early symptoms of adult onset diabetes

This form of diabetes is immune-mediated in over 90% of cases and idiopathic in less than 10%. The rate of pancreatic B cell destruction is quite variable, being rapid in some individuals and slow in others. Type 1 diabetes is usually associated with ketosis in its untreated state. It occurs at any age but most commonly arises in children and young adults with a peak incidence before school age and again at around puberty. It is a catabolic disorder in which circulating insulin is virtually absent, plasma glucagon is elevated, and the pancreatic B cells fail to respond to all insulinogenic stimuli. Exogenous insulin is therefore required to reverse the catabolic state, prevent ketosis, reduce the hyperglucagonemia, and reduce blood glucose.
The highest incidence of immune-mediated type 1 diabetes is in Scandinavia and northern Europe, where the yearly incidence per 100,000 youngsters 14 years of age or less is as high as 37 in Finland, 27 in Sweden, 22 in Norway, and 19 in the United Kingdom. The incidence of type 1 diabetes generally decreases across the rest of Europe to 10 in Greece and 8 in France. Surprisingly, the island of Sardinia has as high an incidence as Finland (37) even though in the rest of Italy, including the island of Sicily, it is only 10 per 100,000 per year. The United States averages 15 per 100,000, with higher incidences in states more densely populated with persons of Scandinavian descent such as Minnesota. The lowest incidence of type 1 diabetes worldwide was found to be less than 1 per 100,000 per year in China and parts of South America.
Certain human leukocyte antigens (HLA) are strongly associated with the development of type 1 diabetes. About 95% of type 1 patients possess either HLA-DR3 or HLA-DR4, compared with 45-50% of white controls. HLA-DQ genes are even more specific markers of type 1 susceptibility, since a particular variety (HLA-DQB1*0302) is found in the DR4 patients with type 1, while a "protective" gene (HLA-DQB1*0602) is often present in the DR4 controls. In addition, most patients with type 1 diabetes at diagnosis have circulating antibodies to islets (islet cell antibodies, ICA), insulin (IAA), glutamic acid decarboxylase (GAD 65), and to tyrosine phosphatases (IA-2 and IA2-ß). These antibodies facilitate screening of siblings of affected children as well as adults with atypical features of type 2 for an autoimmune cause of their diabetes (Table 27-2). The antibody levels decline with increasing duration of the disease. Also, once patients are treated with insulin, low levels of anti-insulin antibodies develop.
Certain unrecognized patients with a milder expression of type 1 diabetes initially retain enough B cell function to avoid ketosis but later in life develop increasing dependency on insulin therapy as their B cell mass diminishes. Islet cell antibody surveys among northern Europeans indicate that up to 15% of "type 2" patients may actually have this mild form of type 1 diabetes (latent autoimmune diabetes of adulthood; LADA).