Type I diabetes usually occurs in people who are below the age 20 and that is why it is also called as juvenile diabetes. In this type, the body becomes partially or completely unable to produce insulin. Type I diabetes is an autoimmune disease. In this, your immune system attacks the pancreas from where the insulin is produced, thereby making the pancreas inefficient or unable to produce insulin. Type I diabetes cannot be prevented, it can only be controlled with healthy lifestyle changes.
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As of 2015 the guidelines called for an HbA1c of around 7% or a fasting glucose of less than 7.2 mmol/L (130 mg/dL); however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy. Despite guidelines recommending that intensive blood sugar control be based on balancing immediate harms and long-term benefits, many people – for example people with a life expectancy of less than nine years – who will not benefit are over-treated and do not experience clinically meaningful benefits.
Anti-diabetic medications are used to control type 2 diabetes mellitus. In this case, body cells are resistant to insulin (injections), therefore medications are given orally to lower the blood glucose levels. In most of the cases, oral hypoglycemic agents are highly effective. One just needs to ascertain which suits him/her the best. There are several classes of anti-diabetic drugs. Largely, their selection depends on the nature of the diabetes, age and situation of the person, as well as other factors.
Unfortunately, most people are not given the benefit of this approach. When diagnosed with diabetes, most people are told to avoid sugar (good step, not the solution). If the problem is bad enough, they are told to take medication to give the body insulin. The problem is, as we saw above, diabetes is a problem with the body’s regulation of insulin, caused by a resistance to insulin and an overproduction to remove toxic amounts of glucose in the bloodstream. Insulin is also dangerous if it is left circulating the the blood. Somehow, treating too much circulating glucose and insulin with more insulin doesn’t seem like the right approach…
Type 2 diabetes is a condition that is characterised by chronically elevated blood sugar levels. However, the main cause as well as the driver for this condition is something called Insulin Resistance. When you eat certain foods, particularly refined carbohydrates, that food is converted to sugar inside your body. Your body’s way of dealing with this sugar is to produce a hormone called insulin. Insulin moves the sugar inside your cells so that it can be used for energy. Sounds great, right?
Storage of liver fat can only occur when daily calorie intake exceeds expenditure. Sucrose overfeeding for 3 weeks has been shown to cause a 30% increase in liver fat content (37). The associated metabolic stress on hepatocytes was reflected by a simultaneous 30% rise in serum alanine aminotransferase (ALT) levels, and both liver fat and serum ALT returned to normal levels during a subsequent hypocaloric diet. Superimposed upon a positive calorie balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver. In groups of both obese and nonobese subjects, it was found that those with higher plasma insulin levels have markedly increased rates of hepatic de novo lipogenesis (2,38,39). Conversely, in type 1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with subnormal liver fat content (40). Initiation of subcutaneous insulin therapy in type 2 diabetes brings about a decrease in portal insulin delivery by suppression of pancreatic insulin secretion and, hence, a decrease in liver fat (41). Hypocaloric diet (42), physical activity (43), or thiazolidinedione use (23,44) each reduces insulin secretion and decreases liver fat content. Newly synthesized triacylglycerol in the liver will be either oxidized, exported, or stored as hepatic triacylglycerol. Because transport of fatty acid into mitochondria for oxidation is inhibited by the malonyl-CoA produced during de novo lipogenesis, newly synthesized triacylglycerol is preferentially directed toward storage or export. Hence, hepatic fat content and plasma VLDL triacylglycerol levels are increased.
In a person with carbohydrate intolerance, type 2 diabetes or prediabetes, this system breaks down. The body loses its insulin sensitivity and more and more insulin is required to remove the excess blood sugar. As a result, blood sugar levels remain high and insulin levels are high as well, and these high insulin levels can make your body even less sensitive to insulin.
Note that these medications used to treat type 2 diabetes are typically not used in pregnant or breastfeeding women. At present the only recommended way of controlling diabetes in women who are pregnant or breastfeeding is by diet, exercise, and insulin therapy. You should speak with your health-care professional if you are taking these medications, are considering becoming pregnant, or if you have become pregnant while taking these medications.