Attenuated GLP-1 secretion in obesity: cause or consequence?
Level 4 - case-series / case-control
Small matched comparative physiological study (case-control design)
PubMed 8984033 · doi:10.1136/gut.38.6.916
What was done
Plasma GLP-1, GIP, glucose, and serum triglyceride responses were evaluated over 180 minutes following oral carbohydrate and fat challenge meals in 6 obese women and 6 age-matched lean control women. Heparin (10,000 units) was administered intravenously at 120 minutes.
What was found
Plasma GLP-1 secretion in response to oral carbohydrate was markedly attenuated in obese subjects compared with lean controls, but GLP-1 responses did not differ between groups after oral fat intake. Plasma GIP responses showed no differences between groups after either carbohydrate or fat ingestion. An apparent fall in plasma GLP-1 occurred in all subjects following heparin administration. The abstract reports no numerical values, variances, or p-values.
Why it matters
This study provides evidence that obesity is associated with impaired postprandial GLP-1 secretion after carbohydrate ingestion, arguing against the hypothesis that hypersecretion of incretins drives hyperinsulinemia in obesity.
Limits
The sample size is very small (n=12 total) and includes only female subjects. The abstract does not provide exact quantitative concentrations or statistical significance values, and the observational cross-sectional design cannot establish whether reduced GLP-1 secretion is a cause or consequence of obesity.
Cited by
- supports A 1996 study published in Gut found that while lean and obese individuals had similar GLP-1 responses to a high-fat meal, obese individuals exhibited no statistically significant GLP-1 increase after a high-carbohydrate meal.