positively through Htr2b and Htr2c. There is very delicate balance between physiological role of gut serotonin and its pathology. Increase in the extracellular content of serotonin results in a complex relay of signals in the osteoblasts culminating in FoxO1/ Creb and ATF4 dependent transcriptional events.
20. These studies have opened a new area of research in bone metabolism that can be potentially harnessed to treat bone mass disorders.
21. In humans, defective signaling of serotonin in the brain may be the root cause of sudden infant death syndrome (SIDS). 
22. Scientists from the European Molecular Biology Laboratory in Monterotondo, Italy genetically modified lab mice to produce low levels of the neurotransmitter serotonin. The results showed the mice suffered drops in heart rate and other symptoms of SIDS, and many of the animals died at an early age. Researchers now believe low levels of serotonin in the animals' brainstems, which control heartbeat and breathing, may have caused sudden death, they said in the July 4, 2008 issue of Science.
23. If neurons that make serotonin — serotonergic neurons — are abnormal in infants, there is a risk of sudden infant death syndrome (SIDS).
24. Serotonin taken orally does not pass into the serotonergic pathways of the central nervous system, because it does not cross the blood–brain barrier (BBB). However, tryptophan and its metabolite 5-hydroxytryptophan (5-HTP), from which serotonin is synthesized, can and do cross the BBB. These agents are available as dietary supplements, and may be effective serotonergic agents. 
25. One product of serotonin breakdown is 5-hydroxyindoleacetic acid (5-HIAA), which is excreted in the urine. 
26. Serotonin and 5-HIAA are sometimes produced in excess amounts by certain tumors or cancers, and levels of these substances may be measured in the urine to test for these tumors.
27. In animals and humans, serotonin is synthesized from the amino acid L-tryptophan by a short metabolic pathway consisting of two enzymes: tryptophan hydroxylase (TPH) and amino acid decarboxylase (DDC). The TPH-mediated reaction is the rate-limiting step in the pathway. TPH has been shown to exist in two forms: TPH1, found in several tissues, and TPH2, which is a neuron-specific isoform.
28. Serotonin can also signal through a nonreceptor mechanism called serotonylation, in which serotonin modifies proteins. This process underlies serotonin effects upon platelet-forming cells (thrombocytes) in which it links to the modification of signaling enzymes called GTPases that then trigger the release of vesicle contents by exocytosis. A similar process underlies the pancreatic release of insulin. 
29. The effects of serotonin upon vascular smooth muscle tone (this is the biological function from which serotonin originally got its name) depend upon the serotonylation of proteins involved in the contractile apparatus of muscle cells.
30. Serotonergic action is terminated primarily via uptake of 5-HT from the synapse. This is accomplished through the specific monoamine transporter for 5-HT, SERT, on the presynaptic neuron. 
31. Various agents can inhibit 5-HT reuptake, including MDMA (ecstasy), amphetamine, cocaine, dextromethorphan (an antitussive), tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs). 
32. Interestingly, a 2006 study conducted by the University of Washington suggested a newly discovered monoamine transporter, known as PMAT, may account for "a significant percentage of 5-HT clearance". 
33. Contrasting with the high-affinity SERT, the PMAT has been identified as a low-affinity transporter, with an apparent Km of 114 micromoles/l for serotonin; approximately 230 times higher than that of SERT. 
34. However, the PMAT, despite its relatively low serotonergic affinity, has a considerably higher transport 'capacity' than SERT, "... resulting in roughly comparable uptake efficiencies to SERT in heterologous expression systems." 
35. The study also suggests some SSRIs, such as fluoxetine and sertraline, inhibit PMAT but at IC50 values which surpass the therapeutic plasma concentrations by up to four orders of magnitude; therefore, SSRI monotherapy is "ineffective" in PMAT inhibition. 
36. At present, no known pharmaceuticals are known to appreciably inhibit PMAT at normal therapeutic doses. The PMAT also suggestively transports dopamine and norepinephrine, albeit at Km values even higher than that of 5-HT (330–15,000 μmoles/L).
37. The 5-HT receptors, the receptors for serotonin, are located on the cell membrane of nerve cells and other cell types in animals, and mediate the effects of serotonin as the endogenous ligand and of a broad range of pharmaceutical and hallucinogenic drugs. 
38. With the exception of the 5-HT3 receptor, a ligand-gated ion channel, all other 5-HT receptors are G protein-coupled, seven transmembrane (or heptahelical) receptors that activate an intracellular second messenger cascade.
39. Several classes of drugs target the 5-HT system, including some antidepressants, antipsychotics, anxiolytics, antiemetics, and antimigraine drugs, as well as the psychedelic drugs and empathogens.
40. The psychedelic drugs psilocin/psilocybin, DMT, mescaline, and LSD are agonists, primarily at 5HT2A/2C receptors. The empathogen-entactogen MDMA releases serotonin from synaptic vesicles of neurons.
41. Drugs which alter serotonin levels are used in depression, generalized anxiety disorder and social phobia. 
42. Monoamine oxidase inhibitors (MAOIs) prevent the breakdown of monoamine neurotransmitters (including serotonin), and therefore increase concentrations of the neurotransmitter in the brain. 
43. MAOI therapy is associated with many adverse drug reactions, and patients are at risk of hypertensive emergency triggered by foods with high tyramine content, and certain drugs. 
44. Some drugs inhibit the reuptake of serotonin, making it stay in the synaptic cleft longer. 
45. The tricyclic antidepressants (TCAs) inhibit the reuptake of both serotonin and norepinephrine. 
46. The newer selective serotonin reuptake inhibitors (SSRIs) have fewer side effects and fewer interactions with other drugs.

http://upload.wikimedia.org/wikipedia/commons/1/1c/Serotonin_biosynthesis.svg
http://upload.wikimedia.org/wikipedia/en/8/88/Dopamineseratonin.png
http://en.wikipedia.org/wiki/Serotonin

Epinephrine (Adrenaline)

1. Lipid mobilization.
2. Glycogenolysis is stimulated by epinephrine and/or norepinephrine.
3. Epinephrine (or adrenaline or adrenalin) is a hormone and a neurotransmitter. 
4. Epinephrine has many functions in the body: regulating heart rate, blood vessel and air passage diameters, and metabolic shifts. 
5. Epinephrine release is a crucial component of the fight-or-flight response of the sympathetic nervous system. 
6. Epinephrine is one of a group of monoamines called the catecholamines. 
7. Adrenaline is used to treat a number of conditions including: cardiac arrest, anaphylaxis, and superficial bleeding. 
8. It has been used historically for bronchospasm and hypoglycemia. 
9. Newer treatments for bronchospasm and hypoglycaemia, such as salbutamol, a synthetic epinephrine derivative, and dextrose, respectively, are currently preferred.
10. Adrenaline is also used as a bronchodilator for asthma if specific β2 agonists are unavailable or ineffective.
11. Adrenaline is used as a drug to treat cardiac arrest and other cardiac dysrhythmias resulting in diminished or absent cardiac output. Its actions are to increase peripheral resistance via α1receptor-dependent vasoconstriction and to increase cardiac output via its binding to β1 receptors.
12. Due to its vasoconstrictive effects, adrenaline is the drug of choice for treating anaphylaxis. Allergy patients undergoing immunotherapy may receive an adrenaline rinse before the allergen extract is administered, thus reducing the immune response to the administered allergen.
13. Adrenaline is added to injectable forms of a number of local anesthetics, such as bupivacaine and lidocaine, as a vasoconstrictor to slow the absorption and, therefore, prolong the action of the anesthetic agent. Due to epinephrine's vasoconstricting abilities, the use of epinephrine in localized anesthetics also helps to diminish the total blood loss the patient sustains during minor surgical procedures.

http://en.wikipedia.org/wiki/Epinephrine

Injectable epinephrine:
http://en.wikipedia.org/wiki/File:Adrenalin_Ampulle.jpg

Catecholamines:
http://en.wikipedia.org/wiki/Catecholamine

Cortisol

CORTISOL

Synonyms

Cortisol (11 b,17,21, trihydroxy-4-pregnene-3,20-dione) (in humans), natural form

Hydrocortisone, this form is prescribed by doctors

Corticosterone (11 b,21,d,hydroxypregn-4-ene-3,20-dione) (in rodents), synthetic form

Cortisol is a stress hormone. It is a steroid hormone, more specifically a glucocorticoid. 

Structure of cortisol

Cortisol is the major natural glucocorticoid. Semisynthetic derivatives with greater hormonal activity than that of cortisol are dexamethasone, prednisone, and triamcinolone

Structure of steroid hormones.

From http://what-when-how.com/molecular-biology/glucocorticoids-molecular-biology/

Production of cortisol

Glucocorticoid secretion is enhanced during stress conditions, such as anxiety, hunger, and trauma.

1. Cortisol is a stress hormone as well as a steroid hormone, and more specifically a glucocorticoid. 
2. It is released in response to stress and a low level of blood glucocorticoids. 

Regulation of cortisol production

The synthesis of glucocorticoids in the zona fasciculata of the adrenal cortex (in the adrenal gland) and their release into the blood circulation is regulated by adrenocorticotropic hormone (ACTH). 

ACTH is produced in the anterior lobe of the hypophysis, in response to stimuli coming either from the neuroendocrine cells of the paraventricular nuclei of the hypothalamus (corticotropin releasing hormone, CRH) or from the periphery (blood cortisol concentration).

High blood cortisol levels reduce (by feedback inhibition) the production of both CRH and ACTH. This regulatory circuit is called the hypothalamus-pituitary-adrenal axis

Regulation of cortisol production by the hypothalamus-pituitary-adrenal axis. 

From http://what-when-how.com/molecular-biology/glucocorticoids-molecular-biology/

Why do we need cortisol?

1. It is the most important human glucocorticoid. 
2. It is essential for life.
3. It regulates or supports a variety of important cardiovascular, metabolic, immunologic, and homeostatic functions.
4. Various synthetic forms of cortisol are used to treat a variety of diseases, eg, hydrocortisone.

Functions of cortisol

1. Its primary functions are to increase blood sugar through gluconeogenesis; suppress the immune system; and aid in fat, protein and carbohydrate metabolism.
2. It also decreases bone formation. 
3. Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis, and inhibits the peripheral utilization of glucose (insulin resistance) by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane. 
4. Cortisol increases glycogen synthesis (glycogenesis) in the liver. The permissive effect of cortisol on insulin action in liver glycogenesis is observed in hepatocyte culture in the laboratory, although the mechanism for this is unknown.

External Links
http://en.wikipedia.org/wiki/Cortisol
http://www.netterimages.com/image/9025.htm

What-When-How
http://what-when-how.com/molecular-biology/glucocorticoids-molecular-biology/

Cortisol for injection
http://upload.wikimedia.org/wikipedia/commons/d/d6/Cortisol_for_injection.jpg

PowerPoints

http://slideplayer.com/search/cortisol/

http://slideplayer.com/slide/3469175/#

http://slideplayer.com/slide/3883704/#

http://slideplayer.com/slide/4404396/#

Steroidogenesis

http://upload.wikimedia.org/wikipedia/commons/1/13/Steroidogenesis.svg

Lipid Metabolism

SEQ: Describe lipid metabolism under fasting state. (10 marks)

MODEL ANSWER:

No.	Details	Marks
1.	During fasting, there are many changes in the body and blood in the following: i.      nutrient storage, supply and levels; ii.     hormone secretions and levels; iii.    blood pH; iv.    Usage of alternative energy resources v.     energy storage, supply and levels;	2
2.	Order of usage of energy resources within the body: i.      Glucose (0-4 hrs), ii.     Glycogen (during sleep), iii.    Proteins (by day 3), and iv.    Lipids (from day 3 onward) v.     Ketones	2
3.	Chemical processes & pathways (catabolism): a.     glycolysis, b.    proteolysis, c.     lipolysis, d.    glycogenolysis, e.     b-oxidation f.     TCA cycle g.    ETC	2
4.	Lipid metabolism in fasting: i.      Hyperglycaemic hormones: Increase ii.     Insulin: Decrease iii.    Exogenous lipoprotein metabolism: No iv.    Endogenous lipoprotein metabolism: Yes v.     Fat mobilization (from adipose tissue): Active vi.    Carnitine shuttle: Active vii.   b-oxidation: Very active viii.  TCA cycle: Active ix.    ETC: Active x.     Ketogenesis: Very active xi.    Ketolysis: Active xii.   Gluconeogenesis (from glycerol): Yes	2
5.	Effects of lipid metabolism during fasting (fasting lipid profile): i.      Blood glucose: low-normal ii.     Blood free fatty acids (FFA): high iii.    Blood ketones: high, acidic --> ketoacidosis iv.    Blood pH: metabolic acidosis, due to high ketones v.     Blood amino acids: low vi.    Blood glycogen: nil	2

STUDENTS' PROBLEMS WITH THIS QUESTION

Wrong answers

Lipid Digestion

Exogenous Lipoprotein Metabolism (Chylomicron metabolism)

Exogenous + Endogenous Lipoprotein Metabolism (CM + VLDL metabolism)

Lipid Digestion: Dietary fat will be combined with bile salt and formed into the water soluble micelles. Then, micelles will be transported to the intestinal absorption site. Once the micelles already absorbed across the intestinal mucosal cell, dietary fat will be reesterified to form into the triglyceride and also cholesterol esters and travels in the blood plasma.

Exogenous Lipoprotein Metabolism: Chylomicron will be released into the blood circulation by travels in lymphatic duct and thoracic duct. Chylomicron will be hydrolysed by the enzyme lipoprotein lipase (LPL) to become monoglyceride, diglyceride and free fatty acid to be uptake by the cells. While chylomicron remnant be uptake by the liver to undergo delipidation to be used to synthesize new lipoprotein and building of plasma membrane.

Gluconeogenesis: Under fasting state, lipid undergo gluconeogenesis to supply glucose. b-oxidation of lipid produce acetyl CoA. Under fasting state, lipid undergo lipolysis, and FFA undergo b-oxidation. Lipid is first breakdown and transfer into mitochondria matrix to form oxaloacetate (OAA). OAA convert to citrate and transported into cytosol. In cytosol, OAA is converted back by citrate. Citrate convert into phosphoenolpyruvate (PEP) by PEP carboxykinase. PEP is converted into fructose-1,6-biphosphate by fructose-1,6-biphosphatase. Fructose-1,6-biphosphate dephosphorylate bt fructose-6-phosphatase into fructose-6-phosphate. Frutose-6-phosphate convert into glucose-6-phosphate by phosphoglucomutase. Glucose-6-phosphate dephosphorylated into glucose by glucose-6-synthase. Glucose enter glycolysis to supply energy.

When fasting, glucose stores are depleted. Other sources of energy are needed by the body such as protein, fatty acids, and ketone bodies. Gluconeogenesis, glycogenolysis are all in the action at higher levels. Glucagon stimulate the secretion of fatty acid lipase to degrade fatty acid. This is termed lipolysis. This leads to increase in free fatty acids, that is degraded  to lactic acid and used in gluconeogenesis for ketone body generation. Ketone bodies are alkaline in nature and this leads to ketoalkalosis. Gluconeogenesis takes place 90% in the liver and 10% in the kidney. Lipolysis increase which leads to increase blood fatty acid and form alkaline urine.

Ambiguous answers

Fatty acyl-CoA will undergo gluconeogenesis to produce glucose.

Gluconeogenesis is process to produce glucose from non carbohydrate molecules.

During fasting, glucose will be breakdown first followed up by lipid breakdown, then only goes to protein breakdown.

Meaningless answers

Lipid –[fasting]--> FA + Glycogen (should be Glycerol)

Lipid will undergo gluconeogenesis

Lipid is hydrolysed to acetyl CoA

Fatty acids with short chain is transported directly into the blood circulation where it binds to ammonia and is stored as triglycerides.

Fatty acids with long chain and glycerol absorbed into the lacteal, then flows into the thoracic duct and finally into the blood.

Fatty acids is added with vitamen A, D, E and K to produce chylomicrons.

The chylomicrons are broken down into fatty acid and glycerol.

Remnents of the chylomicrons are stored in the liver.

Glucose will undergo glycolysis to produce high energy which is ATP.

b-oxidation itself can produce ATP.

Breakdown on lipid into fatty acid and triglycerides.

Lipid ---> FFA  +  TG [this is wrong] vs. Lipid ---> FFA  + Glycerol [this is correct]