Metabolic abnormalities in impaired glucose tolerance.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing mechanistic and physiological literature without systematic methodology
PubMed 9439558 · doi:10.1016/s0026-0495(97)90316-4
What was done
This narrative review summarizes the physiological and metabolic abnormalities present in impaired glucose tolerance (IGT) that precede the onset of diabetes mellitus.
What was found
The abstract reports diagnostic thresholds for IGT as postprandial hyperglycemia (> 7.8 mmol/L or 140 mg/dL) with fasting plasma glucose between > 5.5 and < 7.8 mmol/L (> 100 and < 140 mg/dL). It identifies impaired early insulin release as the most consistent defect, often accompanied by insulin resistance. Postprandial hyperglycemia is primarily caused by impaired suppression of endogenous (hepatic and renal) glucose release, linked to deficient early insulin release and unsuppressed glucagon release. Postprandial glucose disposal is reported as normal or increased due to hyperglycemia and delayed hyperinsulinemia. Postabsorptive rates of glucose release and disposal, as well as circulating levels of free fatty acids, glycerol, ketone bodies, lactate, and alanine, are described as generally normal. No empirical effect sizes or primary sample statistics are provided.
Why it matters
This synthesis clarifies the early pathophysiological sequence of type 2 diabetes development, highlighting that postprandial hyperglycemia in prediabetes is driven by defective hepatic/renal glucose suppression rather than reduced peripheral disposal.
Limits
As a narrative review, it lacks a described systematic literature search, inclusion criteria, or quality assessment. The abstract reports no primary experimental data, sample sizes, or quantitative confidence intervals.
Cited by
- supports Postprandial glucose spikes are among the earliest indicators of metabolic dysfunction before fasting glucose rises.