By checking your own blood sugar levels, you can track your body's changing needs for insulin and work with your doctor to figure out the best insulin dosage. People with diabetes check their blood sugar up to several times a day with an instrument called a glucometer. The glucometer measures glucose levels in a sample of your blood dabbed on a strip of treated paper. Also, there are now devices, called continuous glucose monitoring systems (CGMS), that can be attached to your body to measure your blood sugars every few minutes for up to a week at a time. But these machines check glucose levels from skin rather than blood, and they are less accurate than a traditional glucometer.
^ Jump up to: a b Cox DJ, Kovatchev BP, Anderson SM, Clarke WL, Gonder-Frederick LA (November 2010). "Type 1 diabetic drivers with and without a history of recurrent hypoglycemia-related driving mishaps: physiological and performance differences during euglycemia and the induction of hypoglycemia". Diabetes Care. 33 (11): 2430–35. doi:10.2337/dc09-2130. PMC 2963507. PMID 20699432.
And when I talk about reducing certain carbohydrates, I mainly mean reducing your intake of  refined carbohydrates such as pasta, rice and bread. Non starchy vegetables (such as broccoli, cabbage and cauliflower) are fine and can be eaten in abundance. Many fruits are packed with carbohydrates, so if you’re trying to reduce your carb intake, try and limit your intake to low-carb fruit, such as rhubarb, watermelon, berries, peaches and blackberries.
During this 8-week study, β-cell function was tested by a gold standard method that used a stepped glucose infusion with subsequent arginine bolus (21). In type 2 diabetes, the glucose-induced initial rapid peak of insulin secretion (the first phase insulin response) typically is absent. This was confirmed at baseline in the study, but the first phase response increased gradually over 8 weeks of a very-low-calorie diet to become indistinguishable from that of age- and weight-matched nondiabetic control subjects. The maximum insulin response, as elicited by arginine bolus during hyperglycemia, also normalized. Pancreas fat content decreased gradually during the study period to become the same as that in the control group, a time course matching that of the increase in both first phase and total insulin secretion (Fig. 3). Fat content in the islets was not directly measured, although it is known that islets take up fat avidly (24) and that islet fat content closely reflects total pancreatic fat content in animal models (25). Although a cause-and-effect relationship between raised intraorgan fat levels and metabolic effect has not yet been proven, the time course data following the dietary intervention study are highly suggestive of a causal link (21).
The NIDDK has played an important role in developing “artificial pancreas” technology. An artificial pancreas replaces manual blood glucose testing and the use of insulin shots or a pump. A single system monitors blood glucose levels around the clock and provides insulin or a combination of insulin and a second hormone, glucagon, automatically. The system can also be monitored remotely, for example by parents or medical staff.
Gene therapy can be used to turn duodenum cells and duodenum adult stem cells into beta cells which produce insulin and amylin naturally. By delivering beta cell DNA to the intestine cells in the duodenum, a few intestine cells will turn into beta cells, and subsequently adult stem cells will develop into beta cells. This makes the supply of beta cells in the duodenum self replenishing, and the beta cells will produce insulin in proportional response to carbohydrates consumed.[78]
Grains: Grains, especially gluten-containing grains like wheat, contain large amounts of carbohydrates that are broken down into sugar within only a few minutes of consumption. Gluten can cause intestinal inflammation, which affects hormones like cortisol and leptin, and can lead to spikes in blood sugar. I recommend removing all grains from your diet for 90 days as your body adjusts to this healing program. Then you can try bringing sprouted ancient grains back into your diet in small amounts.

There was a clinical trial conducted at Department of Biochemistry, Postgraduate Institute of Basic Medical Sciences Madras, India that studied 22 patients with type 2 diabetes. It reported that supplementing the body with 400 mg of Gymnema Sylvestre extract daily resulted in remarkable reductions in blood glucose levels, hemoglobin A1c and glycosylated plasma protein levels. What’s even more remarkable is that by the end of this 18 month study, participants were able to reduce the dosage of their prescription diabetes medication. Five were even completely off medication and attaining stable blood sugar levels with Gymnema Sylvestre supplementation alone.

In the study, Fung and his team randomly recruited three men, ages 40 to 67, with type 2 diabetes, who also had high cholesterol and high blood pressure. At the start of the study, the authors recorded the participants’ vitals, including their A1C (a three-month average of their blood sugar levels), their fasting blood glucose levels, their waist circumference, and their weight. All three men were on insulin and oral medication.
Any food that you ingest is processed and metabolized by the body. Food is broken down into the various building blocks the body needs, and what cannot be metabolized or used is processed and removed by the liver. Protein and fats are used for muscle and tissue regeneration and other processes in the body. Carbohydrates are typically a fast fuel for the body, but when more are eaten that the body immediately needs, they must be stored. A simple explanation from a previous post:
In obese young people, decreased β-cell function has recently been shown to predict deterioration of glucose tolerance (4,78). Additionally, the rate of decline in glucose tolerance in first-degree relatives of type 2 diabetic individuals is strongly related to the loss of β-cell function, whereas insulin sensitivity changes little (79). This observation mirrors those in populations with a high incidence of type 2 diabetes in which transition from hyperinsulinemic normal glucose tolerance to overt diabetes involves a large, rapid rise in glucose levels as a result of a relatively small further loss of acute β-cell competence (3). The Whitehall II study showed in a large population followed prospectively that people with diabetes exhibit a sudden rise in fasting glucose as β-cell function deteriorates (Fig. 5) (80). Hence, the ability of the pancreas to mount a normal, brisk insulin response to an increasing plasma glucose level is lost in the 2 years before the detection of diabetes, although fasting plasma glucose levels may have been at the upper limit of normal for several years. This was very different from the widely assumed linear rise in fasting plasma glucose level and gradual β-cell decompensation but is consistent with the time course of markers of increased liver fat before the onset of type 2 diabetes observed in other studies (81). Data from the West of Scotland Coronary Prevention Study demonstrated that plasma triacylglycerol and ALT levels were modestly elevated 2 years before the diagnosis of type 2 diabetes and that there was a steady rise in the level of this liver enzyme in the run-up to the time of diagnosis (75).
Jump up ^ Qaseem A, Vijan S, Snow V, Cross JT, Weiss KB, Owens DK; Vijan; Snow; Cross; Weiss; Owens; Clinical Efficacy Assessment Subcommittee of the American College of Physicians (September 2007). "Glycemic control and type 2 diabetes mellitus: the optimal hemoglobin A1c targets. A guidance statement from the American College of Physicians". Annals of Internal Medicine. 147 (6): 417–22. doi:10.7326/0003-4819-147-6-200709180-00012. PMID 17876024. Retrieved 19 July 2008.
Type 2 diabetes is a chronic disease (meaning there isn’t a “cure”) and tends to be progressive. The longer that someone has been living with Type 2 diabetes the less insulin their beta cells may be producing. This doesn’t mean that lifestyle modification is irrelevant–but does mean that individuals should work on accepting their Type 2 diabetes diagnosis so they can focus on managing their diabetes in the best way possible.
They will always have the pre-diabetes diagnosis and have the potential to develop type 2 diabetes if aggressive dietary, exercise and or medication is not followed. It is possible to achieve a normal non-diabetic HbA1c after this – virtually not having any clinical evidence of the pre-diabetes, however the disease process is still there and being held at bay.

the remedies you have mentioned has given me heart ,as i am having half cup of of karela juice....but i have not taken my blood test as i am fed up and my finger tips are also fed i take my dose of insulin and also the juice.;-)...and hope it works. or is working . i do my daily morning and evening walk of half nothing sweet.or starchy 15th july 08

Within the hepatocyte, fatty acids can only be derived from de novo lipogenesis, uptake of nonesterified fatty acid and LDL, or lipolysis of intracellular triacylglycerol. The fatty acid pool may be oxidized for energy or may be combined with glycerol to form mono-, di-, and then triacylglycerols. It is possible that a lower ability to oxidize fat within the hepatocyte could be one of several susceptibility factors for the accumulation of liver fat (45). Excess diacylglycerol has a profound effect on activating protein kinase C epsilon type (PKCε), which inhibits the signaling pathway from the insulin receptor to insulin receptor substrate 1 (IRS-1), the first postreceptor step in intracellular insulin action (46). Thus, under circumstances of chronic energy excess, a raised level of intracellular diacylglycerol specifically prevents normal insulin action, and hepatic glucose production fails to be controlled (Fig. 4). High-fat feeding of rodents brings about raised levels of diacylglycerol, PKCε activation, and insulin resistance. However, if fatty acids are preferentially oxidized rather than esterified to diacylglycerol, then PKCε activation is prevented, and hepatic insulin sensitivity is maintained. The molecular specificity of this mechanism has been confirmed by use of antisense oligonucleotide to PKCε, which prevents hepatic insulin resistance despite raised diacylglycerol levels during high-fat feeding (47). In obese humans, intrahepatic diacylglycerol concentration has been shown to correlate with hepatic insulin sensitivity (48,49). Additionally, the presence of excess fatty acids promotes ceramide synthesis by esterification with sphingosine. Ceramides cause sequestration of Akt2 and activation of gluconeogenic enzymes (Fig. 4), although no relationship with in vivo insulin resistance could be demonstrated in humans (49). However, the described intracellular regulatory roles of diacylglycerol and ceramide are consistent with the in vivo observations of hepatic steatosis and control of hepatic glucose production (20,21).
Formal recommendations on how to reverse type 2 diabetes in clinical practice must await further studies. In the meantime, it will be helpful for all individuals with newly diagnosed type 2 diabetes to know that they have a metabolic syndrome that is reversible. They should know that if it is not reversed, the consequences for future health and cost of life insurance are dire, although these serious adverse effects must be balanced against the difficulties and privations associated with a substantial and sustained change in eating patterns. For many people, this may prove to be too high a price to pay, but for those who are strongly motivated to escape from type 2 diabetes, the new understanding gives clear direction. Physicians need to accept that long-term weight loss is achievable for a worthwhile proportion of patients (96). In the United States, diabetes costs $174 billion annually (97), and in the United Kingdom, it accounts for 10% of National Health Service expenditure. Even if only a small proportion of patients with type 2 diabetes return to normal glucose control, the savings in disease burden and economic cost will be enormous.
An insulin pump is composed of a reservoir similar to that of an insulin cartridge, a battery-operated pump, and a computer chip that allows the user to control the exact amount of insulin being delivered. The pump is attached to a thin plastic tube (an infusion set) that has a cannula (like a needle but soft) at the end through which insulin passes. This cannula is inserted under the skin, usually on the abdomen.. The pump continuously delivers insulin, 24 hours a day. The amount of insulin is programmed and is administered at a constant rate (basal rate). Often, the amount of insulin needed over the course of 24 hours varies, depending on factors like exercise, activity level, and sleep. The insulin pump allows the user to program many different basal rates to allow for variations in lifestyle. The user can also program the pump to deliver additional insulin during meals, covering the excess demands for insulin caused by eating carbohydrates.