Glucose is a simple sugar found in food. Glucose is an essential nutrient that provides energy for the proper functioning of the body cells. Carbohydrates are broken down in the small intestine and the glucose in digested food is then absorbed by the intestinal cells into the bloodstream, and is carried by the bloodstream to all the cells in the body where it is utilized. However, glucose cannot enter the cells alone and needs insulin to aid in its transport into the cells. Without insulin, the cells become starved of glucose energy despite the presence of abundant glucose in the bloodstream. In certain types of diabetes, the cells' inability to utilize glucose gives rise to the ironic situation of "starvation in the midst of plenty". The abundant, unutilized glucose is wastefully excreted in the urine.
Fasting plasma glucose level: If your blood glucose level is 7.0 mmol/L or higher after having not eaten anything for at least 8 hours – called fasting – your doctor may diagnose diabetes. If your blood glucose level is between 6.1 to 6.9 mmol/L, your doctor may diagnose impaired fasting glucose or prediabetes (a condition that may later develop into diabetes).
Jump up ^ Rubino, F; Nathan, DM; Eckel, RH; Schauer, PR; Alberti, KG; Zimmet, PZ; Del Prato, S; Ji, L; Sadikot, SM; Herman, WH; Amiel, SA; Kaplan, LM; Taroncher-Oldenburg, G; Cummings, DE; Delegates of the 2nd Diabetes Surgery, Summit (June 2016). "Metabolic Surgery in the Treatment Algorithm for Type 2 Diabetes: A Joint Statement by International Diabetes Organizations". Diabetes Care. 39 (6): 861–77. doi:10.2337/dc16-0236. PMID 27222544.
The progression of nephropathy in patients can be significantly slowed by controlling high blood pressure, and by aggressively treating high blood sugar levels. Angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs) used in treating high blood pressure may also benefit kidney disease in patients with diabetes.
For Candace Clark, bariatric surgery meant the difference between struggling with weight issues, including medical problems triggered by obesity, and enjoying renewed health and energy. "I felt like I was slowly dying," says Candace Clark, a 54-year-old Barron, Wisconsin, resident who had dealt with weight issues for years. "I was tired of feeling the way [...]
On behalf of the millions of Americans who live with or are at risk for diabetes, we are committed to helping you understand this chronic disease. Help us set the record straight and educate the world about diabetes and its risk factors by sharing the common questions and answers below. If you're new to type 2 diabetes, join our Living With Type 2 Diabetes program to get more facts.
Type 1 Diabetes: About 5 to 10 percent of those with diabetes have type 1 diabetes. It's an autoimmune disease, meaning the body's own immune system mistakenly attacks and destroys the insulin-producing cells in the pancreas. Patients with type 1 diabetes have very little or no insulin, and must take insulin everyday. Although the condition can appear at any age, typically it's diagnosed in children and young adults, which is why it was previously called juvenile diabetes.
Hypoglycemic reactions are promptly treated by giving carbohydrates (orange juice, hard candy, honey, or any sugary food); if necessary, subcutaneous or intramuscular glucagon or intravenous dextrose (if the patient is not conscious) is administered. Hyperglycemic crises are treated initially with prescribed intravenous fluids and insulin and later with potassium replacement based on laboratory values.
Diabetes insipidus is characterized by excessive urination and thirst, as well as a general feeling of weakness. While these can also be symptoms of diabetes mellitus, if you have diabetes insipidus your blood sugar levels will be normal and no sugar present in your urine. Diabetes insipidus is a problem of fluid balance caused by a problem with the kidneys, where they can't stop the excretion of water. Polyuria (excessive urine) and polydipsia (excessive thirst) occur in diabetes mellitus as a reaction to high blood sugar.
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DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L); 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. SEE ALSO insulin resistance
Say that two people have the same genetic mutation. One of them eats well, watches their cholesterol, and stays physically fit, and the other is overweight (BMI greater than 25) and inactive. The person who is overweight and inactive is much more likely to develop type 2 diabetes because certain lifestyle choices greatly influence how well your body uses insulin.
When the glucose concentration in the blood remains high over time, the kidneys will reach a threshold of reabsorption, and glucose will be excreted in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).
People with type 1 diabetes are unable to produce any insulin at all. People with type 2 diabetes still produce insulin, however, the cells in the muscles, liver and fat tissue are inefficient at absorbing the insulin and cannot regulate glucose well. As a result, the body tries to compensate by having the pancreas pump out more insulin. But the pancreas slowly loses the ability to produce enough insulin, and as a result, the cells don’t get the energy they need to function properly.
Patients need to ensure that their blood glucose levels are kept as normal as possible so that delicate tissues in the body (especially blood vessels in the eyes, kidneys and peripheral nerves) are not damaged by high glucose levels over a long period of time. To achieve this, patients need to measure their glucose regularly and learn how to adjust their insulin doses in order to optimise their glucose levels (diabetes control). Good diabetes control helps to minimise the risk of long-term diabetes complications, as well as short-term symptoms (such as thirst).
Longer-term, the goals of treatment are to prolong life, reduce symptoms, and prevent diabetes-related complications such as blindness, kidney failure, and amputation of limbs. These goals are accomplished through education, insulin use, meal planning and weight control, exercise, foot care, and careful self-testing of blood glucose levels. Self-testing of blood glucose is accomplished through regular use of a blood glucose monitor (pictured, right). This machine can quickly and easily measure the level of blood glucose based by analysing the level from a small drop of blood that is usually obtained from the tip of a finger. You will also require regular tests for glycated haemoglobin (HbA1c). This measures your overall control over several months.
Insulin-dependent diabetes mellitus is believed to result from autoimmune, environmental, and/or genetic factors. Whatever the cause, the end result is destruction of insulin-producing pancreatic beta cells, a dramatic decrease in the secretion of insulin, and hyperglycemia. Non-insulin-dependent diabetes mellitus is presumably heterogeneous in origin. It is associated with older age, obesity, a family history of diabetes, and ethnicity (genetic components). The vast majority of those with non-insulin-dependent diabetes are overweight Kahn (2003). This form of the disorder has a much slower rate of progression than insulin-dependent diabetes. Over time the ability to respond to insulin decreases, resulting in increased levels of blood glucose. The pancreatic secretion of insulin increases in an attempt to compensate for the elevated levels of glucose. If the condition is untreated, the pancreatic production of insulin decreases and may even cease.