Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses, a lack of insulin may also develop.[11] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is a combination of excessive body weight and insufficient exercise.[2]

Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels that result from defects in insulin secretion, or its action, or both. Diabetes mellitus, commonly referred to as diabetes (as it will be in this article) was first identified as a disease associated with "sweet urine," and excessive muscle loss in the ancient world. Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine, hence the term sweet urine.
Diabetes mellitus is a disease in which a person's blood sugar (blood glucose) is either too high (hyperglycemia) or too low (hypoglycemia) due to problems with insulin regulation in the body. There are two main types of diabetes mellitus, type 1 and type 2. Type 1 diabetes usually occurs during childhood, while type 2 diabetes usually occurs during adulthood, however, rates of both types of diabetes in children, adolescents, and teens is increasing. More men than women have diabetes in the US, and the disease can affect men differently than women.
Type 2 diabetes, which is more common, usually occurs in people over 40 and is called adult onset diabetes mellitus. It is also called non insulin-dependent diabetes mellitus. In Type 2, your pancreas makes insulin, but your body does not use it properly. The high blood sugar level often can be controlled by following a diet and/or taking medication, although some patients must take insulin. Type 2 diabetes is particularly prevalent among African Americans, American Indians, Latin Americans and Asian Americans.

That’s a feature that Kelli Rush, 41, a homemaker in Fallon, Nevada, appreciates. She was diagnosed with type 2 diabetes in late 2017, and she’s since made huge strides in improving her A1C. She likes to see the estimated number in the app, and she says it closely matched the lab value when she had the blood test. “It’s nice to know that I’m making progress,” she says.

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.
DIAbetes Genetics Replication And Meta-analysis (DIAGRAM) Consortium; Asian Genetic Epidemiology Network Type 2 Diabetes (AGEN-T2D) Consortium; South Asian Type 2 Diabetes (SAT2D) Consortium; Mexican American Type 2 Diabetes (MAT2D) Consortium; Type 2 Diabetes Genetic Exploration by Nex-generation sequencing in muylti-Ethnic Samples (T2D-GENES) Consortium, Mahajan A, Go MJ, Zhang W, Below JE, Gaulton KJ, Ferreira T, Horikoshi M, Johnson AD, Ng MC, Prokopenko I, Saleheen D, Wang X, Zeggini E, Abecasis GR, Adair LS, Almgren P, Atalay M, Aung T, Baldassarre D, Balkau B, Bao Y, Barnett AH, Barroso I, Basit A, Been LF, Beilby J, Bell GI, Benediktsson R, Bergman RN, Boehm BO, Boerwinkle E, Bonnycastle LL, Burtt N, Cai Q, Campbell H, Carey J, Cauchi S, Caulfield M, Chan JC, Chang LC, Chang TJ, Chang YC, Charpentier G, Chen CH, Chen H, Chen YT, Chia KS, Chidambaram M, Chines PS, Cho NH, Cho YM, Chuang LM, Collins FS, Cornelis MC, Couper DJ, Crenshaw AT, van Dam RM, Danesh J, Das D, de Faire U, Dedoussis G, Deloukas P, Dimas AS, Dina C, Doney AS, Donnelly PJ, Dorkhan M, van Duijn C, Dupuis J, Edkins S, Elliott P, Emilsson V, Erbel R, Eriksson JG, Escobedo J, Esko T, Eury E, Florez JC, Fontanillas P, Forouhi NG, Forsen T, Fox C, Fraser RM, Frayling TM, Froguel P, Frossard P, Gao Y, Gertow K, Gieger C, Gigante B, Grallert H, Grant GB, Grrop LC, Groves CJ, Grundberg E, Guiducci C, Hamsten A, Han BG, Hara K, Hassanali N, Hattersley AT, Hayward C, Hedman AK, Herder C, Hofman A, Holmen OL, Hovingh K, Hreidarsson AB, Hu C, Hu FB, Hui J, Humphries SE, Hunt SE, Hunter DJ, Hveem K, Hydrie ZI, Ikegami H, Illig T, Ingelsson E, Islam M, Isomaa B, Jackson AU, Jafar T, James A, Jia W, Jöckel KH, Jonsson A, Jowett JB, Kadowaki T, Kang HM, Kanoni S, Kao WH, Kathiresan S, Kato N, Katulanda P, Keinanen-Kiukaanniemi KM, Kelly AM, Khan H, Khaw KT, Khor CC, Kim HL, Kim S, Kim YJ, Kinnunen L, Klopp N, Kong A, Korpi-Hyövälti E, Kowlessur S, Kraft P, Kravic J, Kristensen MM, Krithika S, Kumar A, Kumate J, Kuusisto J, Kwak SH, Laakso M, Lagou V, Lakka TA, Langenberg C, Langford C, Lawrence R, Leander K, Lee JM, Lee NR, Li M, Li X, Li Y, Liang J, Liju S, Lim WY, Lind L, Lindgren CM, Lindholm E, Liu CT, Liu JJ, Lobbens S, Long J, Loos RJ, Lu W, Luan J, Lyssenko V, Ma RC, Maeda S, Mägi R, Männisto S, Matthews DR, Meigs JB, Melander O, Metspalu A, Meyer J, Mirza G, Mihailov E, Moebus S, Mohan V, Mohlke KL, Morris AD, Mühleisen TW, Müller-Nurasyid M, Musk B, Nakamura J, Nakashima E, Navarro P, Ng PK, Nica AC, Nilsson PM, Njølstad I, Nöthen MM, Ohnaka K, Ong TH, Owen KR, Palmer CN, Pankow JS, Park KS, Parkin M, Pechlivanis S, Pedersen NL, Peltonen L, Perry JR, Peters A, Pinidiyapathirage JM, Platou CG, Potter S, Price JF, Qi L, Radha V, Rallidis L, Rasheed A, Rathman W, Rauramaa R, Raychaudhuri S, Rayner NW, Rees SD, Rehnberg E, Ripatti S, Robertson N, Roden M, Rossin EJ, Rudan I, Rybin D, Saaristo TE, Salomaa V, Saltevo J, Samuel M, Sanghera DK, Saramies J, Scott J, Scott LJ, Scott RA, Segrè AV, Sehmi J, Sennblad B, Shah N, Shah S, Shera AS, Shu XO, Shuldiner AR, Sigurđsson G, Sijbrands E, Silveira A, Sim X, Sivapalaratnam S, Small KS, So WY, Stančáková A, Stefansson K, Steinbach G, Steinthorsdottir V, Stirrups K, Strawbridge RJ, Stringham HM, Sun Q, Suo C, Syvänen AC, Takayanagi R, Takeuchi F, Tay WT, Teslovich TM, Thorand B, Thorleifsson G, Thorsteinsdottir U, Tikkanen E, Trakalo J, Tremoli E, Trip MD, Tsai FJ, Tuomi T, Tuomilehto J, Uitterlinden AG, Valladares-Salgado A, Vedantam S, Veglia F, Voight BF, Wang C, Wareham NJ, Wennauer R, Wickremasinghe AR, Wilsgaard T, Wilson JF, Wiltshire S, Winckler W, Wong TY, Wood AR, Wu JY, Wu Y, Yamamoto K, Yamauchi T, Yang M, Yengo L, Yokota M, Young R, Zabaneh D, Zhang F, Zhang R, Zheng W, Zimmet PZ, Altshuler D, Bowden DW, Cho YS, Cox NJ, Cruz M, Hanis CL, Kooner J, Lee JY, Seielstad M, Teo YY, Boehnke M, Parra EJ, Chambers JC, Tai ES, McCarthy MI, Morris AP. Genome-wide trans-ancestry meta-analysis provides insight into the genetic architecture of type 2 diabetes susceptibility. Nat Genet. 2014 Mar;46(3):234-44. doi: 10.1038/ng.2897. Epub 2014 Feb 9.
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]
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]
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]
"A little diabetes monster accompanies the kids through the app and gives feedback on their entries. The child can enter data such as blood glucose levels, food and insulin or take a picture of his meals, but they can also request help whenever the parents are not around. All entries can be sent as a push message or email from within the app to the parents' phone. This way, the child can ask for feedback on calculating carbs or the insulin dose." 

Storage of liver fat can only occur when daily calorie intake exceeds expenditure. Sucrose overfeeding for 3 weeks has been shown to cause a 30% increase in liver fat content (37). The associated metabolic stress on hepatocytes was reflected by a simultaneous 30% rise in serum alanine aminotransferase (ALT) levels, and both liver fat and serum ALT returned to normal levels during a subsequent hypocaloric diet. Superimposed upon a positive calorie balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver. In groups of both obese and nonobese subjects, it was found that those with higher plasma insulin levels have markedly increased rates of hepatic de novo lipogenesis (2,38,39). Conversely, in type 1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with subnormal liver fat content (40). Initiation of subcutaneous insulin therapy in type 2 diabetes brings about a decrease in portal insulin delivery by suppression of pancreatic insulin secretion and, hence, a decrease in liver fat (41). Hypocaloric diet (42), physical activity (43), or thiazolidinedione use (23,44) each reduces insulin secretion and decreases liver fat content. Newly synthesized triacylglycerol in the liver will be either oxidized, exported, or stored as hepatic triacylglycerol. Because transport of fatty acid into mitochondria for oxidation is inhibited by the malonyl-CoA produced during de novo lipogenesis, newly synthesized triacylglycerol is preferentially directed toward storage or export. Hence, hepatic fat content and plasma VLDL triacylglycerol levels are increased.
This app is like a digital diary for your meals and physical activity. It tracks your carbs, as well as other nutrients and total calories. It gives you an option to set a weight loss goal and will help you track calories to meet it. It also connects with activity tracking devices to log your exercise. This app syncs with the Sugar Sense glucose tracking app made by the same developer (see below).

Best of them all I was diagnosed LADA a year ago. Downloaded a bunch of apps and used them all for a month. This one’s easily the winner. Extremely comprehensive, a complete set of features and enough customization to track carb intake; initial no pill and no insulin treatment; then medication only treatment; then long lasting insulin treatment. And I know it’s future proof for when I start the short term insulin and then the pump. Thank you!
Type 2 diabetes is the most common type of diabetes, accounting for 90 to 95 percent of all cases. In 2015, more than 23 million people in the United States had diagnosed diabetes and an additional 7 million people likely had undiagnosed diabetes. The prevalence of diabetes increases with age, and the disease currently affects more than 20 percent of Americans over age 65. It is the seventh leading cause of death in the United States.
In late 2015 the family added a Pebble watch to their daughter’s diabetes technology which shows her blood sugar levels on her wrist so that she can check them without taking a phone out in class. If the levels are high or low the watch vibrates to let her know. Hoover and her husband can also send her text messages that show up on the watch so she can get help with what to do.
The treatment of low blood sugar consists of administering a quickly absorbed glucose source. These include glucose containing drinks, such as orange juice, soft drinks (not sugar-free), or glucose tablets in doses of 15-20 grams at a time (for example, the equivalent of half a glass of juice). Even cake frosting applied inside the cheeks can work in a pinch if patient cooperation is difficult. If the individual becomes unconscious, glucagon can be given by intramuscular injection.
American Indian/Alaska Native. American Indian/Alaska Native women have the highest rate of diabetes among all racial and ethnic groups in the United States. It is more than twice as common for American Indian/Alaska Native women to be diagnosed with diabetes compared to white women. But rates of diabetes are different in different regions of the United States. Rates are lowest in Alaska Native people and highest in people who are American Indian and live in certain areas of the Southwest.1
^ Emadian A, Andrews RC, England CY, Wallace V, Thompson JL (November 2015). "The effect of macronutrients on glycaemic control: a systematic review of dietary randomised controlled trials in overweight and obese adults with type 2 diabetes in which there was no difference in weight loss between treatment groups". The British Journal of Nutrition. 114 (10): 1656–66. doi:10.1017/S0007114515003475. PMC 4657029. PMID 26411958.
Monogenic diabetes is caused by mutations, or changes, in a single gene. These changes are usually passed through families, but sometimes the gene mutation happens on its own. Most of these gene mutations cause diabetes by making the pancreas less able to make insulin. The most common types of monogenic diabetes are neonatal diabetes and maturity-onset diabetes of the young (MODY). Neonatal diabetes occurs in the first 6 months of life. Doctors usually diagnose MODY during adolescence or early adulthood, but sometimes the disease is not diagnosed until later in life.