Glucose Wiz keeps your blood sugar and medication logs with time.  Write notes, and see your numbers in chart view to show glucose tendency for before meals, 2 hours after meals and at bedtime.  Export the readings in PDF, CSV, or HTML f0rmat by email to anyone, and print the logs directly from this app. iCloud auto sync is available and you can track and monitor your family members’ readings.

People who are obese -- more than 20% over their ideal body weight for their height -- are at particularly high risk of developing type 2 diabetes and its related medical problems. Obese people have insulin resistance. With insulin resistance, the pancreas has to work overly hard to produce more insulin. But even then, there is not enough insulin to keep sugars normal.

You can manually enter your blood glucose values in the app or buy their special cable to upload your glucometer readings to the app. For every glucose entry, add notes about medications, mood, exercise, and meals (you can even add a photo of your meal for a quick record), and then track your trends over the course of the day and long term. This app also has features for tracking blood pressure, weight, and A1C.

Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors,[40] such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.[40][41] Among dietary factors, data suggest that gliadin (a protein present in gluten) may play a role in the development of type 1 diabetes, but the mechanism is not fully understood.[42][43]
Still, these choices are just the beginning, and there are lots of other options to explore. We’ve listed our top picks for several types of apps, focusing on those that have numerous and consistent good reviews from users and have been updated recently. Many offer similar features, so you may want to download a few and see which is easiest for you to use.

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).
As your kidneys fail, your blood urea nitrogen (BUN) levels will rise as well as the level of creatinine in your blood. You may also experience nausea, vomiting, a loss of appetite, weakness, increasing fatigue, itching, muscle cramps (especially in your legs) and anemia (a low blood count). You may find you need less insulin. This is because diseased kidneys cause less breakdown of insulin. If you develop any of these signs, call your doctor.
Some kids and teens are already using devices that make blood glucose testing and insulin injections easier, less painful, and more effective. One of these is the insulin pump, a mechanical device that can deliver insulin more like the pancreas does. There's also been progress toward the development of a wearable or implantable "artificial pancreas." This consists of an insulin pump linked to a device that measures the person's blood glucose level continuously.
Research has shown that there are some ways of preventing type 2 diabetes, or at least delaying its onset. Lifestyle changes such as becoming more active (or staying active, if you already engage in regular physical activity) and making sure your weight stays in a healthy range are two ways to help ward off type 2 diabetes, but talk to your doctor about what else you can do to prevent or manage the disease.
Fuchsberger C, Flannick J, Teslovich TM, Mahajan A, Agarwala V, Gaulton KJ, Ma C, Fontanillas P, Moutsianas L, McCarthy DJ, Rivas MA, Perry JRB, Sim X, Blackwell TW, Robertson NR, Rayner NW, Cingolani P, Locke AE, Tajes JF, Highland HM, Dupuis J, Chines PS, Lindgren CM, Hartl C, Jackson AU, Chen H, Huyghe JR, van de Bunt M, Pearson RD, Kumar A, Müller-Nurasyid M, Grarup N, Stringham HM, Gamazon ER, Lee J, Chen Y, Scott RA, Below JE, Chen P, Huang J, Go MJ, Stitzel ML, Pasko D, Parker SCJ, Varga TV, Green T, Beer NL, Day-Williams AG, Ferreira T, Fingerlin T, Horikoshi M, Hu C, Huh I, Ikram MK, Kim BJ, Kim Y, Kim YJ, Kwon MS, Lee J, Lee S, Lin KH, Maxwell TJ, Nagai Y, Wang X, Welch RP, Yoon J, Zhang W, Barzilai N, Voight BF, Han BG, Jenkinson CP, Kuulasmaa T, Kuusisto J, Manning A, Ng MCY, Palmer ND, Balkau B, Stančáková A, Abboud HE, Boeing H, Giedraitis V, Prabhakaran D, Gottesman O, Scott J, Carey J, Kwan P, Grant G, Smith JD, Neale BM, Purcell S, Butterworth AS, Howson JMM, Lee HM, Lu Y, Kwak SH, Zhao W, Danesh J, Lam VKL, Park KS, Saleheen D, So WY, Tam CHT, Afzal U, Aguilar D, Arya R, Aung T, Chan E, Navarro C, Cheng CY, Palli D, Correa A, Curran JE, Rybin D, Farook VS, Fowler SP, Freedman BI, Griswold M, Hale DE, Hicks PJ, Khor CC, Kumar S, Lehne B, Thuillier D, Lim WY, Liu J, van der Schouw YT, Loh M, Musani SK, Puppala S, Scott WR, Yengo L, Tan ST, Taylor HA Jr, Thameem F, Wilson G Sr, Wong TY, Njølstad PR, Levy JC, Mangino M, Bonnycastle LL, Schwarzmayr T, Fadista J, Surdulescu GL, Herder C, Groves CJ, Wieland T, Bork-Jensen J, Brandslund I, Christensen C, Koistinen HA, Doney ASF, Kinnunen L, Esko T, Farmer AJ, Hakaste L, Hodgkiss D, Kravic J, Lyssenko V, Hollensted M, Jørgensen ME, Jørgensen T, Ladenvall C, Justesen JM, Käräjämäki A, Kriebel J, Rathmann W, Lannfelt L, Lauritzen T, Narisu N, Linneberg A, Melander O, Milani L, Neville M, Orho-Melander M, Qi L, Qi Q, Roden M, Rolandsson O, Swift A, Rosengren AH, Stirrups K, Wood AR, Mihailov E, Blancher C, Carneiro MO, Maguire J, Poplin R, Shakir K, Fennell T, DePristo M, de Angelis MH, Deloukas P, Gjesing AP, Jun G, Nilsson P, Murphy J, Onofrio R, Thorand B, Hansen T, Meisinger C, Hu FB, Isomaa B, Karpe F, Liang L, Peters A, Huth C, O'Rahilly SP, Palmer CNA, Pedersen O, Rauramaa R, Tuomilehto J, Salomaa V, Watanabe RM, Syvänen AC, Bergman RN, Bharadwaj D, Bottinger EP, Cho YS, Chandak GR, Chan JCN, Chia KS, Daly MJ, Ebrahim SB, Langenberg C, Elliott P, Jablonski KA, Lehman DM, Jia W, Ma RCW, Pollin TI, Sandhu M, Tandon N, Froguel P, Barroso I, Teo YY, Zeggini E, Loos RJF, Small KS, Ried JS, DeFronzo RA, Grallert H, Glaser B, Metspalu A, Wareham NJ, Walker M, Banks E, Gieger C, Ingelsson E, Im HK, Illig T, Franks PW, Buck G, Trakalo J, Buck D, Prokopenko I, Mägi R, Lind L, Farjoun Y, Owen KR, Gloyn AL, Strauch K, Tuomi T, Kooner JS, Lee JY, Park T, Donnelly P, Morris AD, Hattersley AT, Bowden DW, Collins FS, Atzmon G, Chambers JC, Spector TD, Laakso M, Strom TM, Bell GI, Blangero J, Duggirala R, Tai ES, McVean G, Hanis CL, Wilson JG, Seielstad M, Frayling TM, Meigs JB, Cox NJ, Sladek R, Lander ES, Gabriel S, Burtt NP, Mohlke KL, Meitinger T, Groop L, Abecasis G, Florez JC, Scott LJ, Morris AP, Kang HM, Boehnke M, Altshuler D, McCarthy MI. The genetic architecture of type 2 diabetes. Nature. 2016 Aug 4;536(7614):41-47. doi: 10.1038/nature18642. Epub 2016 Jul 11.
With a health care system as complicated as ours, it’s hard to take money from one pot and shift it easily to another. Efficiency in each system is crucial. The fact that a necessary facet of diabetes care is increasingly out of reach — while unnecessary and potentially harmful care is easily overused — illustrates how much work still needs to be done.
Maybe. You should be tested for diabetes if you are between 40 and 70 years old and are overweight or obese. Your doctor may recommend testing earlier than age 40 if you also have other risk factors for diabetes. Also, talk to your doctor about diabetes testing if you have signs or symptoms of diabetes. Your doctor will use a blood test to see if you have diabetes.
Most cases of diabetes involve many genes, with each being a small contributor to an increased probability of becoming a type 2 diabetic.[10] If one identical twin has diabetes, the chance of the other developing diabetes within his lifetime is greater than 90%, while the rate for nonidentical siblings is 25–50%.[13] As of 2011, more than 36 genes had been found that contribute to the risk of type 2 diabetes.[38] All of these genes together still only account for 10% of the total heritable component of the disease.[38] The TCF7L2 allele, for example, increases the risk of developing diabetes by 1.5 times and is the greatest risk of the common genetic variants.[13] Most of the genes linked to diabetes are involved in beta cell functions.[13]
These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease, such as those involving the eyes, kidneys and nerves (microvascular disease), and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply (claudication).
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
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.

A great app to add to the list is Wellocity Health. It helps you manage chronic conditions such as heart disease and diabetes by addressing key risk factors. This free app allows users to track medications, vitals and activity and share reports of your progress with your doctor or coach. Actionable insights and realistic goals make it easy to monitor progress and improve. The app also has a built-in community that allow users to share experiences.

Heart disease and stroke. People who have diabetes are at greater risk for heart disease and stroke. The risk is even greater for people who have diabetes and smoke, have high blood pressure, have a family history of heart disease, or are overweight. Heart disease is easiest to treat when it is caught early. It is very important to see your doctor on a regular basis. He or she can test for early signs of heart disease. This includes checking cholesterol levels. If your cholesterol is higher than the recommended level, your doctor will talk to you about lifestyle changes and medicine to help get your cholesterol under control.

For people with Type 1 diabetes, blood glucose monitoring and insulin administration is the standard of care. Patients need to check their blood sugar a number of times a day, then give themselves insulin to replace what would have been made in the pancreas. Treatment for Type 2 diabetes, however, doesn’t involve these critical calculations of insulin. It’s usually maintained with a pretty regular administration of the same drugs on a set schedule.
What medication is available for diabetes? Diabetes causes blood sugar levels to rise. The body may stop producing insulin, the hormone that regulates blood sugar, and this results in type 1 diabetes. In people with type 2 diabetes, insulin is not working effectively. Learn about the range of treatments for each type and recent medical developments here. Read now