Type 2 diabetes is a metabolic disorder resulting from the body’s inability to properly use insulin. This is called insulin resistance. Insulin resistance means the body does not respond when insulin is present. This is the most common and there is no known cure. Between 2005-2007 diabetes has increased by 13.5%. 24 % of the world’s population goes undiagnosed. Diabetes affects over 150 million over the world. A Yale University study of obese children between the ages 4 and 18 appeared in the March14, 2002, issue of New England Journal of Medicine. It found that nearly a quarter had a condition that’s often a precursor to diabetes (Dr. Bernstein’s, 2003). Type 2 is often associated with obesity, hypertension, elevated cholesterol, and a condition often termed Metabolic syndrome. Secondary causes are:
Cusings syndrome, acromegaly, thyrotoxicosis, cancer, pheochromocytoma, chronic pancreatitis. There does appear to be a genetic factor which causes it to run in some families. People can inherit a tendency to develop type 2 diabetes, Type 2 diabetes may be prevented or delayed by following a program to eliminate or reduce risk factors– losing weight and exercise.
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There are 5 main kinds of oral medication for people that have been diagnosed with this disease. Sulfonylureas, benzoic acid derivatives, biguanides, acarbose and thiazolidinediones. These are medications that come under the general name of oral hypoglycemic agents (OHAs) (American College of Physicians). Future outcomes of Type 2 Diabetes
Ideal treatment would be to prevent diabetes. For type 2 diabetes, control of body weight and regular exercise are known to reduce the chances of developing the condition. The problem with type 2 is more complicated because they may be making insulin but resistant to its action. Losing weight can see a dramatic change in sugar levels, which may allow patients to come off medications. Complications for type 2 diabetes are: Macrovascular (heart attack, stroke, peripheral vascular disease). Microvascular (eyes, kidneys, nerves). (Conquering Diabetes, Peters,)
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A study says diabetes may originate in the intestines. While the role of the pancreas and the liver in the development of diabetes are well described, a recent study conducted by ADA-funded researchers at Washington University in St. Louis suggests that the digestive system may also play a surprising and important role in developing the disease.
Lead investigator Clay F. Semenkovich, MD is the main author on the February 16, 2012 Cell Host ; Microbe publication, which links an insulin-regulated enzyme, called fatty acid synthase (FAS), to chronic inflammation in the gut – a known contributor to insulin resistance and type 2 diabetes. Dr. Semenkovich’s former postdoctoral fellow in an ADA mentorship grant, Xiaochao Wei, PhD, collaborated on the study and is first author on the paper. While humans (and animals) depend on normal gut bacteria to aid with digestion and help produce vitamins, a protective mucus barrier prevents harmful pathogenic bacteria from invading the small intestines and colon. The scientists found that FAS, an enzyme which is critical in lipid and fat production, helps maintain this protective mucus membrane that lines the intestines. Since FAS is regulated by insulin,
people with diabetes have lower levels of the enzyme and thus may be more vulnerable to inflammation in their digestive tract.
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“Diabetes may start in your intestines. When people become insulin resistant, as happens when they gain weight, FAS won’t work properly, which causes inflammation that, leads to developing diabetes,” said Dr. Semenkovich. By identifying mechanisms involved in diabetes, these results could provide future avenues for developing therapeutics to combat the disease.
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American College of Physians (2000). Medications. P.84 Bernstein (2003).Explanation of Type 2 Diabetes. Diabetes Solution, p.33 News.medical.net/health/Diabetes-mellitus-type2-pathophtsicology Peters, A. (2005). Outcome For Type 2 Diabetes. Conquering Diabetes. P.28 ; 29 Semenkovich,C (2012). Diabetes In The Intestines. Cell Host ; Micobe