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| Visitor Q |
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Visitor Q
$25 whore
Joined: 30 Apr 2004
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 Posted: 19:00 - 13 Dec 2006  Post subject: Any type 1 diabetics about? |
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Well i say type 1, i assume thats the one that just pops up at random.
Well ive been having a lot of the symptoms, namely;
Always pissing, especially at night or when exercising but only tiny amounts and luminescent orange even though im trying to drink lots of water.
Always feeling shattered, for instance i got up at 3 oclock yesterday (no shit), went boxing 8.30 - 10 and got back, promptly collapsed at about 11, then physically couldnt get up until 1. Thats 14 hours sleep after being awake 8 hours 
I had a big pasta meal before boxing to give me energy and then for the next hour was really struggling to stay awake.
Also been quite constipated recently.
All of which are symptoms. The question is, how much of a cunt is it to live with?
Any advice they give you you can give me, so i dont do anything that stupid.
Im going to get tested asap and if anyone knows any good ways asides from doctors id be intrigued to hear, ive heard loyds chemist do free tests but dont know any either in bangor or stevenage. So i'm open to suggestions as i imagine doing it through doctors could be a pain
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From September 2014 to January/February 2015 I will not be using any English, nor reading any. As such, I won't be on here. PM at will, but I won't be checking/posting unless in emergencies. Certainly not for the first couple of months. Please berate me savagely if I break that rule... |
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| Mary Jane |
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Mary Jane
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Posted: 20:33 - 13 Dec 2006  Post subject: |
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Type 1 is child onset, Type 2 is adult onset.
I don't have it... yet. I say yet becuase my mother was diagnosed several years ago with pre-diabetes, which she has kept from becoming fully blown diabetes with the use of some prescription drugs and diet. My Dad was diagnosed with the full disease, which he is also managing through pharmaceuticals and diet. My sister has pre-diabetes as well, so as a result I try to be careful about what I eat. I say try, becuase it doesn't always work, although I've been adjusting my diet lately.
Definitely get tested through a doc, becuase they'd be able to provide you information on how to manage it. A doctor would also be able to provide you information on your symptoms and an alternate diagnosis if it turns out not to be diabetes.
Being easy to live with... it can be done. You'd have to watch your carb intake, especially refined carbs, watch your blood glucose levels, and start reading labels on everything you buy from the store.
For instance, until I went shopping with my mom, I didn't realise how much sugar gets put into just about everything. I dont' think it's the same case over there as here, but you find High Fructose Corn Syrup in everything. That's worse than pure sugar; it's concentrated sugar. We read labels on about 20 bottles of spaghetti sauce before finding one that didn't have HFCS or another suagr added to it. And she only uses whole wheat pasta, eats whole wheat bread, and doesn't eat potatoes anymore, becuase the starch in the potatoes turns into sugar in the body. Mostly, she eats proteins and fiber, like from vegetables, gets carbs from whole meal and fruits. And tests her blood sugar after every meal. |
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stinkwheel
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map
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Whosthedaddy
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Posted: 20:13 - 14 Dec 2006  Post subject: |
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| map wrote: | | Mary Jane wrote: | Type 1 is child onset, Type 2 is adult onset..... |
Partly right, just being picky. Type 1 is insulin dependent. That is insulin injections. Whilst this normally occurs in children you can be an adult with insulin dependent diabetes.
Type 2 is late onset diabetes which, as you say, can usually be controlled by diet and/or pills (no needles).
HTH  |
Partly right again.
It takes me long enough to explain to students whats the difference between type I and type II (previsously IDDM and NIDDM), its quite simple in essence but confusing as well.
Here is a section (rough copy  ) from one of my old essays about the the management of diabetes in coronary heart disease:
| Quote: | Since time began, there have been numerous illnesses and diseases that have plagued mankind. One such illness that is more prevalent now than ever, is that of diabetes. Diabetes is older than time itself, and was known to the both Egyptian and Grecian physicians. Even then, the severity of this illness was well known, although today we are aware that there is more to diabetes than the excessive production of sweet ‘sugary’ urine. Watkins (1996) agrees with this, and explains that it’s a worldwide problem with a high morbidity count from blindness, renal failure, amputation and coronary heart disease.
Heller et al, 1987 states that coronary heart disease occurs when the blood supply to the heart muscle is reduced by obstruction in the coronary arteries. This obstruction is due to atheroma, or the formation of hardened fatty plaques within the lining of the epithelial cells of the arteries. The clinical indications of the presence of the coronary heart disease include the development of a myocardial infarction.
A myocardial infarction is a very traumatic event in any individual’s lifetime. It is “always frightening and painful, arousing intense distress in the patient and family, especially the spouse” (Thompson, 1990). However, education is key in explaining the signs and symptoms of the chest pain involved in a myocardial infarction as diabetes can alter the perception of this pain. Cheitlin (1993) states that pain is the classic dominant feature of an acute myocardial infarction that spurs the patient to seek medical help. It may be described as heaviness or tightness or a great weight sitting on the chest rather than pain. During the cardiac counselling session, the various patients explained how the experienced different type of pain, but commonly the most classic includes; possible radiation to the lower jaw and teeth, neck, left shoulder, upper back and, or down the left arm. Cheitlin goes on to state that myocardial infarctions can occur without any pain or discomfort. The incidence of ‘silent’ heart attacks found on subsequent routine ECG’s was in the region of 25% according to the Framingham study. A silent infarct means the classic pain across the chest, down the arm and into the jaw is absent. Not all patients with myocardial ischeamia experience pain; in most cases diabetic patients caused by diabetic autonomic neuropathy witness these ‘silent’ heart attacks.
I have already mentioned that diabetes is responsible for coronary heart disease, which may lead to a myocardial infarction, hence how I met Alan, but what is diabetes? It was in 1995, that Ross and Wilson defined diabetes mellitus as the deficiency or absence of insulin causing varying degrees of disruption to carbohydrate and fat metabolism and its storage, as well as excessive gluconeogenesis from protein catabolism and water electrolyte imbalance. Diabetes according to Dunning, 1994 is considered to be the 4th major cause of death after cardiovascular disease, cancer and musculo-skeletal disease distributed across all age groups and may be classified into two main types, these being type I and type II. Type II diabetes is the most common form of the illness and is usually predominant in people over the age of 40. Diabetes UK stated that in 2000 approximately 1.4 million people were diagnosed with having diabetes, 85% of these being type II. The worrying fact for heath care professionals is that there are approximately 1 million more individuals in the population waiting to be diagnosed.
The division of diabetes has been known and recognised for many years and Watkins (1996) explains how over a century ago Bouchardat described it as having ‘diabete gras’ or ‘diabete maigre’. It wasn’t until the mid part of this century that Bornstein and Lawrence were the first to show that types of diabetes “could be distinguished between insulin dependant diabetes also known as type I, and non-insulin dependant diabetes also known as type II” (Watkins 1996). The author then goes on to explain that the aforementioned terms are misleading and inappropriate.
Type I diabetes indicates the beta cells of the pancreas are damaged and are unable to produce insulin, therefore insulin is required for the individual to survive, whereas in type II diabetes, there is a “relative but not an absolute lack of insulin” (Watkins, 1996). Meaning that the reserves, or, supply of insulin from the beta cells in the pancreas may become diseased in middle age and ultimately “become insufficient to provide adequate insulin for the high carbohydrate intake of the adult” (Watkins, 1996).
There are ultimately three types of fuel available to the human body; carbohydrates, fats or lipids and protein. In order to obtain energy, cells must breakdown these food stuffs (fuels) at a cellular level into a substance called adenosine triphosphate (ATP). As all food carbohydrates are eventually broken down from polysaccharides (complex sugars) into monosaccharides (simple sugars), Marieb (1998) suggests that the story of carbohydrate metabolism may be thought of as the story of glucose metabolism.
Glucose (C6H12O6) enters the various tissue cells of the body by diffusion, which is allowed by insulin. Insulin may be thought of as a key that opens the door for glucose to enter. Once inside the cell, “the glucose is phosphorylated to form glucose-6-phospate by the transfer of a phosphate group to its sixth carbon with the reaction of ATP” (Marieb, 1998). As this newly formed glucose-6-phosphate is different molecule to glucose, the intracellular levels are lower than the extra cellular levels, therefore maintaining a diffusion gradient for more glucose to enter the cell. This glucose-6-phosphate may now go one of two ways. It may be stored as a reserve as glycogen in the liver and muscles to be used later or utilised immediately to form more energy. In order to form more energy (ATP), the glucose-6-phosphate must be oxidised, this involves three main steps as described by Marieb, 1998. The first step is that of glycolysis. The author defines glycolysis as ‘sugar splitting’. This actually is more complex than this and involves a total of ten stages by which glucose is converted into pyruvic acid yielding 2 molecules of ATP. The process of glycolysis is an anaerobic reaction and oxygen is not required, however, if sufficient oxygen is present then the glycolysis reaction may then enter the next stage, the Kreb cycle.
The Kreb cycle occurs in the aqueous mitochondrial matrix and is the process whereby glucose-6-phospahte is converted into acetyl CoA. This process is fuelled by pyruvic acid produced in the earlier stages and by the breakdown of fatty acids resulting in the breakdown of fats. Marieb (1998) explains that one of the pyruvic acid carbons is removed to form carbon dioxide (a waste product), and is diffused into the blood stream. It is at this stage that hydrogen atoms are removed forming acetic acid with coenzyme A (otherwise known as acetyl CoA). This substance may now enter the Krebs cycle and is oxidised through a series of stages to form yet mote ATP.
The final step in glucose metabolism is that of the electron transport chain. Like glycolysis, none of the reactions of the Kreb cycle require oxygen directly. This is the exclusive function of the electron transport chain, which oversees the catabolic reaction in the mitochondria. The hydrogen atoms removed during the oxidation of food fuels are finally combined with molecular oxygen in the presence of a phosphate group ultimately producing ADP (energy). Most energy is produced in this final stage, 36 molecules of ATP.
Shaw (1996) states that CCU management of acute myocardial infarction and diabetes requires particular skilled management and strict guidelines for glycaemic control. Diabetes UK in 2000 stated that a pre meal blood sugar levels should be between 3.9-6.7mmols/l and up to 10mmols/l after the meal. Marieb (1998) states that ordinarily when blood sugars begin to rise, hyperglycaemic hormones are not released, but when this state becomes excessive, the person begins to feel nauseated which then can precipitate the ‘fight or flight’ response. This means that, all the reactions the normally occur in the hypoglycaemic state (fasting) to make glucose readily available respond inappropriately. The result being, the already high blood sugar levels soar even higher, the stress factor being the myocardial infarction.
Watkins, 1996 highlights the aims of education with the diabetic patient. The health care professional must explain the nature of the disease and potential complications that may arise in the future. They must also be made aware of the reason for their treatment and importance of monitoring their blood sugar levels. It is also a good time to stress the importance of good dietary habits and provide them with the up to date literature so the patient can make informed decisions about their own life. Such individuals, whom are specialised to assist the nursing staffs, are that of the diabetic nurse specialist and dietician.
Watkins (1996) states that the diabetic nurse specialist is one of the most important single innovations in the care of the diabetic patient to occur in the last 30 years. The diabetic nurse specialist may act as both educator and liaison to patient and health care staffs. As already stated, education is the key, but so is good communication in order to facilitate a safe discharge. The diabetic nurse will communicate with the hospital staffs; the patients GP and assist in follow up appointments in order for good monitoring, which already highlighted is vital for diabetes to managed effectively.
Blood glucose monitoring is vital in the control of diabetes; especially in an emergency situation like a myocardial infarction. It enables the medical and nursing staffs to titrate the hypoglycaemic medication to the individual’s needs and their lifestyle. Dunning (1994) agrees with this and states that patients should be assessed individually and the regime suited to meet their individual requirements. All patients, including Alan, have their blood sugars taken upon admission; if the random level is above 11mmols/l it should be rechecked within an hour. Blood sugars that remain persistently high should be actively treated. Because of the raised blood sugar of 25mmols/l upon admission, and the fact that Alan was having a myocardial infarction, he was started on intravenous insulin ‘sliding scale’. Jowett and Thompson (1998) justifies this whereby, hyperglycaemia in the peri-infarction state is best treated with insulin as oral hypoglycaemic agents may cause unwanted side effects later. Malmberg (1997) states that diabetic patients are more likely to die after a heart attack than those without this disorder. The Digami trial in Sweden proved this. This was a randomised trial of intensive insulin therapy compared with usual treatment for diabetes and demonstrated that death rates could be reduced by a third in the following 3 and half years following the heart attack. The trial included patients with a blood sugar level of greater than 11 mmols/l. They were given intravenous insulin / glucose for at least 24 hours followed by subcutaneous insulin for 3 months post discharge.
Hyperglycaemic state are treated aggressively as stated by the Digami trial, and the blood monitoring tests as explained by Dunning (1994) are performed every two hours during the initial stage reducing to 3-4 hourly once the blood sugar levels are more stable and within acceptable limits. The subcutaneous insulins that should be commenced consist of both short and long acting insulin, thus giving immediate and long-term cover. Humalog Mix 25, this is analogue insulin, and is to be administered with food, this type of insulin is ideal. Dunning in 1994 states that new diabetic patients are more likely to have a longer stay in the acute environment (e.g. CCU) and the blood sugar levels may normalise during the convalescence period, it is important that the blood sugar levels continue to be monitored throughout this time. Dunning then goes on to state that blood glucose monitoring is performed ideally before meals and before bedtime. These times enable the nursing and medical staffs to ascertain a profile of the current glycaemic control especially now that Alan is on subcutaneous insulin rather than diet alone. It is easy to monitor blood sugar levels and current control whilst in hospital, but what about previous control, carrying out a simple blood test measuring called a ‘HbA1c’ may measure this.
When in excess, circulating blood glucose may attach itself to the haemoglobin in the red blood cells, and undergo a chemical reaction whereby the glucose then becomes permanently fixed. Watkins (1996) states that the haemoglobin is composed of several different components, these being HbA1c, HbA1a and A1b. In a persistent hyperglycaemic state, the HbA becomes modified at a constant rate during the actual life cycle of the red blood cell, Dunning (1994) goes onto explain that the HbA1c can be measured and quantified to give an indication of the metabolic control, in other words the average blood glucose concentration over the last 3 months. The normal ranges for a non-diabetic are 4.5-6.2% as state by Diabetes UK (2000) and the ideal level for a diabetic should be within one per cent of the upper end. This demonstrates that Alan’s glycaemic control was poor and if no changes are made to his monitoring and actual treatment, he runs an increased chance of having further cardiac events in the future.
The Diabetes Control and Complications Trial (DCCT) was a major innovation and ran from 1983-1993. Diabetes UK (2000) states that the DCCT proved that a tight blood sugar control prevents or delays the onset of diabetic complications. Every bit of improvement in the patient’s diabetic control goes some way towards reducing the potential risks. It also worthwhile for patients whom are already experiencing complications like Alan. Watkins (1996) explains that there is evidence that if the patient understands what their HbA1c represents they will achieve better control, as they know have a goal to aim for. The author also explains that HbA1c levels should be monitored routinely on all patients where good control is utmost, i.e. 3-6 monthly.
It is important to note that every patient requires individualised care for his or her individualised needs, therefore, for any nursing care to be effective and personalised there must be good management. According to Bennett (1994), management involves several stages including; planning, organising, co-ordinating and control. Ainsworth (1998) goes on to suggest that management may be thought of as the achievement of objectives through the work of others, i.e. using the various members of the multidisciplinary team. An integral aspect of diabetes is that of education, or in some instances, re-education. Alan is in the unfortunate position of having being diagnosed with having a heart attack and a new diabetic regime at the same time, which will ultimately change his lifestyle permanently. Even though he is undergoing a crisis at this point, he still needs the relevant interventions (education) to overcome this. As a nurse on a coronary care unit, it is vital for one to understand what is involved in a myocardial infarction and the relevant treatment for this life threatening disorder in order to educate the patient. Cheitlin et al, 1993 state that in a myocardial infarction, there is ischaemic necrosis of a viable part of the myocardial tissue due to a sudden occlusion in the coronary blood flow. In other words the heart is being starved of blood and oxygen. This reduction in blood flow may be attributed to either a thrombus in one of the coronary arteries or by a haemorrhage within or below an atherosclerotic plaque. It is this latter reason that poses a major problem for individuals like Alan, whom have uncontrolled diabetes, hypertension and a raised cholesterol, if these are not properly managed in the present or near future, he stands a high risk of having another cardiac event of some description.
Dunning, 1994 highlights the need to stabilise the cardiac status and relieve symptoms of both the myocardial infarction and the raised hyperglycaemic state. Therefore, the nursing staffs must be in a suitable position to list any further episodes of chest pain, thus altering medication to suit Alan and his needs whilst retaining some elements of independence by involving him in the decisions for his management. Also, from a diabetic point of view, to maintain equilibrium with glycaemic medications, i.e. achieve euglycaemia, finally the most important element of management is involving the patient in education and re-education towards a myocardial infarction and diabetes.
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stinkwheel
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ali-b
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Visitor Q
$25 whore
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| Posted: 21:49 - 14 Dec 2006 Post subject: |
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Oh i fucking hate this mouse, has a button on the side that if you casually knock goes 'back' on your browser. Fab.
And thanks for all your kind replies, i know i may have been over reacting but at least this way someone will bully me to get a check up. Im one of those have a panic, it goes a way, go back to avoiding the doctor.
And SW one thing i thought of, obviously im not monitoring all urinations but if the glucose was 'pulling through' water (im not overly fond of that definition but im too lazy to get up and flick through Vanders) that would lead to the dehydration and this concentrated urine possibly.
I mean the other day it looked... well opaque almost. Thats gotta be a high conc. of bile pigments 
Not good.
I'm back on sunday so if anyone feels the urge to pm and hassle me to get checked, but having mentioned it to my dad i will probs get plenty. I will let you know what the result it. Although is it only me that thinks 'high glucose' is a slightly hit and miss way of diagnosing...?
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China traffic/travel bike vid - When I make a sweeping statement, please add the word 'statistically' in to the sentence before you bitch...
From September 2014 to January/February 2015 I will not be using any English, nor reading any. As such, I won't be on here. PM at will, but I won't be checking/posting unless in emergencies. Certainly not for the first couple of months. Please berate me savagely if I break that rule... |
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Louise
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| Posted: 11:38 - 15 Dec 2006 Post subject: |
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Lloyds pharmacy do a check for free I keep meaning to go as a few people in my family have it. |
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craigie b
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JonB
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| Posted: 12:37 - 15 Dec 2006 Post subject: |
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I don't think you have Type I diabetes, my girlfriend's Mum has it and she seems to live with it well anyway. Kind of get used to checking your blood often during the day and injecting with insulin before a meal. She has days where she gets low, cause of hypoglycaemia and her immune system is slightly cancelled out because of diabetes, therefore she gets ill quite often, but she has got used to living with the disease.
Bonny, lay off alcohol, fizzy drinks and orange juice (acidic), when I came to uni I was drinking a lot of the aforementioned drinks and I was getting the same kind of symptoms, now I drink at least 1.5L of water a day, but a 2L bottle in the morning. Feel a lot better now and going for a wee a lot less often. 
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stinkwheel
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Blackrhythms
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| Posted: 22:01 - 16 Dec 2006 Post subject: |
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I'm type I (insulin-dependant) since I was 14. Before being diagnosed, I was permanently shattered with barely enough energy to get out of bed! No matter how much water (or anything) I drank, I was still thirsty - even as I was drinking, the thirst was still there - nothing would relieve it - and as a result, was peeing all the time too - but as Stinkwheel said, your pee should be almost dilute as a result. Also, I was losing weight at a scary rate - by the time I was diagnosed, I was 4 stone (and I was a tiny 4'11"!! )
It's not so bad to live with - as has been said, it becomes a way of life, testing blood regularly, taking injections before every meal, with another long-acting one, once a day. You've been given some great advice and information here already, but if it's a thing that it is diabetes you have (although you probably wouldn't be insulin-dependant) feel free to pm me if you think there's anything I can help you with. Best of luck! 
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Posted: 22:04 - 16 Dec 2006  Post subject: |
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Just as a side note - saw this on the New Scientist website today
https://www.newscientist.com/article/dn10812-breakthrough-sheds-light-on-cause-of-diabetes.html
One of the root causes of type 1 diabetes may need rethinking – the condition may be triggered by faulty nerves in the pancreas, a new study reveals.
Type 1 diabetes has long been described as an autoimmune disease in which the body’s immune system targets islet cells in the pancreas, eventually destroying their ability to produce insulin. Without insulin, the body cannot convert glucose into energy, so people with type 1 diabetes have to regularly inject themselves with insulin to survive.
However, what initiates the original attack on the pancreas had been unclear. It now seems that the nervous system may play a key role, according to researchers in Toronto, Canada. The team eliminated the disease in diabetes-prone mice by knocking out a set of faulty sensory nerves. They believe the finding could chart a new path in treatment of the disease in humans.
Michael Dosch at the Hospital for Sick Children in Toronto, and colleagues, had previously shown that not only islet cells, but the nerve tissue around them was affected as diabetes set in. For this reason, they suspected that certain sensory nerves of the pancreas might be involved. These nerves release a neuropeptide called "substance P" and are usually responsible for ensuring that islet cells produce the right amount of insulin.
The researchers used a chemical to obliterate these nerves in a breed of mice genetically predestined to develop diabetes. “It turns out if you remove these specific sensory nerves, the animals don’t get diabetes,” says Dosch. “It was stunning.”
Single injection
When the researchers examined the nerves of diabetes-prone mice and compared them with normal mice, they found that the nerves of diabetes-prone mice do not producing enough substance P. This causes islet cells to overproduce insulin, leading to insulin-resistance and eventually islet-cell death. It is at this point, says Dosch, that the immune system is called into action, triggering diabetes.
The team wanted to know what would happen if they gave diabetic mice a top-up of substance P, so they injected some directly into the pancreas. Astonishingly, the diabetes disappeared overnight and the mice remained diabetes-free for weeks, and even months in some cases.
If the same were to happen in humans, a single injection could keep the disease at bay for years, says Dosch.
Other mechanisms
“These are interesting and original observations, and could potentially open new avenues for diabetes therapies,” says David Leslie of the Centre for Diabetes and Metabolic Medicine at Barts and The London, Queen Mary’s School of Medicine and Dentistry in London, UK.
The findings also support previous suggestions of a possible connection between autoimmunity and the nervous system. However, “there are almost certainly other mechanisms by which these mice, and indeed humans, get type 1 diabetes,” Leslie says.
About 85% of human diabetics are believed to have impaired sensory nerve function, but it has always been assumed to be a consequence of the disease, rather than a cause, says Dosch.
"This work merits serious consideration,” says Matt Hunt, Science Information Manager at Diabetes UK. However, since the study was carried out on specific neurons in mice, “future work in human populations with high rates of type 1 diabetes, such as Scandinavia, would seem a possible area to pursue," he adds.
From January 2007, Dosch plans to look for evidence of sensory abnormalities in babies born to high-risk families, and will follow them to see if impairment is predictive of disease.
Journal reference: Cell (vol 127, p 1123) |
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Whosthedaddy
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| Posted: 22:10 - 16 Dec 2006 Post subject: |
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| Joe wrote: | Without insulin, the body cannot convert glucose into energy |
Not entirely true.
Insulin is required for cells to aerobically respire and energy is released by the kreb cycle.
| Whosthedaddy wrote: | Glucose (C6H12O6) enters the various tissue cells of the body by diffusion, which is allowed by insulin. Insulin may be thought of as a key that opens the door for glucose to enter. Once inside the cell, “the glucose is phosphorylated to form glucose-6-phospate by the transfer of a phosphate group to its sixth carbon with the reaction of ATP” (Marieb, 1998). As this newly formed glucose-6-phosphate is different molecule to glucose, the intracellular levels are lower than the extra cellular levels, therefore maintaining a diffusion gradient for more glucose to enter the cell. This glucose-6-phosphate may now go one of two ways. It may be stored as a reserve as glycogen in the liver and muscles to be used later or utilised immediately to form more energy. In order to form more energy (ATP), the glucose-6-phosphate must be oxidised, this involves three main steps as described by Marieb, 1998. The first step is that of glycolysis. The author defines glycolysis as ‘sugar splitting’. This actually is more complex than this and involves a total of ten stages by which glucose is converted into pyruvic acid yielding 2 molecules of ATP. The process of glycolysis is an anaerobic reaction and oxygen is not required, however, if sufficient oxygen is present then the glycolysis reaction may then enter the next stage, the Kreb cycle.
The Kreb cycle occurs in the aqueous mitochondrial matrix and is the process whereby glucose-6-phospahte is converted into acetyl CoA. This process is fuelled by pyruvic acid produced in the earlier stages and by the breakdown of fatty acids resulting in the breakdown of fats. Marieb (1998) explains that one of the pyruvic acid carbons is removed to form carbon dioxide (a waste product), and is diffused into the blood stream. It is at this stage that hydrogen atoms are removed forming acetic acid with coenzyme A (otherwise known as acetyl CoA). This substance may now enter the Krebs cycle and is oxidised through a series of stages to form yet mote ATP.
The final step in glucose metabolism is that of the electron transport chain. Like glycolysis, none of the reactions of the Kreb cycle require oxygen directly. This is the exclusive function of the electron transport chain, which oversees the catabolic reaction in the mitochondria. The hydrogen atoms removed during the oxidation of food fuels are finally combined with molecular oxygen in the presence of a phosphate group ultimately producing ADP (energy). Most energy is produced in this final stage, 36 molecules of ATP. |
Even without glucose being able to enter the cells, energy is still obtained through anaerobic respiration, the amount of energy or ATP is less and the byproduct is lactic acid which is a poison 
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Current : MSX 125 Past : CBR 900RR Monkeybike : c50 LAC : ZXR750 H2 : FZR600 : ZX7R P3 : YW100 : TRX850: Trophy 900 T309 : GSXR 600 L0: Monkeybike : XJ6S Whosthedaddy |
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| Blackrhythms |
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Blackrhythms
Scooby Slapper
Joined: 18 Sep 2006
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| Posted: 22:17 - 16 Dec 2006 Post subject: |
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That's really interesting Joe, about diabetes being auto-immune, as I also was recently diagnosed with MS which is also auto-immune and of course, which affects the Central Nervous System. My consultant (for MS) told me that he'll be doing some research into if there's a connection and would I be interested in taking part. By all means, I said, as I'd like to know too!
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| Andy C |
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Andy C
Tree Seeking Missile
Joined: 26 Apr 2005
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| Posted: 22:19 - 16 Dec 2006 Post subject: |
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my sister has had i since she was about 12. If you moniter it then its liviable, i mean its bad but on the grand scale their are many worse things you can have instead.
i dont think you have it either, but got to that place to have a check up for peace on mind
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| stinkwheel |
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stinkwheel
Bovine Proctologist
Joined: 12 Jul 2004
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| Posted: 00:00 - 17 Dec 2006 Post subject: |
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| Whosthedaddy wrote: |
Even without glucose being able to enter the cells, energy is still obtained through anaerobic respiration, the amount of energy or ATP is less and the byproduct is lactic acid which is a poison |
Err. Strictly speaking both wrong.
To carry out anaerobic respiration, the glucose still has to be taken up by the cells. Anaerobic respiration only happens when oxygen is not available to accept the carbon from the Krebbs cycle when a proton is liberated, (Krebbs cycle is now known as the Tricarboxylic acid (TCA) cycle), there is no lack of oxygen in diabetes. In diabetes, the blood glucose levels are extemely high but the tissues are actually hypogloycaemic because the insulin doesn't activate the glucose uptake mechanism.
In the case of severe, uncontrolled diabetes, the body is forced to rely on energy derived from the breakdown of fats. This produces compounds known as ketones, the primary one being beta-hydroxy-butyrate. This 'inserts' into the TCA cycle and allows the cell to produce energy, but not in a very satisfactory or efficient manner.
The downside is that other ketone bodies are also produced, noteably acetone which is useless to the body. Someone who has severe, uncontrolled diabetes has high levels of ketones in the blood, sometimes the breath and urine even smell of nail varnish remover. Ketone bodies will keep you alive in the absence of glucose, but they are ultimately poisonous. Blood pH drops causing acidosis and they cross the blood brain barrier causing intoxication.
Ketoacidosis eventually leads to coma and death, initial treatment consists of aggressive fluid therapy with intravenous saline to 'flush' the ketones through the kidneys and administration of soluable insulin. Once the ketoacidosis is reversed, stabalisation on diet/longer acting insulin can be commenced.
Phew. Eight years since I did that. I used to be able to draw all the intermediate chemical structures too. |
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| Whosthedaddy |
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Whosthedaddy
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| Posted: 00:13 - 17 Dec 2006 Post subject: |
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| stinkwheel wrote: | The downside is that other ketone bodies are also produced, noteably acetone which is useless to the body. Someone who has severe, uncontrolled diabetes has high levels of ketones in the blood, sometimes the breath and urine even smell of nail varnish remover. Ketone bodies will keep you alive in the absence of glucose, but they are ultimately poisonous. Blood pH drops causing acidosis and they cross the blood brain barrier causing intoxication.
Ketoacidosis eventually leads to coma and death, initial treatment consists of aggressive fluid therapy with intravenous saline to 'flush' the ketones through the kidneys and administration of soluable insulin. Once the ketoacidosis is reversed, stabalisation on diet/longer acting insulin can be commenced.
Phew. Eight years since I did that. I used to be able to draw all the intermediate chemical structures too. |
I have nt met a DKA in a while the last was a young bloke that ran out of insulin on a friday and thought that he could last all weekend and then bank holiday monday before he got some more  Needless to say, his BSL was >40mmol/l, and he felt like shite 
I was trying to explain to our staff grade on the ward a naff experiment I did at A'level to highlight the role of mitochoindria in the kreb cycle. I used 2 forms of yeast (one normal? and the other 'petit yeast' with no mitochondria').
The yeast were placeed on various different media such as glucose, lactose, maltose and other gooey stuff. The idea was to show that without mitochondria, the yeast cannot obtain as much energy and fail to reproduce, compared to the normal yeast.
Needless to say, there was major cross contamination and the experiment was a complete flop, but in theory it was cool.
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Current : MSX 125 Past : CBR 900RR Monkeybike : c50 LAC : ZXR750 H2 : FZR600 : ZX7R P3 : YW100 : TRX850: Trophy 900 T309 : GSXR 600 L0: Monkeybike : XJ6S Whosthedaddy |
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| stinkwheel |
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stinkwheel
Bovine Proctologist
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| Posted: 00:34 - 17 Dec 2006 Post subject: |
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My (animal) diabetic patients usually present collapsed and in a ketoacidotic crisis, often in convulsions.
You want to try getting a 23g IV catheter into a fitting, dehydrated cat. 
I deal with ketosis a lot, when dairy cattle start to lactate, they suddenly need to find an extra 5kg of glucose per day. Some of them don't manage (especially fat ones, probably the same idea as why fat people get diabetes) and essentially starve. Cows can go ketotic as hell, you can smell it when you walk into the shed, I'd swear you could strip paint with some of their piss.
Tricky to treat too because if you feed them glucose, their rumen ferments it and turns it into protien. You have to give them a 'bypass' energy source in the form of proponyl glycol. Their body then cleverly reverses the TCA cycle and uses the propinoate to make pyruvate then glucose. |
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| msgander |
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msgander
Brolly Dolly
Joined: 31 Aug 2005
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| Posted: 09:38 - 20 Dec 2006 Post subject: |
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Stinkwheel Rawks!!!
Bonny, GO GET CHECKED FFS it will only take a few mins!!!
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