Diabetes:M is an award-winning diabetes logbook app that was first published in Google Play in April 2013. It was developed by diabetics to meet the needs of people who want to manage all aspects of their condition. Users can track, analyze, review and export data in great detail. Today Diabetes:M is an established tool with nearly 350 000 installations and over 50 000 active users. The application is well known to medical professionals, with many diabetes specialists recommending it to their patients.
Type 2 diabetes is often treated with oral medication because many people with this type of diabetes make some insulin on their own. The pills people take to control type 2 diabetes do not contain insulin. Instead, medications such as metformin, sulfonylureas, alpha-glucosidase inhibitors and many others are used to make the insulin that the body still produces more effective.
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).
The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.
You are more likely to develop type 2 diabetes if you are age 45 or older, have a family history of diabetes, or are overweight. Physical inactivity, race, and certain health problems such as high blood pressure also affect your chance of developing type 2 diabetes. You are also more likely to develop type 2 diabetes if you have prediabetes or had gestational diabetes when you were pregnant. Learn more about risk factors for type 2 diabetes.
You know that your family medical history, along with what you eat and how much you weigh, can affect your risk of developing type 2 diabetes. But did you know that your sleep habits can also play a role? It’s true. In fact, sleep deprivation is an often overlooked but significant risk factor for type 2 diabetes, a disease that involves too much glucose (or sugar) in the blood and increases the risk of heart disease.
With this technology she is also able to monitor her daughter’s blood sugar levels remotely. Hoover says, “She also has a Dexcom Continuous Glucose Monitor with Share. This monitors her blood sugars through a site that we change weekly (sometimes longer), this updates every 5 minutes and is usually within 20 ml of her actual blood sugar. The CGM communicates her blood sugar numbers to a cell phone through the Share app!”
You can develop type 2 diabetes at any age, even during childhood. However, type 2 diabetes occurs most often in middle-aged and older people. You are more likely to develop type 2 diabetes if you are age 45 or older, have a family history of diabetes, or are overweight or obese. Diabetes is more common in people who are African American, Hispanic/Latino, American Indian, Asian American, or Pacific Islander.
To explain what hemoglobin A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these hemoglobin proteins in these cells, it is known as glycosylated hemoglobin or hemoglobin A1c (HBA1c). Measurement of HBA1c gives us an idea of how much sugar is present in the bloodstream for the preceding three months. In most labs, the normal range is 4%-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is <6.5%). The benefits of measuring A1c is that is gives a more reasonable and stable view of what's happening over the course of time (three months), and the value does not vary as much as finger stick blood sugar measurements. There is a direct correlation between A1c levels and average blood sugar levels as follows.
The authors: David Kerr, MD, is the director of research and innovation at the William Sansum Diabetes Center in Santa Barbara, California, and the creator of ’Appy Feet, an app for people with painful diabetic neuropathy, as well as DiabetesTravel.org and ExCarbs.com—two free resources for people with diabetes. Charis Hoppe is a project coordinator at the William Sansum Diabetes Center for the Santa Barbara 1,000 project. Ceara Axelrod is a data analyst and clinical researcher at the William Sansum Diabetes Center.
Type 2 diabetes is usually associated with being overweight (BMI greater than 25), and is harder to control when food choices are not adjusted, and you get no physical activity. And while it’s true that too much body fat and physical inactivity (being sedentary) does increase the likelihood of developing type 2, even people who are fit and trim can develop this type of diabetes.2,3
Up to 40 percent of people with type 2 diabetes eventually develop kidney failure — the kidney's inability to filter waste and fluid from the blood, according to the National Kidney Foundation. As blood flows through tiny vessels in the kidneys, waste products are filtered out and leave the body through urine. Too much sugar in the blood can stress these filters, making it hard for the kidneys to work effectively. After a while, the filters can break down and leak protein into the urine. If kidney damage continues, you may need dialysis or a kidney transplant.
23andMe can tell you if your genetics are associated with a higher than typical likelihood of developing type 2 diabetes. The 23andMe Type 2 Diabetes Health Predisposition report estimates your chances of developing type 2 diabetes by looking at more than 1,000 places in your DNA. The report also equips you with information and tools to help you take action. You can get the Type 2 Diabetes Health Predisposition report and more with 23andMe's Health + Ancestry Service.
When glucose concentration in the blood remains high over time, the kidneys reach a threshold of reabsorption, and the body excretes glucose in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).
Another emerging issue is the effect on public health of new laboratory based criteria, such as introducing the use of A1c for diagnosis of type 2 diabetes or for recognizing high risk for type 2 diabetes. These changes may impact the number of individuals with undiagnosed diabetes and facilitate the introduction of type 2 diabetes prevention at a public health level.
In this simple app, you can record your blood sugar, meals, insulin, and medications. If there’s a feature in the app you don’t need, you can switch it off to keep the interface as clean as possible. The app syncs across multiple devices and creates clear graphs and reports so you can see the big picture of your data. If simplicity is your goal, this may be the right app for you.
In those with impaired glucose tolerance, diet and exercise either alone or in combination with metformin or acar
Change in fasting plasma glucose (A), 2 h post-oral glucose tolerance test (B), and homeostasis model assessment (HOMA-B) insulin secretion (C) during the 16-year follow-up in the Whitehall II study. Of the 6,538 people studied, diabetes developed in 505. Time 0 was taken as the diagnosis of diabetes or as the end of follow-up for those remaining normoglycemic. Redrawn with permission from Tabák et al. (80).
A random blood sugar of greater than 11.1 mmol/l (200 mg/dl) in association with typical symptoms or a glycated hemoglobin (HbA1c) of ≥ 48 mmol/mol (≥ 6.5 DCCT %) is another method of diagnosing diabetes. In 2009 an International Expert Committee that included representatives of the American Diabetes Association (ADA), the International Diabetes Federation (IDF), and the European Association for the Study of Diabetes (EASD) recommended that a threshold of ≥ 48 mmol/mol (≥ 6.5 DCCT %) should be used to diagnose diabetes. This recommendation was adopted by the American Diabetes Association in 2010. Positive tests should be repeated unless the person presents with typical symptoms and blood sugars >11.1 mmol/l (>200 mg/dl).
The extent of weight loss required to reverse type 2 diabetes is much greater than conventionally advised. A clear distinction must be made between weight loss that improves glucose control but leaves blood glucose levels abnormal and weight loss of sufficient degree to normalize pancreatic function. The Belfast diet study provides an example of moderate weight loss leading to reasonably controlled, yet persistent diabetes. This study showed that a mean weight loss of 11 kg decreased fasting blood glucose levels from 10.4 to 7.0 mmol/L but that this abnormal level presaged the all-too-familiar deterioration of control (87).
The body’s immune system is responsible for fighting off foreign invaders, like harmful viruses and bacteria. In people with type 1 diabetes, the immune system mistakes the body’s own healthy cells for foreign invaders. The immune system attacks and destroys the insulin-producing beta cells in the pancreas. After these beta cells are destroyed, the body is unable to produce insulin.
“We usually see patients quarterly for appointments, which means the other 361 days of the year, they’re on their own,” says endocrinologist Amber Champion, MD, at Great Plains Health in North Platte, Nebraska. “They need to have the knowledge and tools to take care of themselves. Diabetes-related apps can be useful to help keep track of all the data and see it visually. They can also help educate and teach patients to spot trends and keep their data organized.”
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).
Insulin serves as a “key” to open your cells, to allow the glucose to enter -- and allow you to use the glucose for energy. Without insulin, there is no “key.” So, the sugar stays -- and builds up-- in the blood. The result: the body’s cells starve from the lack of glucose. And, if left untreated, the high level of “blood sugar” can damage eyes, kidneys, nerves, and the heart, and can also lead to coma and death.