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             The primary cause of insulin-dependent diabetes mellitus (IDDM), or Type 1 diabetes, is inadequate insulin production by the beta cells of the pancreatic islets. In most cells, glucose trans ­port cannot occur in the absence of insulin. When insulin con- -centrations decline, cells can no longer absorb glucose; tissues remain glucose starved, despite the presence of adequate or even excessive amounts of glucose in the bloodstream.
             After a meal rich in glucose, blood glucose concentrations may be ­come so elevated that the kidney cells cannot reclaim all the glucose molecules that enter the urine. The high urinary concentration of glu ­cose limits the ability of the kidneys to conserve water, so the individ ­ual urinates frequently and may become dehydrated. The chronic dehydration leads to disturbances of neural function (blurred vision, < tingling sensations, disorientation, and fatigue) and muscle weakness.
             Despite high blood concentrations, glucose cannot enter en ­docrine tissues, and the endocrine system responds as if glucose were in short supply. Alpha cells release glucagon, and glucocor-ticoid production accelerates. Peripheral tissues then break down lipids and proteins to obtain the energy needed to continue func ­tioning. The breakdown of large numbers of fatty acids promotes the generation of molecules called ketone bodies. These small ; molecules are metabolic acids whose accumulation in large num ­bers can cause a dangerous reduction in blood pH. This condi- , tion, called ketoacidosis, commonly triggers vomiting. In severe cases, it can progress to coma and death.
             If the individual survives (an impossibility without insulin ther ­apy), long-term treatment involves a combination of dietary control, monitoring of blood glucose levels several times a day, and the ad- , ministration of insulin, either by injection or by infusion, using an insulin pump.

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