TYPE 1 DIABETES

A.Diagnosis of type 1 diabetes The onset of type 1 diabetes is typically during childhood or puberty, and symptoms develop suddenly. Patients with type 1 diabetes can usually be recognized by the abrupt appearance of polyuria (frequent urination), polydipsia (excessive thirst), and polyphagia (excessive hunger), often triggered by stress or an illness. These symptoms are usually accompanied by fatigue, weight loss, and weakness. The diagnosis is confirmed by a fasting blood glucose (FBG) greater than or equal to 126 mg/dl, commonly accompanied by ketoacidosis. [Note: A FBG of 100–125 mg/dl is categorized as an impaired FBG.] Fasting is defined as no caloric intake for at least 8 hours. When the diagnosis of type 1 diabetes is uncertain by clinical presentation, testing for circulating islet-cell antibodies is recommended. [Note: The oral glucose tolerance test is not routinely used as a diagnostic tool for diabetes because it is difficult to perform in practice and the results are highly variable; however, it is used to screen pregnant women for gestational diabetes (see p. 342).]

B. Metabolic changes in type 1 diabetes The metabolic abnormalities of type 1 diabetes mellitus result from a deficiency of insulin which profoundly affects metabolism in three tissues: liver, muscle, and adipose tissue. 
1)      Hyperglycemia and ketoacidosis: Elevated levels of blood glucose and ketones are the hallmarks of untreated type 1 diabetes mellitus. Hyperglycemia is caused by increased hepatic production of glucose, combined with diminished peripheral utilization (muscle and adipose have the insulin-sensitive GLUT-4, see p. 97). Ketosis results from increased mobilization of fatty acids from adipose tissue, combined with accelerated hepatic fatty acid β-oxidation and synthesis of 3-hydroxybutyrate and aceto acetate. [Note: Acetyl coenzyme A from β-oxidation is the substrate for ketogenesis and the allosteric effector of pyruvate carboxylase, a glucon eogenic enzyme.] Diabetic ketoacidosis (DKA, a type of metabolic acidosis) occurs in 25–40% of those newly diagnosed with type 1 diabetes, and may recur if the patient becomes ill (most commonly with an infection) or does not comply with therapy. DKA is treated by replacing fluid and electrolytes, and administering short-acting insulin to gradually correct hyperglycemia without precipitating hypoglycemia. 
2)      Hypertriacylglycerolemia: Not all the fatty acids flooding the liver can be disposed of through oxidation or ketone body synthesis. These excess fatty acids are converted to triacylglycerol, which is packaged and secreted in very-low-density lipoproteins (VLDL, see p. 231). Chylom icrons are synthesized from dietary lipids by the intestinal mucosal cells following a meal (see p. 178). Becauselipoprotein degradation catalyzed by lipoprotein lipase in the capillary beds of muscle and adipose tissue (see. p. 228) is low in diabetics ( synthesis of the enzyme is decreased when insulin levels are low), the plasma chylomicron and VLDL levels are elevated, resulting in hypertriacylglycerolemia.
C. Treatment of type 1 diabetes Individuals with type 1 diabetes must rely on  exogenous insulin injected subcutaneously to control the hyperglycemia and ketoacidosis. Two therapeutic regimens are currently in use—standard and intensive insulin treatment.

Daftar Pustaka

Farrier, Dennise .2014.Biokimia Lippincott; Jakarta, Binapura. Ed:6