Insulin is the hormone responsible for reducing blood sugar. In order for insulin to work, our tissues have to be sensitive to its action; otherwise, tissues become resistant and insulin struggles to clear out sugar from the blood. As insulin resistance sets in, the first organ to stop responding to insulin is the liver, followed by the muscles and eventually fat. How does insulin resistance begin? The root of the problem is our diet.
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).

People with diabetes either don't make insulin or their body's cells no longer are able to use the insulin, leading to high blood sugars. By definition, diabetes is having a blood glucose level of greater than or equal to126 milligrams per deciliter (mg/dL) after an 8-hour fast (not eating anything), or by having a non-fasting glucose level greater than or equal to 200 mg/dL along with symptoms of diabetes, or a glucose level of greater than or equal to 200 mg/dL on a 2-hour glucose tolerance test, or an A1C greater than or equal to 6.5%. Unless the person is having obvious symptoms of diabetes or is in a diabetic crisis, the diagnosis must be confirmed with a repeat test.

2.Retinopathy - Diabetes may cause blood vessels in the retina (the light sensitive lining of the eye) to become leaky, blocked, or grow abnormally [Figure 1]. Retinopathy is rare before the age of 10 and the risk increases with the length of time a person has diabetes. Treatments such as laser, injections in the eye, or other procedures may be helpful to prevent visual loss or restore sight. The longer a patient has diabetes, the greater chance of developing an eye problem.  All patients with diabetes are at risk for developing retinopathy, but the risk is higher for patients with worse blood sugar control.  Early retinopathy may have no symptoms, but early treatment is essential to prevent any loss of vision.
^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.
No single environmental trigger has been identified as causing diabetes mellitus, however both infectious agents and dietary factors are thought to be important. Various viruses have been implicated in the development of type I DM. They may act by initiating or modifying the autoimmune process. In particular, the rubella virus and coxsackie viruses have been closely studied. In particular, congenital rubella infection has shown direct relationships with the development of type 1 diabetes mellitus. This is presumably due to the virus (or antibodies against it) damaging the beta cells of the pancreas. Some research has looked at dietary factors that may be associated with type 1 diabetes. In particular, cow’s milk proteins (such as bovine serum albumin) which may have some similarities to pancreatic islet cell markers may be able to trigger the autoimmune process. Other chemicals including nitrosamines have been identified as causes of diabetes mellitus in animal models, but not in humans.
This is specific to type 2 diabetes. It occurs when insulin is produced normally in the pancreas, but the body is still unable move glucose into the cells for fuel. At first, the pancreas will create more insulin to overcome the body’s resistance. Eventually the cells “wear out.” At that point the body slows insulin production, leaving too much glucose in the blood. This is known as prediabetes. A person with prediabetes has a blood sugar level higher than normal but not high enough for a diagnosis of diabetes. Unless tested, the person may not be aware, as there are no clear symptoms. Type 2 diabetes occurs as insulin production continues to decrease and resistance increases.
There are other factors that also fall into the category of environmental (as opposed to genetic) causes of diabetes. Certain injuries to the pancreas, from physical trauma or from drugs, can harm beta cells, leading to diabetes. Studies have also found that people who live in polluted areas are prone to type 2, perhaps because of inflammation. And an alternate theory of insulin resistance places the blame on damage caused by inflammation. Age also factors into type 2; beta cells can wear out over time and become less capable of producing enough insulin to overcome insulin resistance, which is why older people are at greater risk of type 2.
Threshold for diagnosis of diabetes is based on the relationship between results of glucose tolerance tests, fasting glucose or HbA1c and complications such as retinal problems.[10] A fasting or random blood sugar is preferred over the glucose tolerance test, as they are more convenient for people.[10] HbA1c has the advantages that fasting is not required and results are more stable but has the disadvantage that the test is more costly than measurement of blood glucose.[50] It is estimated that 20% of people with diabetes in the United States do not realize that they have the disease.[10]
Jump up ^ Farmer, AJ; Perera, R; Ward, A; Heneghan, C; Oke, J; Barnett, AH; Davidson, MB; Guerci, B; Coates, V; Schwedes, U; O'Malley, S (27 February 2012). "Meta-analysis of individual patient data in randomised trials of self monitoring of blood glucose in people with non-insulin treated type 2 diabetes". The BMJ. 344: e486. doi:10.1136/bmj.e486. PMID 22371867.
Aspirin should be used as secondary prophylaxis in all diabetic people with evidence of macrovascular disease, and it should be strongly considered as primary prevention in diabetic subjects with other risk factors for macrovascular disease, such as hypertension, cigarette smoking, dyslipidemia, obesity, and albuminuria (macro or micro).228 Because of the platelet defects associated with diabetes, it is recommended that the dose of aspirin should be 300 mg per day,228–230 although the American Diabetes Association’s position statement (http://www.diabetes.org/DiabetesCare/supplement198/s45.htm) advocates a dose of 81 to 325 mg enteric-coated aspirin per day. If the patient cannot tolerate aspirin, then clopidogrel231 can be used.

Jump up ^ McBrien, K; Rabi, DM; Campbell, N; Barnieh, L; Clement, F; Hemmelgarn, BR; Tonelli, M; Leiter, LA; Klarenbach, SW; Manns, BJ (6 August 2012). "Intensive and Standard Blood Pressure Targets in Patients With Type 2 Diabetes Mellitus: Systematic Review and Meta-analysis". Archives of Internal Medicine. 172 (17): 1–8. doi:10.1001/archinternmed.2012.3147. PMID 22868819.

People with full-blown type 2 diabetes are not able to use the hormone insulin properly, and have what’s called insulin resistance. Insulin is necessary for glucose, or sugar, to get from your blood into your cells to be used for energy. When there is not enough insulin — or when the hormone doesn’t function as it should — glucose accumulates in the blood instead of being used by the cells. This sugar accumulation may lead to the aforementioned complications.
×