The big news with the use of fig leaves is that they have anti-diabetic properties. The diabetic needs less insulin when on a treatment of using the fig leaf extract. The diabetic should take the extract with breakfast, first thing in the morning. An additional remedy is to boil the leaves of the fig in some freshly filtered waster and drink this as a tea. Read the whole article on fig leaves and diabetes:
While Type 1 Diabetes is an autoimmune disorder that seems to affect people with certain gene types, Type 2 Diabetes is triggered by lifestyle choices, such as poor diet and obesity. Eating sugary and processed foods contributes to weight gain, and that extra body fat can be released into the bloodstream, impeding the absorption of insulin and other chemicals related to metabolism. When metabolism is slowed, weight gain is more likely, and the cycle repeats itself. Treatment for Type 2 Diabetes is multifaceted, often including insulin injections, a host of medications, and lifestyle modifications such as diet changes and exercise regimens.
The first thing to understand when it comes to treating diabetes is your blood glucose level, which is just what it sounds like — the amount of glucose in the blood. Glucose is a sugar that comes from the foods we eat and also is formed and stored inside the body. It's the main source of energy for the cells of the body, and is carried to them through the blood. Glucose gets into the cells with the help of the hormone insulin.

Imagine that you hide your kitchen garbage under the rug instead throwing it outside in the trash. You can’t see it, so you can pretend your house is clean. When there’s no more room underneath the rug, you throw the garbage into your bedroom, and bathroom, too. Anywhere where you don’t have to see it. Eventually, it begins to smell. Really, really bad.
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).
In addition, a strong partnership between the patient and the primary healthcare provider – general practitioner or internist – is an essential tool in the successful management of diabetes. Often the primary care doctor makes the initial diagnosis of diabetes and provides the basic tools to get the patient started on a management program. Regular appointments with the primary care physician and a certified diabetes educator are some of the best things a patient can do in the early weeks after a diagnosis of diabetes. Upon the diagnosis of diabetes, the primary care physician, specialist, or endocrinologist will conduct a full physical and medical examination. A thorough assessment covers topics such as:

The diabetes looks better, since you can only see the blood sugars. Doctors can congratulate themselves on a illusion of a job well done, even as the patient gets continually sicker. Patients require ever increasing doses of medications and yet still suffer with heart attacks, congestive heart failure, strokes, kidney failure, amputations and blindness. “Oh well” the doctor tells himself, “It’s a chronic, progressive disease”.

Diabetic patients must get professional dental cleanings every six months. In cases when dental surgery is needed, it is necessary to take some special precautions such as adjusting diabetes medication or taking antibiotics to prevent infection. Looking for early signs of gum disease (redness, swelling, bleeding gums) and informing the dentist about them is also helpful in preventing further complications. Quitting smoking is recommended to avoid serious diabetes complications and oral diseases.
Type 2 diabetes is on the rise and is associated with insulin resistance. There are many factors which contribute to developing this disease some of which are modifiable and some of which are nonmodifiable. Modifiable risks which individuals can impact include weight, diet and exercise. It has been reported that gastric bypass patients who have T2DM are “cured” of the disease after surgery. That is a more drastic measure which many people are not ready or willing to consider.
These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.