Atherogenicity of postprandial hyperglycemia and lipotoxicity.
Level 5 - mechanism / opinion, no new human data
Narrative review of clinical and mechanistic evidence without systematic review methodology
PubMed 26880302 · doi:10.1007/s11154-016-9341-8
What was done
This narrative review synthesized literature on postprandial glucose and lipid dysregulation in type 2 diabetes, evaluating evidence on how postprandial hyperglycemia and postprandial hypertriglyceridemia contribute to cardiovascular risk.
What was found
The abstract reports no exact quantitative figures or effect sizes. It notes a linear relationship between 2-hour post-load glucose levels (from oral glucose tolerance testing) and cardiovascular mortality. Postprandial hyperglycemia and hypertriglyceridemia each independently associate with cardiovascular risk, and their concurrent presence produces an additive worsening of endothelial function and inflammation, mediated by oxidative stress, even among patients categorized as having good overall metabolic control.
Why it matters
Standard management relying exclusively on fasting plasma glucose and glycated hemoglobin may overlook critical cardiovascular risk driven by transient postprandial metabolic spikes.
Limits
The paper is a non-systematic narrative review providing no quantitative synthesis, sample sizes, or study selection criteria in the abstract. Causality between specific postprandial targets and reduced hard cardiovascular endpoints cannot be established from this summary.
Cited by
- context Postprandial blood glucose spikes above 140 mg/dL cause arterial damage.