The genes identified so far in people with type 2 include many that affect the insulin-producing beta cells of the pancreas, says Craig Hanis, PhD, a professor at the Human Genetics Center at the University of Texas Health Science Center in Houston. And yet he emphasizes that why people get type 2 isn't at all clear yet: "What it tells us is that diabetes is a complicated disease."
Triglycerides are a common form of fat that we digest. Triglycerides are the main ingredient in animal fats and vegetable oils. Elevated levels of triglycerides are a risk factor for heart disease, heart attack, stroke, fatty liver disease, and pancreatitis. Elevated levels of triglycerides are also associated with diseases like diabetes, kidney disease, and medications (for example, diuretics, birth control pills, and beta blockers). Dietary changes, and medication if necessary can help lower triglyceride blood levels.
Environmental factors are important, because even identical twins have only a 30-60% concordance for type 1 diabetes mellitus and because incidence rates vary in genetically similar populations under different living conditions.  No single factor has been identified, but infections and diet are considered the 2 most likely environmental candidates.
Metformin is generally recommended as a first line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose. Several other groups of drugs, mostly given by mouth, may also decrease blood sugar in type II DM. These include agents that increase insulin release, agents that decrease absorption of sugar from the intestines, and agents that make the body more sensitive to insulin. When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications. Doses of insulin are then increased to effect.
Diabetes mellitus is a metabolic condition in which a person's blood sugar (glucose) levels are too high. Over 29.1 million children and adults in the US have diabetes. Of that, 8.1 million people have diabetes and don't even know it. Type 1 diabetes (insulin-dependent, juvenile) is caused by a problem with insulin production by the pancreas. Type 2 diabetes (non-insulin dependent) is caused by:
Patients with type 1 DM, unless they have had a pancreatic transplant, require insulin to live; intensive therapy with insulin to limit hyperglycemia (“tight control”) is more effective than conventional therapy in preventing the progression of serious microvascular complications such as kidney and retinal diseases. Intensive therapy consists of three or more doses of insulin injected or administered by infusion pump daily, with frequent self-monitoring of blood glucose levels as well as frequent changes in therapy as a result of contacts with health care professionals. Some negative aspects of intensive therapy include a three times more frequent occurrence of severe hypoglycemia, weight gain, and an adverse effect on serum lipid levels, i.e., a rise in total cholesterol, LDL cholesterol, and triglycerides and a fall in HDL cholesterol. Participation in an intensive therapy program requires a motivated patient, but it can dramatically reduce eye, nerve, and renal complications compared to conventional therapy. See: insulin pump for illus.
The beta cells may be another place where gene-environment interactions come into play, as suggested by the previously mentioned studies that link beta cell genes with type 2. "Only a fraction of people with insulin resistance go on to develop type 2 diabetes," says Shulman. If beta cells can produce enough insulin to overcome insulin resistance, a factor that may be genetically predetermined, then a person can stay free of diabetes. But if the beta cells don't have good genes propping them up, then diabetes is the more likely outcome in a person with substantial insulin resistance.
Diabetes experts feel that these blood glucose monitoring devices give patients a significant amount of independence to manage their disease process; and they are a great tool for education as well. It is also important to remember that these devices can be used intermittently with fingerstick measurements. For example, a well-controlled patient with diabetes can rely on fingerstick glucose checks a few times a day and do well. If they become ill, if they decide to embark on a new exercise regimen, if they change their diet and so on, they can use the sensor to supplement their fingerstick regimen, providing more information on how they are responding to new lifestyle changes or stressors. This kind of system takes us one step closer to closing the loop, and to the development of an artificial pancreas that senses insulin requirements based on glucose levels and the body's needs and releases insulin accordingly - the ultimate goal.
Jump up ^ Piwernetz K, Home PD, Snorgaard O, Antsiferov M, Staehr-Johansen K, Krans M (May 1993). "Monitoring the targets of the St Vincent Declaration and the implementation of quality management in diabetes care: the DIABCARE initiative. The DIABCARE Monitoring Group of the St Vincent Declaration Steering Committee". Diabetic Medicine. 10 (4): 371–7. doi:10.1111/j.1464-5491.1993.tb00083.x. PMID 8508624.
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells).
If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more "off limits" to people with diabetes than they are to people without diabetes. The key to sweets is to have a very small portion and save them for special occasions so you focus your meal on more healthful foods.
diabetes mel´litus a broadly applied term used to denote a complex group of syndromes that have in common a disturbance in the oxidation and utilization of glucose, which may be secondary to a malfunction of the beta cells of the pancreas, whose function is the production and release of insulin. Because insulin is involved in the metabolism of carbohydrates, proteins, and fats, diabetes is not limited to a disturbance of glucose homeostasis alone. Insulin resistance may also sometimes play a role in the etiology of diabetes.
Jump up ^ Imperatore, Giuseppina; Boyle, James P.; Thompson, Theodore J.; Case, Doug; Dabelea, Dana; Hamman, Richard F.; Lawrence, Jean M.; Liese, Angela D.; Liu, Lenna L. (December 2012). "Projections of Type 1 and Type 2 Diabetes Burden in the U.S. Population Aged <20 Years Through 2050". Diabetes Care. 35 (12): 2515–20. doi:10.2337/dc12-0669. ISSN 0149-5992. PMC 3507562. PMID 23173134. Archived from the original on 2016-08-14.
How to prevent type 2 diabetes: Six useful steps What are the risks factors for developing type 2 diabetes, and how can we prevent it? Some factors such as blood sugar levels, body weight, fiber intake, and stress can be controlled to some extent, but others, such as age and family history cannot. Find out more about reducing the risk of developing this condition. Read now
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
Sasigarn A Bowden, MD Associate Professor of Pediatrics, Section of Pediatric Endocrinology, Metabolism and Diabetes, Department of Pediatrics, Ohio State University College of Medicine; Pediatric Endocrinologist, Associate Fellowship Program Director, Division of Endocrinology, Nationwide Children’s Hospital; Affiliate Faculty/Principal Investigator, Center for Clinical Translational Research, Research Institute at Nationwide Children’s Hospital
interventions The goal of treatment is to maintain insulin glucose homeostasis. Type 1 diabetes is controlled by insulin, meal planning, and exercise. The Diabetes Control and Complications Trial (DCCT), completed in mid-1993, demonstrated that tight control of blood glucose levels (i.e., frequent monitoring and maintenance at as close to normal as possible to the level of nondiabetics) significantly reduces complications such as eye disease, kidney disease, and nerve damage. Type 2 diabetes is controlled by meal planning; exercise; one or more oral agents, in combination with oral agents; and insulin. The results of the United Kingdom Prospective Diabetes Study, which involved more than 5000 people with newly diagnosed type 2 diabetes in the United Kingdom, were comparable to those of the DCCT where a relationship in microvascular complications. Stress of any kind may require medication adjustment in both type 1 and type 2 diabetes.
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Diabetes mellitus (DM) is best defined as a syndrome characterized by inappropriate fasting or postprandial hyperglycemia, caused by absolute or relative insulin deficiency and its metabolic consequences, which include disturbed metabolism of protein and fat. This syndrome results from a combination of deficiency of insulin secretion and its action. Diabetes mellitus occurs when the normal constant of the product of insulin secretion times insulin sensitivity, a parabolic function termed the “disposition index” (Figure 19-1), is inadequate to prevent hyperglycemia and its clinical consequences of polyuria, polydipsia, and weight loss. At high degrees of insulin sensitivity, small declines in the ability to secrete insulin cause only mild, clinically imperceptible defects in glucose metabolism. However, irrespective of insulin sensitivity, a minimum amount of insulin is necessary for normal metabolism. Thus, near absolute deficiency of insulin must result in severe metabolic disturbance as occurs in type 1 diabetes mellitus (T1DM). By contrast, with decreasing sensitivity to its action, higher amounts of insulin secretion are required for a normal disposition index. At a critical point in the disposition index curve (see Figure 19-1), a further small decrement in insulin sensitivity requires a large increase in insulin secretion; those who can mount these higher rates of insulin secretion retain normal glucose metabolism, whereas those who cannot increase their insulin secretion because of genetic or acquired defects now manifest clinical diabetes as occurs in type 2 diabetes (T2DM).
In addition to learning about diabetes itself, older people may have to learn how to fit management of diabetes in with their management of other disorders. Learning about how to avoid complications, such as dehydration, skin breakdown, and circulation problems, and to manage factors that can contribute to complications of diabetes, such as high blood pressure and high cholesterol levels, is especially important. Such problems become more common as people age, whether they have diabetes or not.
The ketogenic, or keto, diet calls for dramatically increasing your fat intake and consuming a moderate amount of protein and a very low amount of carbs, with the aim of kicking your body into a natural metabolic state called ketosis, in which it relies on burning fat rather than carbs for energy. Ketosis is different from diabetic ketoacidosis, a health emergency that occurs when insulin levels are low in conjunction with high levels of ketones. (37) Ketones are by-products of metabolism that are released in the blood when carb intake is low.
Manage mild hypoglycemia by giving rapidly absorbed oral carbohydrate or glucose; for a comatose patient, administer an intramuscular injection of the hormone glucagon, which stimulates the release of liver glycogen and releases glucose into the circulation. Where appropriate, an alternative therapy is intravenous glucose (preferably no more than a 10% glucose solution). All treatments for hypoglycemia provide recovery in approximately 10 minutes. (See Treatment.)
In this health topic, we discuss hyperglycemic hyperosmolar nonketotic syndrome (HHNS), an extremely serious complication that can lead to diabetic coma and even death in type 2 diabetes. This serious condition occurs when the blood sugar gets too high and the body becomes severely dehydrated. To prevent HHNS and diabetic coma in type 2 diabetes, check your blood sugar regularly as recommended by your health care provider; check your blood sugar more frequently when you are sick, drink plenty of fluids, and watch for signs of dehydration.