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Answer- The ? oxidation accounts for the bulk of the energy production from fatty acids in human. 3) Peroxisomal fatty acid oxidation- Occurs for the chain shortening of very long chain fatty acids. There are systems in many tissues for the hydroxylation of ? –carbon of shorter chain fatty acids in order to start their oxidation. Although the use of the ?- Oxidation scheme is relatively less in terms of total energy production, but it is significant in the metabolism of dietary fatty acids that are methylated. 1)  ?- Oxidation  is most suited for the oxidation of phytanic acid, produced from dietary phytol, a constituent of chlorophyll of plants.
Figure-1- Phytanic acid is oxidised by Phytanic acid ? oxidase (?- hydroxylase enzyme) to yield CO2 and odd chain fatty acid Pristanic acid that can be subsequently oxidised by beta oxidation.This process involves hydroxylation of the alpha carbon, removal of the terminal carboxyl group and concomitant conversion of the alpha hydroxyl group to a terminal carboxyl group, and linkage of CoA to the terminal carboxyl group. 3) Odd chain fatty acid produced upon decarboxylation in this pathway, can be used for the synthesis of sphingolipids and can also undergo beta oxidation  to form propionyl co A and Acetyl co A .The number of acetyl co A depend upon the chain length. Refsum disease (RD) is a neurocutaneous syndrome that is characterized biochemically by the accumulation of phytanic acid in plasma and tissues. Peripheral polyneuropathy, cerebellar ataxia, retinitis pigmentosa, and  Ichthyosis (rough, dry and scaly skin) are the major clinical components. Refsum disease is an Autosomal recessive disorder characterized by defective alpha-oxidation of phytanic acid.Consequently, this unusual, exogenous C20-branched-chain (3, 7, 11, 15-tetramethylhexadecanoic acid) fatty acid accumulates in brain, blood and other tissues.
Classic Refsum disease manifests in children aged 2-7 years; however, diagnosis usually is delayed until early adulthood. The children usually have moderately dysmorphic features that may include epicanthal folds, a flat bridge of the nose, and low-set ears. Levels of plasma cholesterol and high- and low-density lipoprotein are often moderately reduced. Routine laboratory investigations of blood and urine do not reveal any consistent diagnostic abnormalities. The major dietary exclusions are green vegetables (source of phytanic acid) and animal fat (phytol). Plasmapheresis – Patients may also require plasma exchange (Plasmapheresis) in which blood is drawn, filtered, and reinfused back into the body, to control the buildup of phytanic acid.
The main indication for Plasmapheresis in patients with Refsum disease is a severe or rapidly worsening clinical condition. A minor indication is failure of dietary management to reduce a high plasma phytanic acid level. In early diagnosed and treated cases, phytanic acid decreases slowly, followed by improvement of the skin scaling and, to a variable degree, reversal of recent neurological signs.
Another minor pathway for the fatty acid oxidation also involves hydroxylation and occurs in the endoplasmic reticulum of many tissues.
It uses the “mixed function oxidase” type of reaction requiring cytochrome P450, O2 and NADPH, as well as the necessary enzymes. Hydroxy fatty acids can be further oxidised to a dicarboxylic acid via sequential reactions of Alcohol dehydrogenase and aldehyde dehydrogenases.
The dicarboxylic acids so formed can be activated at either end of molecule to form a Co A ester, which can undergo beta oxidation to produce shorter chain dicarboxylic acids such as Adipic acids(C6) and succinic acid (C4). The microsomal (endoplasmic reticulum, ER) pathway of fatty acid ?-oxidation represents a minor pathway of overall fatty acid oxidation. Although most fatty acid oxidation takes place in mitochondria, some oxidation takes place in cellular organelles called peroxisomes (Figure-2). Peroxisomes are a class of sub cellular organelles with distinctive morphological and chemical characteristics.
These organelles are characterized by high concentrations of the enzyme catalase, which catalyzes the dismutation of hydrogen peroxide into water and molecular oxygen. Fatty acid oxidation in these organelles, which halts at octanyl CoA, may serve to shorten long chains to make them better substrates of b-oxidation in mitochondria. Figure-2- Initiation of Peroxisomal Fatty Acid Degradation, The first dehydration in the degradation of fatty acids in peroxisomes requires a flavoprotein dehydrogenase that transfers electrons to O2 to yield H2O2. Zellweger syndrome, also called cerebrohepatorenal syndrome is a rare, congenital disorder (present at birth), characterized by the reduction or absence of Peroxisomes in the cells of the liver, kidneys, and brain. The most common features of Zellweger syndrome include enlarged liver, high levels of iron and copper in the blood stream, and vision disturbances. There are several noninvasive laboratory tests that permit precise and early diagnosis of peroxisomal disorders.  The  abnormally high levels of VLCFA( Very long chain fatty acids ), are most diagnostic.
The prognosis for infants with Zellweger syndrome is poor.  Most infants do not survive past the first 6 months, and usually succumb to respiratory distress, gastrointestinal bleeding, or liver failure. Symptoms of diabetes include excessive thirst, increased urination, weight loss and fatigue. The classical symptoms of diabetes include excessive thirst, increased urination, weight loss and fatigue. Will the 2017 sugar tax on sugar-sweetened soft drinks put you off drinking this type of beverage? Science, Technology and Medicine open access publisher.Publish, read and share novel research. Neither the service provider nor the domain owner maintain any relationship with the advertisers. These reactions must be supplemented by other mechanisms, so that all types of ingested fatty acids can be oxidised.
Phytanic acid is a significant constituent of milk lipids and animal fats and normally it is metabolized by an initial ?- hydroxylation followed by dehydrogenation and decarboxylation. Propionyl co A is converted to Succinyl co A to gain entry in to TCA cycle for further oxidation. The symptoms evolve slowly and insidiously from childhood through adolescence and early adulthood. It is almost exclusively of exogenous origin and is delivered mainly from dietary plant chlorophyll and, to a lesser extent, from animal sources. Dysfunction of myelinated nerve fibers and the cardiac conduction system leads to central and peripheral neuropathic symptoms, impaired vision, and cardiac arrhythmias.
In this case hydroxylation takes place on the methyl carbon at the other end of the molecule from the carboxyl group or on the carbon next to the methyl end.
It has been suggested that peroxisomes may function in a protective role against oxygen toxicity. Peroxisomal oxidation differs from beta oxidation in the initial dehydrogenation reaction (Figure–2). Thus peroxisomal enzymes function to shorten the chain length of relatively long chain fatty acids to a point at which beta oxidation can be completed in mitochondria. It is important to recognise these symptoms as, left untreated, diabetes can cause coma and even death.
In case of trademark issues please contact the domain owner directly (contact information can be found in whois). Beta oxidation can not occur initially because of the presence of 3- methyl groups, but it can proceed after decarboxylation. Patients with Refsum disease are unable to degrade phytanic acid because of a deficient activity of Phytanic acid oxidase enzyme catalyzing the first step of phytanic acid alpha-oxidation.

In peroxisomes, a flavoprotein dehydrogenase transfers electrons to O2 to yield H2O2 instead of capturing the high-energy electrons as FADH2, as occurs in mitochondrial beta oxidation. Other peroxisomal reactions include chain shortening of dicarboxylic acids, conversion of cholesterol to bile acids and formation of ether lipids. In non-diabetic individuals (left), activation of the insulin receptor can result in activation of both vasodilatation and vasoconstriction. Upon binding of insulin, insulin receptors are autophophorylated and subsequently bind IRS proteins. A number of drugs used clinically to decrease triglyceride levels in patients cause a marked increase in peroxisomes. Catalase is needed to convert the hydrogen peroxide produced in the initial reaction into water and oxygen. Given these diverse metabolic roles it is not surprising that the congenital absence of functional peroxisomes, an inherited defect , known as Zellwegar syndrome, has such devastating effects. Under normative conditions, there is a balance of both processes to regulate the immediate metabolic requirements of various tissues. IRS proteins are then phsophorylated by activated insulin receptors and complex with PI3K resulting in PI3K activation.
Vascular dysfunction resulting from type 2 diabetes results in a state of cerebral hypoperfusion, leading to significant energy depletion in the brain. Phytanic acid replaces other fatty acids, including such essential ones as Linoleic and Arachidonic acids, in lipid moieties of various tissues.
Subsequent steps are identical with their mitochondrial counterparts, although they are carried out by different isoforms of the enzymes. However, the first sign of type 1 diabetes can also be a coma, or near coma, as a result of an event called diabetic ketoacidosis in which the levels of glucose in the blood are so high that this life-threatening state occurs. In type 2 diabetic patients (right), factors such as an increase in free fatty acids and hyperglycemia have been shown to specifically inhibit the Akt pathway while the MAPK pathway remains unaffected.
Activated PI3K produces phospholipid secondary messengers by catalyzing the conversion of phosphatidylinositol 4,5-bisphosphate (PIP2) to phosphatidylinositol 3,4,5-trisphosphate (PIP3).
Boniface Hospital Research Centre, Winnipeg, MB, Canada[2] Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, MB, Canada1. This situation leads to an essential fatty acid deficiency, which is associated with the development of ichthyosis. Of central diagnostic importance are the typical facial appearance (high forehead, unslanting palpebral fissures, hypo plastic supraorbital ridges, and epicanthal folds.
Due to a lack of insulin, the glucose in the blood cannot enter the cells where it is desperately needed.
This leads to an imbalance in homeostatic regulation of vascular function and hemodynamics (1).
T2DM also causes (7) hyperinsulinemia which exacerbates IDE deficiencies because (8) excess insulin occupies IDE binding sites rendering them unavailable for A?. The resultant decrease in nutrient availability to affected tissues results in an increase in oxidative stress and ROS production and an increased inflammatory response (2).
Akt is further activated by phosphorylation at Ser 473 by mammalian target of rapamyicin 2 (mTORC2). The increased amyloidogenic processing that occurs in insulin resistance combined with decreased A? clearance by IDE results in a deleterious positive-feedback cycle as (9) A? oligomers contribute to insulin resistance in the brain. Ketones can be used as food by the cells, for example cells in the brain, even in the absence of insulin. Released pro-inflammatory cytokines and macrophage recruitment instigates the onset of atherosclerosis, ultimately leading to macrovascular complications (3).3.
Targets of activated Akt include pro-apoptotic mediators (in red) as well as pro-survival machinery (in green).
As A? levels continue to rise, insulin resistance worsens leading to further production of the toxic peptide.6. But starvation or surgery are unnecessarily painful ways to do it.Luckily diabetics can eat real food to satiety, as long as they avoid sugar and starch. Loss of insulin signaling (at sites labeled with numbers 1-6 in purple) allows FoxO and p53 transcription factors to remain active and (1) transcribe genes for pro-apoptotic proteins such as BIM, BAX and FasL. Akt inhibits the activity of GSK-3? that, when active, (2) causes increased amyloidogenic processing and hyperphosphorylation of tau. They might have nausea and vomiting and loss of appetite.They urinate excessively, and if the condition is not recognised and treated urgently, the person becomes drowsy and eventually comatose. Other pro-apoptotic proteins inhibited by Akt include (3) caspase-9, which forms an apoptotic structure known as the apoptosome, and (6) Bad, which blocks activity of the ant-apoptotic protein Bcl-xL.
Number two: the smaller amounts of starch you eat is not digestedd as easily as the duodenum with the starch-digesting enzyme amylase is diverted from direct contact with the food.
I don't consider it a "disease" to be "cured," but a symptom, along with obesity, high blood pressure, coronary artery disease, etc. Often the diagnosis is made coincidentally, or after the patient presents with a complication caused by the condition. Symptoms of type 2 diabetes, when they do occur, might be similar to the symptoms found in type 1 diabetes, but not as severe:- Excessive thirst - Increased urination - Blurred vision - Weight loss - Fatigue Early in the course of the disease there might be subtle signs such as greater susceptibility to infection, poor wound healing, and fatigue.
That condition cannot be cured, in most cases, but the symptoms can be prevented and reversed. An early sign in men is occasional erectile dysfunction.Candida infection of the tip of the penis (Candida balanitis) is also common. Certainly gastric bypass and starvation will eliminate high blood glucose as a symptom of carbohydrate intolerance just as you have been reporting. I completely agree that those are drastic and miserable ways to do so when we know that there is a simple and healthy way. Classical signs of diabetes are often confused with symptoms common to pregnancy, for example, fatigue and frequency of urinating (micturition). It is amazing that the medical community would promote those two methods for treating "type II" but rant and rave about the dangers of HFLC diets.
Now, all of that said, my lovely sister would disagree adamantly with most of what I have written.
My sister is the only one of us who had received the dreaded diagnosis of "Type II Diabetes,' which she still fully accepts as a disease for which is being seen regularly, with blood tests and medications. For whatever reason that I cannot fathom, the low-carb diet has not controlled her blood sugar. Although she is not grossly obese, in spite of the diet and exercise, she still carries alot of abdominal fat and I would expect her waist size would put her in the category of obese. She has high fasting blood sugars, usually around 150, although if has so much as a cold it can be above 200.
This is a conundrum and is really messing with my belief that "Type II" is not a disease and is an easily managed symptom!
She has good cholesterol readings and doesn't seem to be having any of the other complications associated with the "disease," but I'm concerned that at age 60, if this isn't resolved, she may begin to have other problems. One has no symptoms anymore after being 100% compliant with my recommendations - no starches, moderate saturated fat, high monosaturated fats, high quality protein. The other is 80 and is so bound to the American culture of eating grains, he is struggling with it.

He and his wife just have a hard time with the concept of lunch without a sandwich, breakfast without bread, cereal, or oatmeal, dinner without bread, corn, rice, and so on. No starches, no grains, only true, green leafy vegetables, and the high fiber part of the diet is always eaten first. That means start with a salad with high fat dressing, no croutons, no fruit - you get the picture. Mary Vernon, who has had great success treating patients with type II diabetes (or insulin resistance or whatever you want to call it) with a very low carb diet. Vernon will figure it out and help her reach success.As for the article in the Guardian--such rubbish!
I was still ‘out of control’ even when doing everything I had been told to do by ‘experts’. I said no way, there has to be something else because nothing is getting better even when I follow your rules. He didn't appreciate my opinion and told me I would get sicker and die faster if I didn't accept a new prescription.
On drugs and a 'diabetic diet' I had trouble sleeping, I was tired all day, and I lost very little weight even with increased exercise.
I was irritable and depressed, my work performance was declining since I couldn't keep up because I was so tired and my family was worried sick about me. I followed a self made regimen from research that I did (layman’s amateur research) and as far as energy and mood I actually felt better within 2 days of starting, but my sugars were staying at 250-300 all the time. I stumbled across an Edutainment Documentary ‘Fat Head’ and was truly shocked by the evidence that it provided for a LCHF diet. I have more energy, my mood is significantly improved and although my sugar levels are high (and coming down daily) all of the symptoms I had been experiencing are gone. Of course I am not a medical professional, but like has been said above; your sister may be eating hidden sugars. Whole milk and cream are great, but high in lactose (sugar) for someone trying to come down. Fruits and veggies are great, but until sugars are in control and the body is working properly again, it may be a good idea to go ‘no carb’ until progress is made with glucose control. I don’t know if she takes vitamins or supplements, but it could also be of great worth to investigate high dosage vitamin therapy. But I’m not an orthomolecular (natural) physician or a nutritionist, just a new convert to the right way of thinking and I am passionately involved. And the starvation isn’t even necessary to do that."It is frequently reported (and is reported in the comments above) that certain individuals apparently do not respond to low carb diets. An argument can be made that they are 'cheating' and consuming carbs, or perhaps more likely their body takes longer to normalize than is typical.
Therefore, it is clear that this eating style can be permanently adopted if necessary.12SteveNovember 12 20112 weeks ago I was diagnosed with type 2 diabetes. Due to stress, poor diet choices and being about 15 kilos overweight, as well as being addicted to coffee, I ended up in hospital with a heart rate of 145 (atrial flutter) and blood glucose in the 16-21 range.
I was kept on a heart rate monitor and small doses of insulin and beta blockers were prescribed while doctors conducted a number of tests on my heart. After a week in hospital I was discharged, having lost almost 5 kilograms in a short time.I found the University of UK article and additionally read carefully the scientific paper which was downloadable in PDF form.
I immediately began the same program, even imitating the type of diet shake used in the Newcastle University Study. I was emailed the following day by a researcher from Sydney Uni whose first sentence moved to dismiss and minimize the UK research. I replied that I wasn't very enthusiastic, but attached the PDF file of the Uni Newcastle research, which is a scholarly and well researched piece.
I'm taking several weeks off work, which I think is a worthwhile investment in my long term health. I'm trying to rest and keep my environment as stress free as possible.My program is to swim about a kilometre a day, at a gentle pace. Around 3pm I have a bowl of non starchy vegetables like asparagus, capsicum, baby spinach, tomato, celery, avocado with a garnish of a teaspoon of organic flaxseed oil. I add a sprinkle of black chia seeds.I've added a single high grade multivitamin tablet and a Bilberry tablet to my morning shake.
My heart beat has been fully normalized since discharge from the hospital, however one day I took 2 x 500mg Ginseng tablets which gave me additional energy but seemed to cause a rapid heart rate that evening. I immediately stopped taking Ginseng.Apart from the total normalization of my blood glucose without medication, I've noticed that my previously blurry distance vision has become completely sharp and in focus. Unfortunately, I seem to have to use reading glasses all the time, which was not the case before.This type of diet, if initiated on a large scale, would probably require additional support from a government agency.
I have needed to take only a few units of insulin on this diet because of low starch vegetables, and eating protein.
Chronically overload the body cells with more glucose then they can burn results in cells being saturated with glucose.Issue is to ensure that energy consumption, plus liver leakage throwback need to be balanced out by process and energy burn - hearty exercise.
As those muscles glucose storage are one way in, hearty exercise is mandatory to burning that off on a daily basis. However, you insulin expects “natural fat” around every cell in your body for the past 4M years – evolution! So Insulin is “confused” by the new molecular structure of the fat membrane around you cells.
By replacing the “man-made” fat by natural fat (from walnuts) over 7 months you insulin works as intended , opens the cell wall and lets the sugar in to be consumed as energy. 1)My diet is low carbohydrate but its also limited to those foods defined in Leviticus 11, I don’t eat meat or fish which is outside the scope of biblical definition (no Pork, no shell fish etc…) 2)The second half of eating right as a diabetic is understanding your daily routine and sticking with it. Within 4 hours of the end of that period, you should not intake any carbohydrates at all and you should stop eating any food. I would be willing to bet your sister eats low carbohydrate meals but places them in a traditional fashion (breakfast, Lunch and Dinner). No carbs (unless in green vegetables or peppers) the odd bit of fruit and a good old work out every day (swimming or gym). Sometimes when I test after a hard session my BG goes up - I suspect that this is stored glucose being released to make up for the energy being burnt.
Now I eat more dense foods, more nutritious foods,more quantities also and feel much more healthier. I'm sure Dr Fung says that high sugar levels when fasting is normal as it is the sugar flooding into the blood as a result of lower insulin (high insulin pushes sugar levels down). Learn more about the Diet Doctor organisation and join us in empowering people to revolutionise their health.

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