Objective: The aim of this study is to screen the polyherbal preparation for antidiabetic activity in rats. ANTI-LIPID PEROXIDATIVE ACTIVITY OF GONGRONEMA LATIFOLIUM IN STREPTOZOTOCIN-INDUCED DIABETIC RATS. The prevalence of hyperglycaemia depends on the diagnostic criteria used in epidemiological surveys. The prevalence of diabetes was relatively consistent across the income groupings of countries. The results of any blood glucose estimation are subject to quite a few variable factors which may interfere with the correct estimation and give a variation on the same sample of blood to the tune of 30-50mg%! The Somogyi-Nelson and the Hoffman methods although better that the Folin-Wu method should also be discarded and only the methods which will give the true glucose values like those using the Glucose oxidase system should be used. Until we reach a stage where the method of estimating the blood glucose levels becomes unversally standardised, we would have to take the method by which any blood glucose is reported into consideration whilst interpreting a report especially if the report is to be compared with any previous results. Often they go to the nearest place available to where they are on the day the test has to be done.
Even if the methods and the material on which the glucose is estimated are the same, the problem is still compounded by other factors. Some laboratories have started using the pinprick method to collect a drop of blood from the fingertips and this capillary blood is known to show glucose values which are again anywhere between 10-20mg% higher than what would be estimated in a simultaneously collected venous sample! The time that elapses between the collection of the blood sample and its estimation also affects the results. In view of such variability in the test results, it is not possible to make any valid comparison between the latest and any previous report.
Such, occasional blood glucose estimates cannot be used to correctly adjust the treatment and these estimates should really be called guesstimates (as the Americans with their penchant for joining two words call it), and accepted as such. I would also like to point out the fallacy of presuming that one can judge blood glucose control on the basis of these occasional blood glucose reports.
When we talk of control we mean the average blood glucose levels at all times and not only at the time of the test !
Conversely, we take the example of a patient who has kept to his diet, exercise and medications in the months since the last test and has been in acceptable control in he sense that his blood glucose levels have been in a good range throughout the three months. Blood glucose control is to be judged over a span of time and it is obvious that occasional blood glucose test will NOT give us any idea about the true control. An estimation of the glycosylated hemoglobin (HbA1c) levels allows us to assess the blood glucose control over the previous two months.
Therefore, if one were to estimate the amount of amino acids (protein) to which glucose has become attached, one would be able to gauge the amount of glucose to which the protein had been exposed. If all this sounds confusing, another way of looking at this would be to imagine that a needle has been inserted into the blood stream and this needle leads into a computer. Estimation of the HbA1c levels has some definite advantages over the occasional testing for blood glucose levels at intervals of 2-3 months, that we have previously discussed. Let us take the same two examples that we considered to show the fallacy of trying to judge blood glucose control by the occassional test for blood glucose levels. Conversely, the patient who has been in good control, but due to some reason like suffering from a 'flu' attack, shows a higher than acceptable blood glucose level would manifest a basically an acceptable HbA1c level as the deterioration in the blood glucose values in the past couple of days would not significantly alter the levels. It is possible to get a fairly good idea of the average blood glucose levels over the past two months based on a correctly carried out HbA1c reading. Although, HbA1c levels do give an excellent idea of the blood glucose control over the previous 60 days, there is one other, clinical aspect that needs to be considered. The other, and definitely better alternative is for the patients to self monitor their blood glucose levels (SMBG). SMBG by the patient himself has, in my opinion, completely revolutionised the modern management of diabetes.
Ideally, all patients should self monitor their blood glucose levels, using test trips and meters which are now available. It should be clear that in many these conditions one would not have the luxury of waiting for HBA1c levels, it may not be possible to go to the laboratory at odd times and so frequently, and in many of such conditions, the urine tests are fraught with too many errors for them to be of any use. Patients who may not fall in these "critical" categories, are asked to test the blood glucose daily at different times for about 1-2 weeks or until they are confident about the method of testing and are optimally controlled. All doctors treating patients who have diabetes must use a glucose meter as a part of their medical equipment, just as they carry a stethoscope and a BP apparatus. Carrying a meter with you would also be of help in certain emergencies which you may attend. One problem with the use of glucose meters and strips is that the strips may spoil rapidly in the high ambient temperatures and the degree of humidity that occurs in our country.
Patients especially if they have to test themselves often complain about the pain of pinpricks.
One fear that has been expressed with the routine use of self monitoring is that one may make patients neurotic about their blood glucose control. In conclusion, self monitoring of the blood glucose levels by the patient along with an estimation of the HbA1c level at 2-3 monthly intervals allows us to offer the most optimal method to judge blood glucose control at present. Most importantly, it must be realized that monitoring blood glucose levels is not the same as monitoring diabetes.
Besides glycemic control, optimal monitoring in diabetes, implies optimising weight, blood pressure, lipid abnormalities, and importantly, the diagnosis of the presence of long term complications in their early, initial stages. The Rosedale Diet is the most scientifically advanced diet in the world, that has been shown to mimic the amazing effects of caloric restriction on health and life extension, without having to even think about restricting calories. A carbohydrate diet is currently the diet of choice by the American Heart Association, The American Diabetes Association, The American Cancer Association, most weight loss experts, most nutritionists, and also, I should say, most sports physiologists. Let’s talk a little bit about hyperinsulinemia, because a high carbohydrate diet certainly causes high insulin levels.
In the last, well, especially 15 years, but even 20 or 30 years, our consumption of fat has declined.
The sugar goes to the receptors throughout the body, especially fat and muscle cells, and that stimulates the number of reactions which cause glucose uptake and utilization, glycogen synthesis, and then decreased serum glucose, straight forward.
A quick chart, and I will not draw on it too long, but it shows the rise in incidence of coronary disease, with fasting serum insulin. Gerald Ravin is one of the pioneers in insulin resistance research, and I won’t dwell too long on this, but he is talking about some of the diseases that are clustered in insulin resistance. This talk was given in 1995, and it is quite surprising that it is still new information today. This entry was posted in Articles, Interviews and tagged diabetes, Hormones and Diet, insulin, insulin resistance, Low-carbohydrate Diet, mTOR, rosedale.
I am wondering if you have some info about tests of these key measures in the United States. The insulin tolerance test with 15 minutes of readings on glucose response sounds like a low-impact and great test. This post mentions that insulin may upregulate HMG CoA Reductase, resulting in more endogenous cholesterol production. 1) Measure active levels of HMG CoA Reductase, so that we could establish some baseline against a larger population of people who have normal glucose metabolism? Familial hypercholesterolemia involves various kinds of defects in the LDL receptors, with the result being that the body cannot extract cholesterol out of LDL, and excess LDL sits in the blood unprocessed.
It sound like you are saying that the fat stored in an animal manufactured from carbohydrates is worse than other saturated fat found in an animal. Background: The oxidative stress is known to cause mutation-related disorders in diabetic patients.
Antigenotoxic effects of a polyherbal drug septilin against the genotoxicity of cyclophosphamide in mice. Yet the levels of glucose in the bloodstream are maintained within narrow limits by two key hormones-insulin and glucagon-working to prevent hyperglycemia (abnormally high glucose levels) or hypoglycemia (low glucose). Susceptibility of hippocampus and cerebral cortex to oxidative damage in streptozotocin treated mice: Prevention by extracts of Withania somnifera and Aloe vera. Hypoglycemic effects of Aloe vera gel on streptozotocin-induced diabetes in experimental rats.
Treatment with extracts of Momordica charantia and Eugenia jambolana prevents hyperglycemia and hyperinsulinaemia in fructose fed rats. Patients are usually seen at 2-3 monthly intervals and the fasting and the 2 hour post lunch blood glucose levels are estimated. Firstly, it should be clear that, at present times in our country, there is no accepted standard method to estimate the blood glucose levels. When the patient goes for his blood glucose one must make sure that the laboratory does utilize the oxidase method.
I have often come across patients who come with two or three previous results and it becomes impossible to compare results because the methods by which the blood glucose have been estimated each, time are entirely different! Thus one of the reports may be from the hospital where the patient may be seen, the next may be from a laboratory near the house of the patient and the third, especially if it is a post meal report, would be from a place of work of the patient.
At the same time, it should be added that the newer glucose meters come calibrated to show the equivalent venous plasma glucose levels. A red blood cell has an average life span of 120 days, and therefore, more red blood cells are being constantly made and released into the bloodstream. Usually, the patient would come to the doctor after a period of two months with blood glucose tests and also HbA1c levels.
This is basically the same as HbA1c estimations, but estimates the attachment of glucose molecules to albumin in the blood. Not only will this allow you to diagnose diabetes in your patients at an early stage before complications have set in, but even in your patients who are known to have diabetes, you would be in a unique position to test their blood glucose levels at different times of the day. Well, a gentleman by the name of Iden Cogburn, who is the founder of the Paleopathology Association (this is a group of pathologists and other physicians who are very interested in studying scientifically the remains of ancient societies), wrote a book called MUMMIES, DISEASE, AND ANCIENT CULTURES.
You talk about insulin, and you think about decreasing blood sugar, and insulin is there to lower blood sugar. You eat sugar, you eat carbohydrates, cause an increase in blood sugar, at least to the release of insulin from the pancreas, and the production of the insulin in the pancreas, which is important. Glucagon is also manufactured in the pancreas, right next to where insulin is manufactured, in the alpha cells. That is really, in a 24-hour period, how insulin lowers your blood sugar, not so much by transporting into cells.
Well, short-term, it’s not good because it can create an osmotic gradient in the kidney, and we pee a lot. Syndrome X you might have heard about, and we call it CAOS, which stands for coronary artery disease, hypertension, hyperlipidemia, adult onset diabetes, obesity, and stroke. We chose chickens because birds develop similar atherosclerosis as humans, and chickens in particular, because they are omnivorous. It talks about hypertension, glucose intolerance, hyperglycemia, upper body obesity, and they found out further now that there is a – hypertension resistance to the insulin hyperinsulinemia, glucose intolerance, increased VLDL triglyceride, reduced HDL cholesterol activator inhibitor, and fibrinogen levels. Hypertension can cause insulin resistance by altering delivery of insulin, and glucose into the muscle cells, resulting in impaired glucose uptake.” You have a vicious cycle.
Obesity can also lead to insulin resistance, but it isn’t the obesity that is causing the hypertension, and all these other problems; it’s the insulin.
Several population studies have shown that hyperinsulinemia is the independent risk factor for atheroschlerosis.” I think we are figuring that out. This is a Japanese group, out of Osaka, Japan, that decided to do angiograms, and measure insulin.
Hyperinsulinemia may stimulate the artheromatous process.” This is in DIABETES CARE, January 1996.
Also if I wanted to do a feast or famine style diet how many days do you think I should fast.
If insulin tells the liver to make fat cells because of sugar floating in the blood stream and also tells the liver to produce more cholesterol because it is required in the manufacturing of all the cells, and that is why you have high cholesterol; then how come my fast insulin level is 3 (which means my blood stream is not loaded with sugar) but my total cholesterol is 320. Lalbagh Main Gate, Hosur Road, Bangalore, India2 Department of Pharmacognosy, Al-Ameen College of Pharmacy, Opp. Failure to detect the anti-mutagenic effect of insulin in experimental type-2 diabetic rats.
Early and preventable changes of peripheral nerve structure and function in insulin-deficient diabetic rats. Alterations in free radical tissue-defense mechanisms in streptozotocin-induced diabetes in rats. Experimental NIDDM: Development of new model in adult rats administered streptozotocin and nicotinamide. Chronic effect of insulin on monoamine oxidase and antioxidant enzyme activities in the rat brain stem. Generation of superoxide radical during autoxidation of hydroxylamine and an assay for superoxide dismutase. In vivo chromosome damaging effects of an inosine monophosphate dehydrogenase inhibitor: Ribavirin in mice. Induction of chromosome aberrations, micronucleus formation and sperm abnormalities in mouse following carbafuran exposure. Incomplete development of human spermatozoa is associated with increased creatine phosphokinase concentration and abnormal head morphology. In vitro effect of gliclazide on DNA damage and repair in patients with type 2 diabetes mellitus (T2DM). Inhibitory effect of glimepiride on nicotinamide-streptozotocin induced nuclear damages and sperm abnormality in diabetic Wistar rats.
Protective role of glibenclamide against nicotinamide-streptozotocin induced nuclear damage in diabetic Wistar rats.
Failure to detect an anti-mutagenic effect of chloramphenicol in ultraviolet polar cap cells (early germ track) of drosophila.
Lack of the anti-mutagenic effect of ascorbic acid on the genotoxicity of albendazole in mouse bone marrow cells. Lack of modulatory effect of asparagus, tomato and grape juice on cyclophosphamide-induced genotoxicity in mice.
Catalase, and poly (ADP-ribose) synthetase inhibitors against alloxan-and streptozotocin-induced islet DNA strand breaks and against the inhibition of proinsulin synthesis. On the basis of these levels, it is presumed that one can judge blood glucose control, compare this with previous values and judge whether the control is better or has deteriorated and, also make adjustments in the treatment regimen of the patient.
Many laboratories and even some hospitals still continue to use the outdated Folin-Wu method for the estimation of the blood sugar levels. One would have to make sure that the meter which one is using is properly calibrated and know what reading it gives in order to correctly analyse the test results. Due to the relatively shorter half life in the blood of albumin, serum fructosamine estimations give an idea of the average control over the past fortnight. This would allow you to get a profile of the blood glucose values, allowing a more rational adjustment of their treatment.

Although manufacturer's advise that the strips can be used for about 3-4 months after the bottle is opened, in my experience, the strips spoil within 2-3 weeks.
A number of fine point, plastic coated lancets are available which are definitely easier to use and less painful especially if used with a companion lancet plunger. The reason actually that I am speaking is that John asked me to, after the last AAEM meeting, and a very prominent speaker lectured on merits of a high carbohydrate diet. That includes coronary artery disease, hypertension, cancer, stroke, diabetes, of course, obesity, autoimmune disorders, and mental disease and decline.
Anthropologists can almost immediately identify a particular society of people when they do diggings, and dig up a bunch of bones. There are considered to be more mummies than there are currently Egyptians, and many of these were preserved very well.
I’d like to quote him: “Atheromatous disease of the arteries is a common finding in mummies. Anywhere between 70 to 90% of the calories derived in Eskimo diets are from fat, depending on the season. We’ve got nonfat Fig Newtons, nonfat cheese cake, and nonfat everything – fat has gone down, I mean, Snackwell’s from Nabisco is one of the hottest companies, nonfat cookies. I wasn’t around at the time, but I don’t think that was really the reason that insulin came about.
Your total amount of blood sugar in a 24-hour period is increased more by gluconeogenesis in the liver than it is by your dietary intake. After 19 weeks, he examined their aortas, and found that there was a great increase in lipid deposits in the aortas of the insulin treated chickens as opposed to the ones who didn’t have insulin. Would it be okay if I exercised and fasted for say 12 hours after awaking and gorged on high fiber veggies and protein at night while being active for 3 hours after the feast.
If so, I find this intriguing – do you know if there are any references for the difference in the types of fats generated by different processes in an animal? Bone marrow micronucleus (MN) test and caudal epididymal sperm abnormalities were detected to find the somatic and germinal cell mutations, respectively. This can be evident from the presence of higher levels of DNA damaged products such as 8-hydroxy-2-deoxy guanosine (8-OHdG) in the blood of diabetic patients. When this happens the way it should, the level of sugar in the blood goes down and our bodies have the energy for a full and active life.
Such occasional blood glucose estimations cannot give adequate information to allow us to rationally make these suppositions. This is the oldest method that was used to estimation of the blood sugar levels and its real place should be in the archives or a museum!
Unfortunately, this estimation is not widely available and should preferably be done in special situations such as pregnancy where one wants a tight control throughout, without having the luxury to wait for 2 months to decide if the patient is in good control as would be seen with HbA1c estimations!
Correct and early treatment can save the person's life and this differential diagnosis can easily be made if you have a glucose meter with you. I hope that the manufacturers of the strips will make the individually packed strips available here soon. At the end of the talk, during the question-answer period, John got up, asked a reasonable question, “What about insulin?” The lecturer, who has written multiple books, basically just derided John, and said that he just hadn’t been keeping up the with the literature.
In fact, I think you’ll come to know, and it is not just my opinion, that it may be the chemical mediator of all of the degenerative diseases of aging. When you’re talking about obesity, and when you’re talking about anything that has to do with fat, or coronary disease, you cannot ignore insulin.
It stimulates the burning effect, it stimulates the breakdown of glycogen to increase blood sugar, it stimulates gluconeogenesis, the manufacturer of sugar from amino acids, and it increases your blood sugar, and it is secreted in response to eating proteins, and not carbohydrates. You try to go on a diet, and you have high insulin levels, you might lose weight, but you’re not going to burn fat.
Diabetes type I is a different story and the two diabetes are really two totally different diseases with the same name. We eat a high carbohydrate diet, our insulin levels are high, and we have what’s known as impaired glucose tolerance.
He quotes that this provides further evidence in favor of the hypothesis that insulin and atheroma are causally related.” This was in 1970. We go on in our research about the detrimental effects of lipids, and first it was cholesterol, and if not cholesterol, it’s LDL cholesterol and cholesterol is good, and then we find that it is oxidized LDL. Management should include attempts to reduce insulin resistance, and certainly not increase it.” Remember that!
The antioxidant status was determined by estimating serum lipid peroxidation, catalase, superoxide dismutase and glutathione peroxidase levels.
Nabil Abu-Heakal Asian Journal of Animal and Veterinary Advances. One should also remember that hypoglycemia can mimic many other critical states such as strokes etc., If you find a low blood glucose in such a patient and are able to administer glucose, the patient may show a " miraculous" recovery of the paralysis was due to hypoglycemia! This should not be problem as they do market them in such individually wrapped foils abroad.
I find that the thinner needles, like No.23 give a much better drop of blood as compared to the thicker needles.
This started a little bit of a heated discussion that went back and forth, and John knew of my interest in insulin for a long time. Once modern diet is factored in the high incidence of this disorder in our present-day industrialized civilization, but the etiological influences were certainly there in the ancient world, and this thought should be taken into account in any theorizing regarding causation.” It is well known that ancient Egyptians had a very high incidence of coronary disease. In a very short period of time, in the last 12 years, the incidence of clinical obesity, which is considered 20% over ideal weight by the Metropolitan Life Insurance tables, has gone from 25% to 33%.
Way back when, I don’t think lowering blood sugar was a major problem; there wasn’t that much of it. One of the main effects of insulin is to turn off the liver’s production of glucose, and we will get to that a little bit later, too. You eat a bunch of carbohydrates, this forms a bunch of blood sugar, and your pancreas senses that you’ve got a very high blood sugar level, so it just dumps all those insulin granules, to try and get that blood sugar stored. It’s also known that when a protein becomes glycosylated, it is a much greater target for oxidation. There is a type of LDL particle that is called a small, dense LDL particle, and that is the type of particle that is preferentially manufactured in the liver by insulin. Rosedale mostly does his tests through LabCorp, they do offer a discount if payment is paid in full right there and then.
The somatic cell nuclear damages can cause diseases such as cancer, heart ailments, neurological defects and aging, while germinal cell defect can result in infertility and inheritable disorders in newborns. Like the Benedicts test for urine sugar, it is not very specific and estimates not only glucose but evaluates the presence and amount of any reducing substance in the blood. Although there may be some additional cost, patients would rather pay this little extra rather than have their money wasted on spoilt strips. Pricking on the lateral aspect of the middle three fingers further to the distal finger joint often causes less pain.
There are multiple records in the papyrus writings, and in the examinations of the digestive systems of the Egyptians were very excellent documentations of the diets of the ancient Egyptians. In analyzing the arteries, and they had a high incidence of calcified plaque in the arteries, and these people did not live long. Of course, we know it is made in the pancreas, in the beta cells of the islet cells of the pancreas, it is initially stored as granules, and those granules are released when there is a sensation of blood sugar, and that quick release is lost in type II diabetes.
There is a strong autoimmune component, and there are autoimmune antibodies that are floating around, and something destroys the beta cells.
I found a study on sitting time and it found that for people on the standard american diet risk goes up with every hour of sitting so I started walking while working and studying and this has allowed me to get very lean almost too lean. Blood samples were collected from the tail vein method at 0, 0.5, 1, 2, 4, 8, 12, and 24 h in normal rats and in diabetic rats at 0, 1, 3, 7, 15, and 30 days.
Therefore, besides, many drugs and medications, even substances which are normally present in the blood stream will give rise to abnormal results. More important than the wastage of the money, is the fact that if the strips are spoilt even a bit, they may register low readings and their may be a false sense of complacency that the blood glucose levels are under good control.
They died young; even at a young age, their plaque was highly calcified, indicating it had been there for a while. Sugar becomes also a sticky baggage for that protein, and the protein can no longer function properly. Also I found out that sprinting exercise is so effective because it empties muscle and liver glycogen which increases insulin sensitivity rapidly. Antioxidant exerts multiple effects to overcome the oxidative stress mediated damage on the nucleus, such as scavenging the free radical, increasing the host antioxidant enzyme levels and repairing the damaged nucleus. One thing I do want to mention is, in the molecule itself, there is a small peptide called C-peptide, and that C-peptide is cleaved when it is released into the blood stream.
Your body puts out the multitude of regulatory hormones to increase blood sugar that has evolved over the years, many years ago. Insulin tells your liver to make fat from your excess sugar floating around that you’re not burning. There was a recent study one to two months ago in Science And Medicine that showed that insulin resistance can actually begin in utero. A lot of people implicate weak protein, but there is some sort of autoimmune reactions that is wiping out the beta cells.
Most of us, and most cardiologists, and endocrinologists have totally forgotten about this. If I wanted to do the one meal a day thing I know I would have to do sprinting and walking.
The data were compared statistically by using the one-way ANOVA method followed by the Dunnett multiple component test. They ate a lot of lettuce, cucumbers, garlic, onion, lentils, peas, and they used a lot of olive oil. The mother is eating a high-carbohydrate diet, eating a lot of sugar, — partial beta cell burnout in the fetus.
A true type I has very little autogenous insulin production, and that person is likely going to need insulin the rest of their life. Constant sugar in the diet also depletes magnesium, manganese, chromium, it depletes manganese SOD, and it also reduces receptor activity. Sprinting takes very little time about 40 minutes a day broken up into 15 minute segments so I now I could empty my sugar stores. Insulin therapy is reported to benefit the diabetic patients in reducing the complications associated with hyperglycemia. Now of course, when we take pictures in magazines, we only take pictures of beautiful, live models. So, if you have a patient who is on insulin, how can you tell if their own pancreas is working? It was titled “The effect of Intra-arterial Insulin on Tissue Cholesterol, And Fatty Acids In Diabetic Dogs.” They made dogs diabetics, and they infused insulin into the femoral arteries of those dogs for eight months. Sounds like Mevacor, only without the adverse side affects of stopping co Q-10 production, (and other enzymatic reactions in the liver). Walking burns more fat than sugar but for some reason studies say calorie for calorie walking is just as good as sprinting though sprinting takes less time and goes straight for the sugar. How much insulin are they actually manufacturing themselves, without getting poisoned by exogenous insulin? It’s probably your main stress: the constant stress on the adrenal to produce cortisone to raise your blood sugar after it has gone too high, and then too low. They sacrificed the dogs and examined them, and lo and behold, the femoral artery that had the insulin effused was covered with fatty streaks.
We had a lot of it sometime, and we didn’t have a lot of it sometimes, especially in the wintertime. Conclusion: The polyherbal preparation-I showed a significant glucose lowering effect in normal rats and polyherbal preparation-I, II, and III in diabetic rats. They ate a lot of bread, and the bread was made by freshly stone-grinding wheat and barley. Well, you can measure the C-peptide level, and you can know whether they are producing their own insulin or not.
There are a few tissues in our body that actually prefer to burn sugar; that’s our RBC’s, our retinas, and certain tissues in our gonads.
It goes up and down and up and down, and it’s a constant cycle that we are going through all day long.
Again, insulin is an anabolic hormone; it manufactures fat, and it also manufactures the house for it.
Supplementing with good polyunsaturated fat, omega 3, increases insulin sensitivity, and does so quite strongly. If this imbalanced homeostasis dose not return to normal and continues for a protracted period of time, it leads to hyperglycemia that in due course turns into a syndrome called diabetes mellitus. They had a lot of infection, a lot of parasites, and they were not a healthy society, and yet, they ate a diet that would be the choice of diet that is currently recommended. That is a very important test, because that is going to tell you ultimately whether that person really needs to be on insulin or not. The rest of the body would prefer to burn fat, but it is due to the tissue’s requiring glucose that we need to maintain a certain level of blood sugar, and so we have developed multiple hormones to keep the sugar up, if we are not taking in very much carbohydratewhich, millions of years ago, just wasn’t there.
There are not enough cells to hold it, so it tells your body to manufacture more fat cells.
I cannot really go into the talk about fats, because there is s lot of controversy, but the controversy really arises in that fats can either be the healthiest component of your diet, or the most toxic. The diet that the Egyptians ate, and the diet that is currently recommended, is a high-carbohydrate diet.
In addition, we have sugar attached to a protein, and if there is also an attached lipid, it increases the likelihood of poor oxidation of that lipid, which also increases the oxidizability of lipoprotein. Hence, the present research is aimed evaluate the anti-mutagenic activity of insulin in diabetic Wistar rats, using bone marrow micronucleus (MN) and sperm abnormality tests. Therefore, we have selected three different plants products in our study, namely wheat germ oil, fresh juice of Coriandrum sativum, and Aloe vera. Now, their diet was a very high complex carbohydrate diet; there was nothing refined at all about it, yet they were not very healthy. Now, that insulin is turning off the production of sugar, and it signals the brain when that sugar is low, to crave sugar and carbohydrates. It’s caused by insulin resistance; it is when insulin reduction can no longer keep up with insulin resistance. It decreases natural killer cells, and it increases cancer because of that, it decreases T-helper cells. They ate a little bit of fish, they ate some chicken, and of course, it was free-range chicken.

When your levels drop, one of the main effects is that you crave carbohydrates to get that sugar back up.
So, as it is telling your body to manufacture cells, it is telling it to manufacture cholesterol. Type II diabetics produce too much insulin; I should say they produce much more insulin than the non-diabetic.
There is an article called “The World Of Oxidative Stress and The Development of Complications of Diabetes.” This is in DIABETES, Volume 40, April 1991. Insulin increases fluid retention, it increases the excretion of magnesium, potassium, and it increases sympathetic tone.
It’s not a problem with not producing enough insulin, it’s a problem with insulin resistance, as cells aren’t listening, and so, the pancreas has to put out a ton of insulin to get the job done. The experiments were conducted after obtaining prior approval from the Institutional Animal Ethics Committee.Induction of type-2 diabetesExperimental T2DM was developed in adult rats by administering streptozotocin (STZ) and nicotinamide (NA). Your body has a ton of mechanisms to protect the polyunsaturated fats from becoming oxidized, and that’s really the main purpose of vitamin E.
If you want to go into details, you’re considered a diabetic if your fasting blood sugar is greater than 140, or if it is greater than 200 within the first two hours of glucose tolerance testing.
Because of the interplay between glycation and oxidation in their formation, we have termed these compounds glycosidation products.
This is entitled “The Development of Vascular Lesions In Insulin Treated Animals Fed A Normal Diet.” This was done in Belfast. Sounds like a diet that was previously recommended in this mornings talk as being a very excellent and healthy diet. We’ll talk about this a bit later, but if you want to lower somebody’s cholesterol, pay attention to insulin, because you can do so very quickly and very powerfully. It enhances endothelial cell production, and if there is ever a prescription for high blood pressure, that’s it. I’m not big on numbers, but that means that if your fasting blood sugar is 139, you’re non-diabetic.
Because these products accumulate in collagen normally as a function of age, and at an accelerated rate in diabetes mellitus, diabetes mellitus may be legitimately described at the chemical level as a disease characterized by accelerated aging of collagen by glycative and oxidative mechanisms. Blood sugars go way up again, and we repeat the cycle, day in and day out, week after week, year after year.
You get fat thighs, and you might not look so great, but you’re not hurting your health as much. You can take cholesterol levels that were 400 or 500, and get them down to 200 in weeks if you lower a person’s insulin. Insulin puts it in your belly, packs it in your liver, packs it in your kidneys, and inhibits function. Cortisol becomes increased both by a direct effect of insulin, and as a secondary effect by lowering blood sugar. One saying to avoid polyunsaturated fats because it can oxidize readily is like saying avoid oxygen because it can oxygenate tissues. You talk a lot about endothelial health, and there is a lot of work, especially by George Kindness, who spoke this morning, about platelet adhesiveness.
That’s very important, because the pancreas is free to churn out sugar, and continues to make a lot of sugar. We all know that it’s really the clot that ends up actually killing us in coronary disease. When the blood is hypercoagulatable, if that’ a word, you’re going to be much more prone to coronary disease and stroke, and all sorts of other illnesses.
You can use the analogy: If you eat a lot of salt, (you start using salt to salt your foods, you never did before, but you do now), you start burning out the taste receptors for salt. Again, most of the blood sugar in a 24-hour period is from hepatic production, not immediately from your diet.
One of the definitions of type II diabetes is that it is a disorder in control of gluconeogenesis normally inhibited by insulin. Pretty soon, you have to use five tablespoons of salt, whereas a pinch of salt would have tasted just as salty months ago. There is also decreased muscle and fat glucose uptake, and also not on there, there is a decrease in the amino acid uptake in muscles, when you have insulin resistance. It’s very important, it gives you a fine, end-stage diabetic when the cells are no longer listening to insulin, and they cannot absorb amino acids, and they become muscle-depleted, approaching wasting. Marrow suspension from femur and tibia bones prepared in 5% bovine serum albumin (BSA) was centrifuged at 1000 rpm for 8 min and the pellet was resuspended in a required quantity of BSA.
A drop of this suspension was taken on a clean glass slide and smear was prepared on glass slide and air-dried.
About 2000 PCEs and corresponding NCEs were scanned for the presence of MN using 100Χ oil immersion objective. A cell becomes resistant to insulin in the same way after constantly being bombarded with it. One thousand sperms per animal were screened to find the different types of abnormality in one of the cauda epididymis. Six types of abnormalities such as amorphous, hookless, banana shape, fused, double headed and double tailed were evaluated and finally represented as percentage total abnormality. They know that there are a fewer number of receptors when cells are constantly bombarded with insulin. The spermatozoa count was obtained by counting the number of sperm cells in the four WBC chambers using a Neubauer's slide. I’m not going to get into it, because that would be an hour’s discussion right there, but there are multiple proteins involved. The insulin receptor transcends the entire membrane, and there are a number of chemical reactions that go along, — that transmit the signal into the cell. The principle depends on the reaction between thiobarbituric acid with malondialdehyde, a secondary product of lipid peroxidation, at pH 4. The Coriander juice, 1.0 ml, was added at the time of continuous trituration until a light green product with clicking sound is produced.
Most of them are proteins, and somehow, that receptor becomes burned out, and doesn’t work as well. The reddish pink color developed was estimated at 532 nm, which indicates the extent of peroxidation. You need more insulin to do the job, and you get what’s called hyperinsulinemic; you have hyperinsulinemia, to maintain your blood sugar. This solution was added at a time to the primary emulsion with continuous and rapid trituration. Sometimes, it takes ten times as much, and we have seen patients who are putting out ten times as much insulin as a normal person to maintain their blood sugar. During the oxidation, nitroblue tetrazolium (NBT) was reduced and nitrite was produced in the presence of ethylenediaminetetraacetic acid (EDTA), which could be detected colorimetrically at 560 nm.
Coriander juice 1 ml was added at the time of continuous trituration until a light green product with clicking sound is produced. Administration of insulin produced no significant alteration in the sperm shape and sperm count defects in the diabetic rats.
However, none of the tested doses of insulin reversed significantly the diminished antioxidant profile in the diabetic animals [Table 3]. The emulsion was used for the study.Polyherbal preparation-IIIIt consists of wheat germ oil, fresh juice of C. We’ll talk a little bit more about that later, but one of the problems of high blood sugar is that that sugar combines with proteins, and causes glycosylation, and most people here have probably heard about hemoglobin A1C. The blood glucose estimation indicated that insulin exhibited a dose-dependent reduction in the NA-STZ-induced hyperglycemia.
NA-STZ-induced diabetic model in Wistar rats is commonly used since different levels of stable hyperglycemia can be produced, which are suitable for long-term studies. Further, this method of chemical diabetes is reported to mimic the clinical T2DM, especially in terms of insulin secretion in response to glucose load. The mechanism suggested for these responses is the partial protection offered by the NA against the STZ mediated oxidative damage to the pancreatic beta cells. Bone marrow MN test and sperm abnormalities test are commonly employed assays to determine the mutations in somatic and germinal cells, respectively. MN in young erythrocytes arises primarily from chromosomal fragments or lagging chromosomes that are not incorporated into daughter nucleus at the time of cell division in the erythropoietic blast cells, and the changes in the incidences of MN are considered to reflect the chromosomal damage in somatic cells. The emulsion was used for the study.Experimental animalsAnimalsFor pharmacological experiments, Wistar albino rats (160-250 g) of either sex were used. These agents are reported to benefit the diabetic patients in reducing both hyperglycemia and also the mutagenic complications associated with enhanced oxidative stress.
After one week when the condition of diabetes was stabilized, the animals were fasted again for 14 h before blood collection withdrawal from retro orbital plexus. The tail was cleaned with spirit and allowed to dry; tail vein was dilated by focusing a low voltage electric lamp at the tip of tail for few seconds. The plasma was obtained by centrifuging the blood samples at 3000 rpm for 10 min, decanting supernatant fluid into the clean, dry test tube. Subsequently, other chemical and enzymatic methods were developed to overcome this problem. Trinder's method (1964) utilizes two enzymes GOD and POD along with the chromogen 4-amino antipyrine and phenol.
There was no interference due to the substances such as creatinine, fructose, galactose, reduced glutathione, ascorbic acid, and xylose. Glucose present in the blood is oxidized by the enzyme GOD to give d-gluconic acid and hydrogen peroxide.
Hydrogen peroxide further reacts with 4-aminoantipyrine and phenol in the presence of the enzyme POD to undergo oxidation to produce a red-color quinoneimine dye.
The intensity of the color produced is directly proportional to the glucose concentration in the sample.Preparation of the working reagentOne vial (3 ml) of enzyme powder was transferred to one bottle (100 ml) of buffer solution and mixed gently to dissolve which is ready to use.
All the reagents were stored at 2-8 °C, which is stable till the expiry date, reagents were not freeze. The reagents should not be used if caking is observed due to possible moisture penetration. This process is duplicated to confirm the calibration value and was considered as correct if the value was within 5% of the original value.
The data were analysed by using Student's t-test using one-way analysis of variance (ANOVA) followed by the Dunnett multiple component test. The above observations show that the treatment of diabetic rats with polyherbal preparation-I reduces the fasting plasma glucose of diabetic rats at all the tested dose levels, but the high dose of polyherbal preparation-I (i.e. The above observations show that the treatment of diabetic rats with polyherbal preparation-II reduces the fasting plasma glucose of diabetic rats at all the tested dose levels, but the high dose of polyherbal preparation-I (i.e. The above observations show that the treatment of diabetic rats with polyherbal preparation-III reduces the fasting plasma glucose of diabetic rats at all the tested dose levels, but the high dose of polyherbal preparation-III (i.e. Traditional plant medicines are used throughout the world for the range of diabetic complications as an alternative for conventional hypoglycaemic agents because hypoglycemic or antidiabetic drugs in NIDDM or insulin in IDDM have a limited role to play. The risk of drug tolerance is high with oral hypoglycaemic agents, thereby causing a raise in dosage or a change of drug. Ayurvedic medicines may help as "potentiators" for these drugs or play a supportive role in regulating the dosage of hypoglycemics and maintain the quality of the diabetic life.In the indigenous Indian system of medicine (Ayurveda) a mention was made on a good number of plants for the cure of diabetes, but the bioreactivity of single plant preparation is disappointing and most of these remedies have moderate potency as well as toxicity thus are not fast acting nor overtly dangerous whereas in the polyherbal preparation forms, they are likely to contain several bioreactive components which can act together and elicit additive or synergistic effects which shows optimal therapeutics response that are not apparent when the bioreactive compounds are used independently. Various herbal formulations such as diamed, [21] coagent db, [22] hyponidd, [23] and SMK001 [24] are reported in the literature as an antidiabetic formulation while we have made an attempt to use three different plants products in our study namely wheat germ oil, fresh juice of C. We have also observed that Ph p-I treated normal group of rats produce a progressive and significant reduction in the fasting plasma glucose level during the period of study when compared with normal untreated rats at all the selected dose levels, i.e.
In agreement with the present results, several studies have shown antidiabetic [25] activity upon glibenclamide treatment. Following its administration, alloxan is concentrated in the islets and it is reduced to dialuric acid. This acid is unstable in aqueous solutions and undergoes oxidation back to alloxan, accompanied by generation of O 2− , hydrogen peroxide, and hydroxyl radicals by the Fenton type reaction.
It is well established that sulfonylureas produce hypoglycemia by increasing the secretion of insulin from pancreas, and these compounds are active in mild alloxan-induced diabetes whereas they are inactive in intense alloxan diabetes (nearly all β-cells have been destroyed). Since our results showed that glibenclamide reduced blood glucose levels in hyperglycemic animals, the state of diabetes is not severe. Alloxan-treated animals receiving the polyherbal preparation showed reduction of blood glucose levels in comparison to control, and this could be due to the possibility that some β-cells are still surviving to act upon by Ph p to exert its insulin releasing effect.
Moreover, like sulfonylureas oral administration of Ph p produced hypoglycemia in normal animals. This suggests that the mode of action of the active ingredients of polyherbal preparation is probably mediated by an enhanced secretion of insulin, such as sulfonylureas.The possibility of antidiabetic effects of polyherbal preparation may be due to the effect of active constituents of different plants, namely vitamins such vit C, minerals such as chromium, manganese, magnesium, zinc, and hydrosoluble fiber glucomannan from A. Chromium via the enzyme insulin receptor tyrosine kinase catalyses the phosphorylation in the presence of insulin. Additionally, chromium inhibits tyrosine phosphates, which is responsible for terminating the insulin receptor response.
Thus, by both increasing activation and inhibiting termination of insulin receptor-mediated responses, chromium can significantly influence glucose utilization by peripheral tissues and regulate glucose levels. Magnesium is a co-factor in glucose oxidation, and modulates glucose transport across cell membranes. Manganese, zinc, [22],[23],[24] and iron are co-factors for superoxide dismutase (SODs) that catalyse the breakdown of the superoxide anion into oxygen and hydrogen peroxide which further reduce to give water and protect β-cells from the toxic effects of reactive oxygen species. Vitamin E is lipophilic and inhibits lipid peroxidation which occurs in the plasma membrane and damages the membrane structure and permeability, scavenging lipid peroxyl radicals to yield lipid peroxides and the tocophroxyl radicals and protects the membrane from oxidation. On the basis of above results, it could be concluded that polyherbal preparation, a combination of three herbal plants exert a significant antidiabetic effect.
This could be due to different types of active principles, each with a single or a diverse range of biological activities, which serves as a good adjuvant in the present armamentarium of antidiabetic drugs. Antidiabetic animals were treated with different doses of polyherbal preparation-I, II, and III to assess the effect of the drugs.
This study suggests that polyherbal preparation-I, II, and III possess antidiabetic activity and is going to be a promising antidiabetic preparation for masses.
An exact mechanism underlying this effect is not clear, but apparently may be due to preserving β-cell function in diabetic rats.

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  1. 24.03.2014 at 20:20:39

    Breast cancer than those with a fasting glucose level below pancreas that controls the many newly.

    Author: oO
  2. 24.03.2014 at 10:10:40

    Child's?age, ability to recognize hypoglycemia symptoms.

    Author: aftos
  3. 24.03.2014 at 23:26:14

    Percentage point (although metformin has been found to be more efficacious than caused.

    Author: AXMEDIK_666