Many manufacturers offer pen delivery systems. Such systems resemble the ink cartridge in a fountain pen. A small, pen-sized device holds an insulin cartridge (usually containing 300 units). Cartridges are available for the most widely used insulin formulations. The amount of insulin to be injected is dialed in, by turning the bottom of the pen until the required number of units is seen in the dose-viewing window. The tip of the pen consists of a needle that is replaced with each injection. A release mechanism allows the needle to penetrate just under the skin and deliver the required amount of insulin.
Evidence linking hepatic insulin sensitivity to intraorgan triglyceride content has been steadily accumulating. In insulin-treated type 2 diabetes, insulin dose correlates with the extent of fatty liver (35), and in turn, this is associated with insulin sensitivity to suppression of hepatic glucose production (36). Decreasing the fat content of liver is associated with improvement in insulin suppression of glucose production and, thereby, with improvement in fasting plasma glucose (20,23).
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
The aptly named bitter melon is thought to help cells use glucose more effectively and block sugar absorption in the intestine. When Philippine researchers had men and women take bitter melon in capsule form for three months, they had slight, but consistently, lower blood sugar than those taking a placebo. Gastrointestinal problems are possible side effects. You can reverse diabetes with these science-backed strategies.
Diabetes can be very complicated, and the physician needs to have as much information as possible to help the patient establish an effective management plan. Physicians may often experience data overload resulting from hundreds of blood-glucose readings, insulin dosages and other health factors occurring between regular office visits which must be deciphered during a relatively brief visit with the patient to determine patterns and establish or modify a treatment plan.[5]
Jambul fruit is an effective anti-diabetes agent considering its effect on the pancreas. The fruit, its seed, and juice, all are helpful in treatment of diabetes. Jambul fruit seeds contain a glucoside compound called "jamboline", which, supposedly, has the power to check the pathological conversion of starch into sugar in cases of increased production of glucose. Regular intake of jambul fruit can trigger pancreas to release insulin. Also, it can bring down blood sugar levels considerably. Therefore, jambul is an excellent anti-diabetes agent. It is one of the best home remedies for diabetes.
Mechanism of interaction between excess amounts of fatty acids, diacylglycerol, and ceramide and insulin action within the hepatocyte. Diacylglycerol activates PKCε and inhibits activation of IRS-1 by the insulin receptor. Ceramides cause sequestration of Akt2 by PKCζ and inhibit insulin control of gluconeogenesis. These mechanisms have recently been reviewed (99). FFA, free-fatty acid; TG, triacylglycerol.
Peripheral artery disease (PAD), which commonly affects the legs, is the hardening and narrowing of the arteries that can result from a build-up of plaque or fatty deposits in blood vessels outside the heart or brain. Because diabetics sometimes have reduced feeling in their feet and legs, they often do not feel symptoms of PAD and it goes undiagnosed and untreated. The Diabetes Treatment Center at Desert Springs Hospital take a proactive approach to PAD and provides free Ankle Brachial Index screenings for patients.
Even if you don’t have any underlying glucose issues, testing your blood sugar occasionally will help you pin point which carbohydrates you tolerate well and which you don’t. It can help you have a better understanding of your body’s reaction to foods and take control of your health. It is also an accurate alternative to the pregnancy test for gestational diabetes, so talk to your doctor if you’d prefer to test yourself, though you may have to explain your reasons!
Your care team may recommend that you use a continuous glucose monitor (CGM). A CGM is a wearable device that can measure blood sugar every few minutes around the clock. It's measured by a thread-like sensor inserted under the skin and secured in place. The more frequent CGM blood sugar readings can help you and the care team do an even better job of troubleshooting and adjusting your insulin doses and diabetes management plan to improve blood sugar control.
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”.

Big pharma are in the early stages of developing their own cell therapy approaches for diabetes. Novo Nordisk, one of the largest providers of diabetes treatments, is bidding for stem cells and an encapsulation device, stating that the first clinical trial could take place in the “next few years.” Sanofi, also a big name in diabetes, is working with the German Evotec in a beta cell replacement therapy for diabetics.

Although a close relationship exists among raised liver fat levels, insulin resistance, and raised liver enzyme levels (52), high levels of liver fat are not inevitably associated with hepatic insulin resistance. This is analogous to the discordance observed in the muscle of trained athletes in whom raised intramyocellular triacylglycerol is associated with high insulin sensitivity (53). This relationship is also seen in muscle of mice overexpressing the enzyme DGAT-1, which rapidly esterifies diacylglycerol to metabolically inert triacylglycerol (54). In both circumstances, raised intracellular triacylglycerol stores coexist with normal insulin sensitivity. When a variant of PNPLA3 was described as determining increased hepatic fat levels, it appeared that a major factor underlying nonalcoholic fatty liver disease and insulin resistance was identified (55). However, this relatively rare genetic variant is not associated with hepatic insulin resistance (56). Because the responsible G allele of PNPLA3 is believed to code for a lipase that is ineffective in triacylglycerol hydrolysis, it appears that diacylglycerol and fatty acids are sequestered as inert triacylglycerol, preventing any inhibitory effect on insulin signaling.


These three are the axis of evil in the nutrition world. They are all new introductions to the human diet, especially in the forms they are most eaten in (processed flour, table sugar and High Fructose Corn Syrup and vegetable oils).As we already know, grains (especially in a highly processed form) not only raise insulin levels but can damage the lining of the gut, even in those with no official celiac disease. Grains also cause inflammation in the body and can initiate an immune response.

Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
×