top of page
​英訳サンプル:       7​


Any rise in glycemia is the net result of glucose influx exceeding glucose outflow from the plasma compartment. In the fasting state, hyperglycemia is directly related to increased hepatic glucose production. In the postprandial state, further glucose excursions result from the combination of insufficient suppression of this glucose output and defective insulin stimulation of glucose disposal in target tissues, mainly skeletal muscle. Once the renal tubular transport maximum for glucose is exceeded, glycosuria curbs, though does not prevent, further hyperglycemia.


Abnormal islet cell function is a key and requisite feature of type 2 diabetes. In early disease stages, insulin production is normal or increased in absolute terms, but disproportionately low for the degree of insulin sensitivity, which is typically reduced. However, insulin kinetics, such as the ability of the pancreatic b-cell to release adequate hormone in phase with rising glycemia, are profoundly compromised. This functional islet incompetence is the main quantitative determinant of hyperglycemia and progresses over time. In addition, in type 2 diabetes, pancreatic a-cells hypersecrete glucagon, further promoting hepatic glucose production.


The presence of spreading infection is potentially life and/or limb threatening and so requires aggressive treatment. Individuals demonstrating clinical signs of systemic infection should have blood cultures taken and appropriate systemic antibiotic therapy should be implemented immediately.


bottom of page