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Insulin resistance and impaired insulin secretion are the main pathophysiological defects responsible for the development of hyperglycemia in type 2 diabetes (1, 2).
Type 2 diabetes is a complex metabolic disease that results from two main pathophysiological defects: impaired insulin sensitivity (IS) and β-cell failure (1).
Theoretically, the best antiglycemic treatment is to aim at restoring the main pathophysiological defects in type 2 diabetes: decreased first-phase insulin secretion, peripheral insulin resistance, and elevated hepatic gluconeogenesis.
NGT 1h-high individuals may represent an intermediate state of glucose intolerance between NGT and type 2 diabetes characterized by insulin resistance and reduced β-cell function, the two main pathophysiological defects responsible for the development of type 2 diabetes.
In this study, we provide evidence that subjects with NGT, whose 1-h postload plasma glucose is ≥155 mg/dL, have a reduction in both insulin sensitivity and β-cell dysfunction, the two main pathophysiological defects responsible for the development of type 2 diabetes.
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The association of β-cell dysfunction with insulin resistance represents the main pathophysiological defect responsible for the development of type 2 diabetes.
Our understanding of the pathophysiology of diabetes has progressed over time with recent research identifying eight pathophysiological defects, termed the "ominous octet," involved in the development of diabetes.
The main pathophysiological phenotype of SAKI is tubular damage.
It has been assumed that specific epilepsy syndromes are associated with specific underlying pathophysiological defects.
The immune dysfunction is the main pathophysiological process in septic patients.
Figure 2 The main pathophysiological mechanisms involved in acute traumatic coagulopathy and transfusion strategy.
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