Tag Archives: Oxidative phosphorylation

Obesity and weight lose

Leptin concentration in relation to obesity

January 24, 2017
Leptin concentration

Leptin concentration in relation to obesity. In fact, Leptin concentrations adjust in response to obesity and contribute to insulin resistance

Leptin concentration in relation to obesity: Insulin resistance

Leptin regulates energy metabolism and balance in conjunction with the brain’s hypothalamus. Leptin is currently being touted as having cardio-protective benefits among its others roles in metabolism. Leptin concentrations adjust in response to obesity and contribute to insulin resistance. Besides that, doctor Dalal Akoury MD, President, and founder of AWAREmed health and wellness resource center register that, the changes in leptin concentration have also been associated with the risk factors for coronary heart disease. In the same way, increased resistin concentrations correlate with obesity-related inflammation and may be associated with the initiation and progression of atherosclerotic lesions. Resistins also promotes insulin resistance, although the actual mechanism is still not very clear.

Insulin resistance due to adipokines dysfunction is further influenced by free fatty acids liberated directly into the liver from the visceral fat tissue. Visceral fat releases chemicals and fatty acids into the portal system where they act on the connecting organs. The portal circulation system is a specialized network of blood vessels that connect the visceral organs to the liver. The excess fat in the portal circulation has detrimental effects on insulin action, which is worsened by sympathetic hyperactivity in response to obesity. Sympathetic hyperactivity causes heightened lypolytic action resulting in excess free fatty acids in the blood. These actions combined with beta cell hypersecretion and reduced insulin clearance resulting in hyperinsulemia, lead to early stage diabetes.

Leptin concentration in relation to obesity: Interleukin-6 (IL-6) 

Interleukin-6 (IL-6) is possibly another factor associated with inflammatory detriment within the portal system. High levels of IL-6 are a marker for inflammation and vascular pathology. Obese subjects demonstrated a 50% greater portal vein IL-6 concentration, demonstrating, again, the profound effect visceral fat has on pathogenic indicators. Portal vein IL-6 correlates with systemic C-reactive protein concentrations. And remember that the C-reactive protein is associated with cardio and peripheral vascular disease. C-reactive protein and oxidative stress are now presumed to interact in the early inflammatory processes of atherosclerosis. This is significant for young obese individuals. Although more research is necessary for a conclusive association, the C-reactive protein may be a new risk factor for CAD in individuals under 25 years of age.

The imbalance between increased inflammatory stimuli with a concurrent reduction in anti-inflammatory activity may be the foundation for the accelerated endothelial dysfunction and insulin resistance associated with obesity and the comorbid disorders of metabolic disease. However, more research is needed to clearly delineate the particular relationships, though it seems evident that the low-grade inflammation caused by obesity and visceral adiposity lead to the premature development of the disease. This, more so than ever before, identifies the importance of weight management during the developmental years and ongoing efforts to control weight throughout one’s lifespan.

Finally, for current obese people, there is still plenty of hope. Weight loss is related to the reduction of oxidative stress and inflammation, and these beneficial effects are likely to translate into the reduction of cardiovascular risk in obese individuals. Likewise, exercise and dietary management, along with pharmacologic intervention can lead to the atherosclerotic reversal in the earlier stages of CAD. Individuals with central adiposity, poor blood lipid profiles, hypertension, or insulin resistance should seek immediate professional assistance to prevent further health detriment by scheduling an appointment with AWAREmed health center now.

Leptin concentration in relation to obesity: Insulin resistance

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Glycolysis Inhibitors Help in Fighting Cancer

August 4, 2014

 

The Role of Glycolysis Inhibitors In Fighting Cancer

The best way of killing cancer cells is to starve them. This is the safest way of killing cancer cell as the normal healthy cells are not affected by this way of killing the cancerous cells. In the past it was a big problem finding a way of killing the cancerous cells without affecting the healthy body cells. This is because all the cancer cells as well as the healthy body cells depend on glucose as their energy source that they need to survive. However very many researchers have done work on the subject of cancer cell metabolism and the discovery by Otto Warburg that the cancer cells depended entirely on glucose for source of energy unlike the healthy body cells that can adapt to other sources of energy like fats helps a lot in selective killing of cancer cells without hurting the healthy body cells. The cancerous cells undergo increased glycolysis and rely on this pathway for generation of ATP energy as their sole source of energy for growth and survival.

Basing arguments on the Warburg effect, doctors have come up with different cancer therapies to help in killing the cancer cells effectively without hurting the healthy body cells. The cancer cell overdependence on the glycolitic pathway for generation of ATP energy as the sole source of survival has provided a great loophole through which the cancer cells can be selectively killed without affecting any other healthy cell by inhibiting glycolysis.

There are Glycolytic inhibitors that can be used in maiming the cancer cells by denying them their source of livelihood. By inhibiting glycolysis they exert an anticancer effect on the cancer cells hence help in killing the cancer cells.

Glycolytic inhibitors can be used mostly in fighting cancer cells that have mitochondrial defects or in hypoxic conditions. These cells often become resistant to conventional medication such as chemotherapy or radiation therapy. However increased glycolysis is a common characteristic of all tumor cells and glycolysis inhibition can be used in wide range in treating cancer patients.

Though it may be difficult to understand the molecular and biochemical mechanisms that lead to increased aerobic glycolysis in the cancer cells, the metabolic repercussions of this increased glycolysis is very clear. The malignant cells become dependent or other addicted to the glycolysis pathway as the sole source of ATP energy. Researchers opine that the increased glycolysis in cancer cells may be caused by such factors as; hypoxia, oncogenic signals as well as mitochondrial dysfunction.

The cancer cells have to access a reliable supply of glucose in order to live. Unlike oxidative phosphorylation which generates more ATP energy per glucose the ATP generation of ATP through glycolysis is too little. Typically oxidative phosphorylation produces 36 ATP per glucose while glycolysis produces 2 ATP per glucose. This therefore forces the cancer cells to eat more glucose for effective metabolism as well as to accomplish other activities. The cancer cells therefore need to maintain glycolitic activities in order to grow and live on.

This metabolic characteristic of the cancer cells has availed a better way of killing cancer cells. Researchers have now proved that by inhibiting glycolysis the cancer cell will stop production of the ATP energy that they depend on and so they will die out of starvation.

When there is glycolysis inhibition the normal body cells will be able to adapt to other metabolic pathways to generate the ATP energy through the TCA cycle and oxidative phosphorylation in the mitochondria. The cancer cells however cannot adapt to other sources of ATP as they have defects hence will die as they will not be able to live without another source of ATP energy. The healthy body cells will be able to adapt to new sources of energy like fatty acids and amino acids to produce metabolic intermediates channeled to the TCA cycle for ATP production through respiration. Glycolysis inhibition is therefore a clever way of killing the cancer cells without harm on the healthy body cells.

DCA as a Glycolysis inhibitor

The way DCA works as a glycolysis inhibitor is very interesting; it forces the cancer cells to generate ATP through glucose oxidation but the cancer cells are not able to do this and they get starved and die. The healthy body cells can adapt to metabolic changes unlike the cancerous cells. The first way through which the body cells get energy is through glucose oxidation which happens in the mitochondria of every cell in the body and requires oxygen. Glucose respiration is the mostly utilized form of metabolism in the healthy cells. However in absence of oxygen the cells turn to glycolysis which takes place in the cell cytoplasm for energy generation. Glycolysis does not avail adequate ATP energy for normal cells; however it is the best for cancer cells. Glycolysis depends on sugar. This gives the healthy cell advantage as they have a backup plan in case the oxygen supply is interrupted. However to oxidize glucose there must be pyruvate. Pyruvate entry into the mitochondria is inhibited by an enzyme known as pyruvate dehydrogenase kinase (PDK). In case the PDK is strong then it will limit the transportation of pyruvate into the mitochondria and the healthy cells will have to depend on glycolysis even in presence of oxygen but incase its weak the pyruvate will be transported with ease to mitochondria even when the oxygen is low.

Cancer cells have the most active PDK than the healthy cells and they are adapted to glycolysis. When PDK is weak then the cancer cells are disadvantaged and this is what the DCA does. It weakens PDK forcing the cancer cells to rely on glucose oxidation which does not favor them. Hence they will starve and die.

Dr. Dalal Akoury is an experienced integrative cancer doctor who has seen very many cancer patients journey to victory in their fight against cancer. She is available for consultations. Just call her now and begin your journey to victory against cancer.

The Role of Glycolysis Inhibitors In Fighting Cancer

 

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MITOCHONDRIAL RESTORATION TO TREAT ADDICTION

July 29, 2014

What is a mitochondrion?

They are also sometimes referred to as the powerhouses. It is a membrane bound organelle which is found in most of the cells (eukaryotic cells) that make up living things.

What is the function of mitochondria?

mitochondrial restorationAs we mentioned earlier, mitochondria are also referred to as powerhouse due to the functions that they do in our bodies. Their main work is to generate the energy that our body cells require in order to execute their jobs. One of such cells which need a lot of energy is the brain cells. The brain cells are responsible for the communication to all the other parts of the body and thus these mitochondria must be transported along the cells.

Mitochondria generate chemical energy similarly to the one we normally get from batteries. This energy which is generated by the mitochondria in the form of chemical is referred to as Adenosine Triphosphate or simply ATP. This is an energy currency that every ling thing cell can use and this is what makes it possible for us to be kept alive.

What principle makes mitochondrial restoration able to treat addiction?

Most of the addictive drugs cause damage in the body organs. For instance, alcohol may cause damage to the liver, muscle weakness as well as brain damage in severe cases. Any attempt to help the patent recover from the addiction must therefore apart from treating the addiction itself focus on the damage that has been caused by the addictive drug on the various body organs.

Any cure for addiction that doesn’t address the damage caused by the drug is considered incomplete since even after the patient recovers from the addiction, he/she will suffer from other illnesses which may come as a result of the damage caused by the drug. On top of this, some of the prescription addiction recovery drugs have been found to have residual effects on the body of the addict even after recovering from the addiction.

Mitochondrial restoration is a natural process that seeks to restore the various body organs which have been previously cellular affected to their normal working state. The mitochondrial restoration targets the organs that have been affected by the addictive drug and hence whose functional capacity has been also been affected but the drug and then restores its functional state.

Addiction is known to first affect the human brain before the drug even has any effect to the other related organs. In this case therefore, the treatment of addiction must address the damage that has been caused to the brain by the drug. Mitochondrial restoration is an appropriate natural way of treating addiction, since it helps in the restoration of the various body organs to their normal working states.

The mitochondrial energy

As earlier mentioned, the core mandate of mitochondria in the body is to produce the energy required by the cells in the body. The mitochondrial energy production is usually accompanied by two very closely linked metabolic processes. These processes are; a) the citric acid cycle also known as the Krebs/ biological fuel and b) an oxidative phosphorylation (OXPHOS).

mitochondrial restoration

  • The citric acid cycle

This is usually a series of chemical reactions which are used by all aerobic organisms to generate energy via the process of oxidation of acetate which is derived from the food. The acetate is converted into carbon dioxide and chemical energy in the form of adenosine triphosphate (ATP). This cycle also provides some precursors of certain amino acids as well as the reduction of the NADH that is used in a number of other biochemical reactions in the body.

  • Oxidative phosphorylation

This is the pathway through which the mitochondrion which is released by the oxidation of nutrients is transported to the cells. They use its structure, enzymes and energy released by the oxidation processes to reform ATP. ATP is an important molecule in the body, as it works to supply energy to all the metabolic processes.

OXPHOS operates through a network of electrons, five protein complexes which are attached in the inner membrane of the mitochondria. The five protein complexes are: –

The oxidative phosphorylation converts adenosine di-phosphate (ADP) to adenosine triphosphate (ATP). This is the chemical currency of cells and can then be transported to the cells where work needs to be done.

Does mitochondrial restoration provide a permanent solution to the drug addict?

The aim of mitochondrial restoration is to ensure that the cells in the body are provided with the energy that they need to function. By ensuring that the cells are working correctly, makes it possible for the addict’s body organs to heal from the damage caused by the drugs. This ensures that the addict is healed inside out from the addiction and its damages it had caused to the addict’s body. This also helps to ensure that the recovery process doesn’t experience withdrawal symptoms and craving. This process though may take some time to complete; it provides a permanent solution to the addict as well as improving the overall well-being.

MITOCHONDRIAL RESTORATION TO TREAT ADDICTION

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