A child with glycosuria, polyuria, polydipsia, and weight loss despite increased appetite is likely to have type 1 diabetes mellitus. This form of diabetes has an impoant autoimmune component to its etiology. As many as 85% of patients have islet cell autoantibodies in their blood in the first few weeks after onset of the disease. Most of these antibodies are directed against glutamic acid decarboxylase, an enzyme that is present in b cells. Insulin deficiency leads to decreased glucose uptake and hyperglycemia. The increase in blood glucose results in increased glycosylation of hemoglobin in red blood cells. Hence, the hemoglobin A1c concentration will be increased, not decreased, reflecting long-standing hyperglycemia. Another consequence of the increased blood glucose is increased serum osmolarity (not decreased). If the osmolarity exceeds 330 mOsm/L, consciousness begins to be impaired.beta; cell destruction in type 1 diabetes leads to decreased secretion of insulin. Since insulin and C-peptide are released on a 1:1 ratio by the beta; cells, the secretion of C-peptide is also decreased . Insulin is first synthesized as preproinsulin, with an initial leader sequence of hydrophobic amino acids that allows the developing protein to be extruded from the ribosomes into the rough endoplasmic reticulum. The "pre" segment is then cleaved off, leaving proinsulin. Proinsulin is packaged into secretory granules within the Golgi, and as the granules bud off, enzymes cleave the precursor into insulin and C-peptide. Ref: Klein U. (2012). Chapter 17. Oral Medicine & Dentistry. In W.W. Hay, Jr., M.J. Levin, R.R. Deterding, J.J. Ross, J.M. Sondheimer (Eds), CURRENT Diagnosis & Treatment: Pediatrics, 21e.