Injections of insulin may either be added to oral medication or used alone.[24] Most people do not initially need insulin.[13] When it is used, a long-acting formulation is typically added at night, with oral medications being continued.[23][24] Doses are then increased to effect (blood sugar levels being well controlled).[24] When nightly insulin is insufficient, twice daily insulin may achieve better control.[23] The long acting insulins glargine and detemir are equally safe and effective,[100] and do not appear much better than neutral protamine Hagedorn (NPH) insulin, but as they are significantly more expensive, they are not cost effective as of 2010.[101] In those who are pregnant insulin is generally the treatment of choice.[23]
"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used.[38] Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, frequently with ketosis, and sometimes with serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease).[38] These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.[39]

Your doctor may recommend working with a registered dietitian and a personal trainer to help you set up a diabetes weight loss plan. "Diet and exercise is always encouraged as the first line of therapy, but it works better for some people than others," says Sullivan. If you’re obese and having trouble losing weight with diet and exercise alone, your doctor may recommend medications to suppress your appetite and promote weight loss, or even gastric bypass surgery.ause of nontraumatic blindness and kidney failure.[24] It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia.[25] Other complications include acanthosis nigricans, sexual dysfunction, and frequent infections.[23]
Medications used to treat diabetes do so by lowering blood sugar levels. There is broad consensus that when people with diabetes maintain tight glucose control (also called "tight glycemic control") – keeping the glucose levels in their blood within normal ranges – that they experience fewer complications like kidney problems and eye problems.[84][85] There is however debate as to whether this is cost effective for people later in life.[86]
Inhalable insulin has been developed.[125] The original products were withdrawn due to side effects.[125] Afrezza, under development by the pharmaceuticals company MannKind Corporation, was approved by the United States Food and Drug Administration (FDA) for general sale in June 2014.[126] An advantage to inhaled insulin is that it may be more convenient and easy to use.[127]
It is recommended that all people with type 2 diabetes get regular eye examination.[13] There is weak evidence suggesting that treating gum disease by scaling and root planing may result in a small short-term improvement in blood sugar levels for people with diabetes.[81] There is no evidence to suggest that this improvement in blood sugar levels is maintained longer than 4 months.[81] There is also not enough evidence to determine if medications to treat gum disease are effective at lowering blood sugar levels.[81]

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.[110]
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 term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis.[108] The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career.[108] This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).[110]
In type 1 diabetes, the pancreas loses its ability to make insulin because the body's immune system attacks and destroys the cells that produce insulin. No one knows exactly why this happens, but scientists think it has something to do with genes. But just getting the genes for diabetes isn't usually enough. A person probably would then have to be exposed to something else — like a virus — to get type 1 diabetes.
In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood.
Prediabetes is a condition in which blood glucose levels are higher than normal, but a person does not yet have diabetes. Prediabetes and high blood glucose levels are a risk factor for developing diabetes, heart disease, and other health problems. Other warning signs prediabetes may include increased urination, feeling you need to urinate more often, and/or increased thirst.
BlueStar Diabetes is an FDA-approved, Class 2 medical app which provides approved diabetics with 24/7, real-time coaching from a certified diabetes specialist. This comprehensive app is available only by prescription and offers an impressive range of tools tailored to the individual. When registered, users can receive personalized guidance based on their blood glucose, medications, current health, and a review of lifestyle factors.
Type 1 diabetes occurs because the insulin-producing cells of the pancreas (beta cells) are damaged. In type 1 diabetes, the pancreas makes little or no insulin, so sugar cannot get into the body's cells for use as energy. People with type 1 diabetes must use insulin injections to control their blood glucose. Type 1 is the most common form of diabetes in people who are under age 30, but it can occur at any age. Ten percent of people with diabetes are diagnosed with type 1.
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.
Lifestyle factors are important to the development of type 2 diabetes, including obesity and being overweight (defined by a body mass index of greater than 25), lack of physical activity, poor diet, stress, and urbanization.[10][31] Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of cases in Pima Indians and Pacific Islanders.[13] Among those who are not obese, a high waist–hip ratio is often present.[13] Smoking appears to increase the risk of type 2 diabetes mellitus.[32]

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.
Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered.

Rates of type 2 diabetes have increased markedly since 1960 in parallel with obesity.[17] As of 2015 there were approximately 392 million people diagnosed with the disease compared to around 30 million in 1985.[11][18] Typically it begins in middle or older age,[6] although rates of type 2 diabetes are increasing in young people.[19][20] Type 2 diabetes is associated with a ten-year-shorter life expectancy.[10] Diabetes was one of the first diseases described.[21] The importance of insulin in the disease was determined in the 1920s.[22]

Weight loss. Obesity is a leading risk factor for diabetes. Calculate your BMI to see whether you’re at a healthy weight. If you’re overweight or obese, start making small changes to your eating habits and get more physical activity. Even a small amount of weight loss (7%, or about 14 pounds for a 200-pound woman) can delay or even prevent type 2 diabetes.


How long will diabetes stay away after weight loss? Long-term normal blood glucose control in previously diabetic individuals after bariatric surgery demonstrates that diabetes does not recur for up to 10 years, unless substantial weight gain occurs (86). These observations are consistent with the twin cycle hypothesis and the existence of a trigger level for adverse metabolic effects of fat in the pancreas. Hence, for a given individual with type 2 diabetes, reducing the liver and pancreas fat content below his or her personal trigger levels would be expected to result in a release from the fatty acid–mediated dysfunction. Individual tolerance of different degrees of fat exposure vary, and understanding this liposusceptibility will underpin the future understanding of genetically determined risk in any given environment. However, this should not obscure the central point: If a person has type 2 diabetes, there is more fat in the liver and pancreas than he or she can cope with.
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.
Creatinine is a chemical waste molecule that is generated from muscle metabolism. Creatinine is produced from creatine, a molecule of major importance for energy production in muscles. Creatinine has been found to be a fairly reliable indicator of kidney function. As the kidneys become impaired the creatinine level in the blood will rise. Normal levels of creatinine in the blood vary from gender and age of the individual.
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger).[20] Symptoms may develop rapidly (weeks or months) in type 1 DM, while they usually develop much more slowly and may be subtle or absent in type 2 DM. Other symptoms of diabetes mellitus include weight loss and tiredness.[21]
When Dan Hamilton was diagnosed with T1D in 1972, the doctor told him he wouldn’t live past 50. Fast forward 45 years, and Dan is strong and healthy at 59. He credits his health to the advancements in treatment and care over the years. He has been an early adopter of every technology that has come along, and exercises regularly as part of a healthy lifestyle.
^ Sarwar N, Gao P, Seshasai SR, Gobin R, Kaptoge S, Di Angelantonio E, Ingelsson E, Lawlor DA, Selvin E, Stampfer M, Stehouwer CD, Lewington S, Pennells L, Thompson A, Sattar N, White IR, Ray KK, Danesh J (June 2010). "Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies". Lancet. 375 (9733): 2215–22. doi:10.1016/S0140-6736(10)60484-9. PMC 2904878. PMID 20609967.
Diabetes is a serious complex condition which can affect the entire body. Diabetes requires daily self care and if complications develop, diabetes can have a significant impact on quality of life and can reduce life expectancy. While there is currently no cure for diabetes, you can live an enjoyable life by learning about the condition and effectively managing it.
Diabetes affects your body’s ability to process sugar. All food you eat is turned to sugar and used for energy. In Type I diabetes, the body doesn’t make enough insulin, a hormone that carries sugar from your blood to the cells that need it for energy. In Type II diabetes, the body stops responding to insulin. Both cases result in high blood sugar levels, which can cause problems with your eyes, nerves, kidneys, heart and other parts of your body.
Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance.[13] Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue.[45] In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood.[10] The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion.[13]
The role of physical activity must be considered. Increased levels of daily activity bring about decreases in liver fat stores (43), and a single bout of exercise substantially decreases both de novo lipogenesis (39) and plasma VLDL (92). Several studies demonstrated that calorie control combined with exercise is much more successful than calorie restriction alone (93). However, exercise programs alone produce no weight loss for overweight middle-aged people (94). The necessary initial major loss of body weight demands a substantial reduction in energy intake. After weight loss, steady weight is most effectively achieved by a combination of dietary restriction and physical activity. Both aerobic and resistance exercise are effective (95). The critical factor is sustainability.
This is a special edition of the iCookbook app just for people with diabetes. The app delivers new, free diabetes-friendly recipes every month. It also has built-in kitchen tools like conversion charts and timers and voice activation, so the user can proceed through a recipe even with messy hands. The user can save and share recipes or even pull up a random one by shaking the phone.
A second oral agent of another class or insulin may be added if metformin is not sufficient after three months.[78] Other classes of medications include: sulfonylureas, thiazolidinediones, dipeptidyl peptidase-4 inhibitors, SGLT2 inhibitors, and glucagon-like peptide-1 analogs.[78] As of 2015 there was no significant difference between these agents.[78] A 2018 review found that SGLT2 inhibitors may be better than glucagon-like peptide-1 analogs or dipeptidyl peptidase-4 inhibitors.[94]
^ Cheng J, Zhang W, Zhang X, Han F, Li X, He X, Li Q, Chen J (May 2014). "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis". JAMA Internal Medicine. 174 (5): 773–85. doi:10.1001/jamainternmed.2014.348. PMID 24687000.
Home blood sugar (glucose) testing is an important part of controlling blood sugar. One important goal of diabetes treatment is to keep the blood glucose levels near the normal range of 70 to 120 mg/dl before meals and under 140 mg/dl at two hours after eating. Blood glucose levels are usually tested before and after meals, and at bedtime. The blood sugar level is typically determined by pricking a fingertip with a lancing device and applying the blood to a glucose meter, which reads the value. There are many meters on the market, for example, Accu-Check Advantage, One Touch Ultra, Sure Step and Freestyle. Each meter has its own advantages and disadvantages (some use less blood, some have a larger digital readout, some take a shorter time to give you results, etc.). The test results are then used to help patients make adjustments in medications, diets, and physical activities.
The WHO estimates that diabetes mellitus resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death.[12][101] However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes.[101][104] For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide,[8] using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.[8]
The major eye complication of diabetes is called diabetic retinopathy. Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina. Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms), and new but brittle blood vessels (neovascularization). Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision.
Metformin is generally recommended as a first line treatment for type 2 diabetes, as there is good evidence that it decreases mortality.[6] It works by decreasing the liver's production of glucose.[87] Several other groups of drugs, mostly given by mouth, may also decrease blood sugar in type II DM. These include agents that increase insulin release, agents that decrease absorption of sugar from the intestines, and agents that make the body more sensitive to insulin.[87] When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.[6] Doses of insulin are then increased to effect.[6][88]
Several vision complications can result from type 2 diabetes, from glaucoma to cataracts to the most common, diabetic retinopathy. Over time, high blood sugar levels can damage the blood vessels in the eyes, Sullivan says. If left untreated, diabetic retinopathy can cause severe vision loss and even blindness. Nearly half of everyone diagnosed with diabetes has some degree of diabetic retinopathy, according to the National Eye Institute.
Health2Sync helps you log your blood sugar, blood pressure, weight, medication, diet, exercise, and even your mood through the app.  Health2Sync provides you helpful feedback based on your blood sugar records to help you manage diabetes.  View current and past trends in your health.  The app provides a diabetes support community.  Invite your friends and family members to join you on your journey. Premium Features of the app include a PDF report feature.
In type 1 diabetes, the pancreas loses its ability to make insulin because the body's immune system attacks and destroys the cells that produce insulin. No one knows exactly why this happens, but scientists think it has something to do with genes. But just getting the genes for diabetes isn't usually enough. A person probably would then have to be exposed to something else — like a virus — to get type 1 diabetes.
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature.[citation needed]
For our bodies to work properly we need to convert glucose (sugar) from food into energy. A hormone called insulin is essential for the conversion of glucose into energy. In people with diabetes, insulin is no longer produced or not produced in sufficient amounts by the body. When people with diabetes eat glucose, which is in foods such as breads, cereals, fruit and starchy vegetables, legumes, milk, yoghurt and sweets, it can’t be converted into energy.
Diabetes Companion is one of two apps on the list by mySugr, an Austrian company that raised money earlier this year. The company adds a little bit of gamification to the traditional diabetes management app. "The Companion is a charming, sometimes outspoken diabetes manager that focuses on making your diabetes data useful in everyday life," the app store description says. "Adding elements of fun, gamification, and immediate feedback (with attitude!) through a diabetes monster to help keep you motivated and involved in your therapy." The app works with Sanofi-Aventis' iPhone-connected IGBStar meter and is a registered class I medical device. 
Reversal of type 2 diabetes to normal metabolic control by either bariatric surgery or hypocaloric diet allows for the time sequence of underlying pathophysiologic mechanisms to be observed. In reverse order, the same mechanisms are likely to determine the events leading to the onset of hyperglycemia and permit insight into the etiology of type 2 diabetes. Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content. The difference in time course of these two processes is striking. Recent information on the intracellular effects of excess lipid intermediaries explains the likely biochemical basis, which simplifies both the basic understanding of the condition and the concepts used to determine appropriate management. Recent large, long-duration population studies on time course of plasma glucose and insulin secretion before the diagnosis of diabetes are consistent with this new understanding. Type 2 diabetes has long been regarded as inevitably progressive, requiring increasing numbers of oral hypoglycemic agents and eventually insulin, but it is now certain that the disease process can be halted with restoration of normal carbohydrate and fat metabolism. Type 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat.
^ Imperatore G, Boyle JP, Thompson TJ, Case D, Dabelea D, Hamman RF, Lawrence JM, Liese AD, Liu LL, Mayer-Davis EJ, Rodriguez BL, Standiford D (December 2012). "Projections of type 1 and type 2 diabetes burden in the U.S. population aged <20 years through 2050: dynamic modeling of incidence, mortality, and population growth". Diabetes Care. 35 (12): 2515–20. doi:10.2337/dc12-0669. PMC 3507562. PMID 23173134. Archived from the original on 2016-08-14.
Diabetes mellitus is classified into four broad categories: type 1, type 2, gestational diabetes, and "other specific types".[10] The "other specific types" are a collection of a few dozen individual causes.[10] Diabetes is a more variable disease than once thought and people may have combinations of forms.[36] The term "diabetes", without qualification, usually refers to diabetes mellitus.

Type 2 diabetes, the most common type of diabetes, is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes mainly from the food you eat. Insulin, a hormone made by the pancreas, helps glucose get into your cells to be used for energy. In type 2 diabetes, your body doesn’t make enough insulin or doesn’t use insulin well. Too much glucose then stays in your blood, and not enough reaches your cells.


This app, named one of the top diabetes apps by Healthline from 2015 to 2017, offers two options: basic and pro. The basic app function is designed to help manage blood glucose patterns for individuals with Type 1 and Type 2 diabetes. There is a section to enter data regarding diet, medications, and blood glucose levels. The upgraded pro version provides features like blood glucose reminders, multi-device syncing, basal rates for pump usersm and priority support. MySugr coaching is one of the newest features by which users can receive personalized advice from certified diabetes educators.


In type 1 diabetes, the pancreas loses its ability to make insulin because the body's immune system attacks and destroys the cells that produce insulin. No one knows exactly why this happens, but scientists think it has something to do with genes. But just getting the genes for diabetes isn't usually enough. A person probably would then have to be exposed to something else — like a virus — to get type 1 diabetes.
Diabetic ketoacidosis can be caused by infections, stress, or trauma, all of which may increase insulin requirements. In addition, missing doses of insulin is also an obvious risk factor for developing diabetic ketoacidosis. Urgent treatment of diabetic ketoacidosis involves the intravenous administration of fluid, electrolytes, and insulin, usually in a hospital intensive care unit. Dehydration can be very severe, and it is not unusual to need to replace 6-7 liters of fluid when a person presents in diabetic ketoacidosis. Antibiotics are given for infections. With treatment, abnormal blood sugar levels, ketone production, acidosis, and dehydration can be reversed rapidly, and patients can recover remarkably well.
Yes. Once you get a new kidney, you may need a higher dose of insulin. Your appetite will improve so your new kidney will break down insulin better than your injured one. You will use steroids to keep your body from rejecting your new kidney. If your new kidney fails, dialysis treatment can be started while you wait for another kidney. To learn more about kidney transplant click here.
Your doctor will test your blood sugar every 3 months with an A1C test. Also, you can test your blood sugar on your own throughout the day. You will need to use a blood glucose monitor to check it on your own. This involves pricking your finger for blood and putting a test strip in the blood to get the results. If your blood sugar gets too low, you might feel tired, experience problems with muscle coordination, sweat, have difficulty thinking or speaking clearly, twitch, feel like you’re going to faint, become pale, lose consciousness, or have a seizure. At the earliest sign of any of these symptoms, eat or drink something that will raise your blood sugar fast. This could include candy, juice, milk, or raisins. If you don’t feel better in 15 minutes or if monitoring shows that your blood sugar level is still too low, eat or drink another item to raise your blood sugar fast. Always keep a supply of these items on hand for emergencies.
The GoMeals “Today’s Plate” feature helps monitor each day’s calorie intake, as well as the distribution of carbohydrates, fats and proteins. These three nutrient categories are also represented in a pie chart on the touch screen. A restaurant locator feature helps users locate restaurants based on their current location and the type of cuisine they prefer, as well.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
^ Jump up to: a b Picot J, Jones J, Colquitt JL, Gospodarevskaya E, Loveman E, Baxter L, Clegg AJ (September 2009). "The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation". Health Technology Assessment. 13 (41): 1–190, 215–357, iii–iv. doi:10.3310/hta13410. PMID 19726018.
Diabetes Educational Services (DES) has established this website to provide information and education to health care professionals. Nothing in this website constitutes medical advice nor is it a substitute for medical advice. References in this website to any and all specific products, services or processes do not constitute or imply an endorsement or recommendation by Diabetes Educational Services.
^ Jump up to: a b c d Inzucchi SE, Bergenstal RM, Buse JB, Diamant M, Ferrannini E, Nauck M, Peters AL, Tsapas A, Wender R, Matthews DR (March 2015). "Management of hyperglycaemia in type 2 diabetes, 2015: a patient-centred approach. Update to a position statement of the American Diabetes Association and the European Association for the Study of Diabetes". Diabetologia. 58 (3): 429–42. doi:10.1007/s00125-014-3460-0. PMID 25583541.
With gestational diabetes, risks to the unborn baby are even greater than risks to the mother. Risks to the baby include abnormal weight gain before birth, breathing problems at birth, and higher obesity and diabetes risk later in life. Risks to the mother include needing a cesarean section due to an overly large baby, as well as damage to heart, kidney, nerves, and eye.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).

The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
^ Imperatore G, Boyle JP, Thompson TJ, Case D, Dabelea D, Hamman RF, Lawrence JM, Liese AD, Liu LL, Mayer-Davis EJ, Rodriguez BL, Standiford D (December 2012). "Projections of type 1 and type 2 diabetes burden in the U.S. population aged <20 years through 2050: dynamic modeling of incidence, mortality, and population growth". Diabetes Care. 35 (12): 2515–20. doi:10.2337/dc12-0669. PMC 3507562. PMID 23173134. Archived from the original on 2016-08-14.
Type 2 diabetes, the most common type of diabetes, is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes mainly from the food you eat. Insulin, a hormone made by the pancreas, helps glucose get into your cells to be used for energy. In type 2 diabetes, your body doesn’t make enough insulin or doesn’t use insulin well. Too much glucose then stays in your blood, and not enough reaches your cells.
But for most people with Type 2 diabetes not on insulin, testing is inappropriate most of the time. That message is not getting through. At the end of last year, another study was published in JAMA Internal Medicine that quantified the prevalence of glucose testing in adults. Researchers examined a database that contained data on more than 370,000 commercial health insurance and Medicare Advantage beneficiaries who had Type 2 diabetes.
Also, know that while apps can be incredibly valuable tools, they can’t — and shouldn’t try to — replace individualized medical advice. “It’s still not a person. It’s still not the team,” says Ilkowitz. She advises walking through your apps with your certified diabetes educator to be sure they are appropriate tools for you and that you’re using them correctly.

^ Jump up to: a b Cheng J, Zhang W, Zhang X, Han F, Li X, He X, Li Q, Chen J (May 2014). "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis". JAMA Internal Medicine. 174 (5): 773–85. doi:10.1001/jamainternmed.2014.348. PMID 24687000.
Type 2 diabetes: Type 2 diabetes affects the way the body uses insulin. While the body still makes insulin, unlike in type I, the cells in the body do not respond to it as effectively as they once did. This is the most common type of diabetes, according to the National Institute of Diabetes and Digestive and Kidney Diseases, and it has strong links with obesity.
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