Diabetes mellitus (DM) is a strong predictor of cardiovascular morbidity and mortality and is associated with both micro- and macrovascular complications.1 Cardiovascular disease (CVD) causes up to 70% of all deaths in people with DM. The epidemic of DM will thus be followed by a burden of diabetes-related vascular diseases. The number of DM patients increases with aging of the population, in part because of the increasing prevalence of obesity and sedentary lifestyle. Although the mortality from coronary artery disease (CAD) in patients without DM has declined since the 1990s, the mortality in men with type 2 diabetes (T2DM) has not changed significantly.2 Moreover, DM is an independent risk factor for heart failure. Heart failure is closely related to diabetic cardiomyopathy: changes in the structure and function of the myocardium are not directly linked to CAD or hypertension. Diabetic cardiomyopathy is clinically characterized by an initial increase in left ventricular stiffness and subclinical diastolic dysfunction, gradually compromising left ventricular systolic function with loss of contractile function and progress into overt congestive heart failure. DM accounts for a significant percentage of patients with a diagnosis of heart failure in epidemiologic studies such as the Framingham Study and the UK Prospective Diabetes Study (UKPDS).2 A 1% increase in glycated hemoglobin (HbA1c) correlates to an increment of 8% in heart failure.3 The prevalence of heart failure in elderly diabetic patients is up to 30%.3

Morbidity and mortality stem from the metabolic derangements and from the long-term complications that affect small and large vessels, resulting in retinopathy, nephropathy, neuropathy, ischemic heart disease, and arterial obstruction with gangrene of extremities.2 The acute clinical manifestations can be fully understood in the context of current knowledge of the secretion and action of insulin.3 Genetic and other etiologic considerations implicate autoimmune mechanisms in the evolution of the most common form of childhood diabetes, known as type 1a diabetes.4,5 Genetic defects in insulin secretion are increasingly recognized and understood as defining the causes of monogenic forms of diabetes such as maturity-onset diabetes of youth (MODY) and neonatal DM and contributing to the spectrum of T2DM.6

Jump up ^ Feinman, RD; Pogozelski, WK; Astrup, A; Bernstein, RK; Fine, EJ; Westman, EC; Accurso, A; Frassetto, L; Gower, BA; McFarlane, SI; Nielsen, JV; Krarup, T; Saslow, L; Roth, KS; Vernon, MC; Volek, JS; Wilshire, GB; Dahlqvist, A; Sundberg, R; Childers, A; Morrison, K; Manninen, AH; Dashti, HM; Wood, RJ; Wortman, J; Worm, N (January 2015). "Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base". Nutrition. Burbank, Los Angeles County, Calif. 31 (1): 1–13. doi:10.1016/j.nut.2014.06.011. PMID 25287761.
Diabetes can occur temporarily during pregnancy, and reports suggest that it occurs in 2% to 10% of all pregnancies. Significant hormonal changes during pregnancy can lead to blood sugar elevation in genetically predisposed individuals. Blood sugar elevation during pregnancy is called gestational diabetes. Gestational diabetes usually resolves once the baby is born. However, 35% to 60% of women with gestational diabetes will eventually develop type 2 diabetes over the next 10 to 20 years, especially in those who require insulin during pregnancy and those who remain overweight after their delivery. Women with gestational diabetes are usually asked to undergo an oral glucose tolerance test about six weeks after giving birth to determine if their diabetes has persisted beyond the pregnancy, or if any evidence (such as impaired glucose tolerance) is present that may be a clue to a risk for developing diabetes.
The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body.[60] Insulin plays a critical role in balancing glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.[60]
An article published in November 2012 in the journal Global Public Health found that countries with more access to HFCS tended to have higher rates of the disease. Though it’s likely that these countries’ overall eating habits play a role in their populations’ diabetes risk, a study published in February 2013 in the journal PLoS One found limiting access to HFCS in particular may help reduce rates of the diagnosis.
Jump up ^ Ahlqvist, Emma; Storm, Petter; Käräjämäki, Annemari; Martinell, Mats; Dorkhan, Mozhgan; Carlsson, Annelie; Vikman, Petter; Prasad, Rashmi B; Aly, Dina Mansour (2018). "Novel subgroups of adult-onset diabetes and their association with outcomes: a data-driven cluster analysis of six variables". The Lancet Diabetes & Endocrinology. 0 (5): 361–369. doi:10.1016/S2213-8587(18)30051-2. ISSN 2213-8587. PMID 29503172.
Insulin resistance is the most common cause of type 2 diabetes, but it is possible to have type 2 and not be insulin resistant. You can have a form of type 2 where you body simply doesn’t produce enough insulin; that’s not as common. Researchers aren’t sure what exactly keeps some people from producing enough insulin, but that’s another thing they’re working hard to figure out.
While it's conceivable that scientists will isolate a single factor as causing type 1 and type 2, the much more likely outcome is that there is more than one cause. Each person seems to take a unique path in developing diabetes. Someday, doctors may be able to assess an individual's genetic risk for diabetes, allowing him or her to dodge the particular environmental factors that would trigger the disease. And perhaps if the baffling question of why a person gets diabetes can be put to rest, the answer will also offer a cure for the disease.
In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are also more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.[123]
Infections. Poorly controlled diabetes can lead to a variety of tissue infections. The most commonly encountered is a yeast infection (Candida) and the presence of dry mouth further increases one’s risk (see PATIENT INFORMATION SHEET – Oral Yeast Infections). Typically, affected areas appear redder than the surrounding tissue and commonly affected sites include the tongue, palate, cheeks, gums, or corners of the mouth (see Right). There is conflicting data regarding cavity risk in the diabetic patient, but those who have dry mouth are clearly at increased risk for developing cavities.
High blood glucose sets up a domino effect of sorts within your body. High blood sugar leads to increased production of urine and the need to urinate more often. Frequent urination causes you to lose a lot of fluid and become dehydrated. Consequently, you develop a dry mouth and feel thirsty more often. If you notice that you are drinking more than usual, or that your mouth often feels dry and you feel thirsty more often, these could be signs of type 2 diabetes.