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St. Kitts & Nevis
I'm a physician doctor with an MD degree. My passion for teaching has always been appreciated by students with whom I have shared my knowledge. I'm a passionate teacher of medical biochemistry and would like to share my knowledge about this beautiful subject with all those who is interested to learn to understand the cellular metabolic events and to understand the metabolic disease process. I would like to learn new things by keeping myself updated with current research in the field. Let us share the knowledge each other!!

Tuesday, March 24, 2015

Worth reading - article on sugar, processed food and heart diseases.


Wednesday, March 11, 2015

Explanation for CNS changes seen in hyperammonemia!

Explanation for CNS changes seen in hyperammonemia! 

High levels of ammonia 5-10 fold higher than normal induces metabolic changes with alteration in the function of central nervous system. High ammonia levels leads to increased extracellular concentration of glutamate in the brain and results in activation of the N -methyl D-aspartate (NMDA) receptor. Activation of this receptor mediates ATP depletion and ammonia toxicity; Activation of NMDA receptors is believed to be responsible for seizures seen in hyperammonemia. 

Hyperammonemia leads to downregulation of glutamate receptors secondary to excessive extrasynaptic accumulation of glutamate. In addition, changes in the glutamate-nitric oxide-cGMP pathway result in impairment of signal transduction associated with NMDA receptors, leading to alteration in cognition and learning. There is also increased GABAergic tone resulting from benzodiazepine receptor overstimulation by endogenous benzodiazepines and neurosteroids. These changes probably contribute to deterioration of intellectual function, decreased consciousness, and coma. 

Ammonia also increases the transport of aromatic amino acids (eg, tryptophan) across the blood-brain barrier. This leads to an increase in the level of serotonin, which is the basis for anorexia in hyperammonemia.

Other metabolic changes that are not mediated by activation of the NMDA receptor and thus are not involved directly in ammonia-induced ATP depletion or neurotoxicity. These include increases in brain levels of lactate, pyruvate, glutamine, and free glucose, and decreases in brain levels of glycogen, ketone bodies, and glutamate.

Wednesday, February 25, 2015

Energy sources for brain and other tissues during fasting and starvation.

During fasting and starvation as a physiological adaptation mechanism different reserves are used in our body to provide the energy needs of different tissues in.ucding brain and RBCs. Initial energy source is glycogen and then it shifts to protein breakdown and lipolysis. Please watch the video below to learn more. 

Tuesday, February 24, 2015

Energy yield from breakdown of glycogen

Are you wondering how many ATPs you get from the glucose 1-phosphate released from glycogen? Please watch my video on this topic. 


Energy from complete oxidation of glucose.

Want to know how many ATPs you get on oxidation of glucose then please my video on energy yield from complete oxidation of glucose to 6 CO2.