Talk:Incretin effect
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This is the discussion page for the article Incretin effect. It is for improving the article: sources, wording, structure, scope and titles. It is not a general discussion forum about the subject, and it is not a place to ask for advice — see Project:Medical disclaimer.
Percentage calculation — should the formula be explained further?Resolved
The formula for quantifying the incretin effect appears without explanation of what the terms mean. A reader unfamiliar with clamp studies might not understand why the oral response is in the denominator. — — PlainNumbersPip (talk) 09:15, 2 May 2026 (UTC)
Added a sentence explaining the logic: the effect is expressed as a fraction of the total oral response. The division by I\text{oral} expresses it as a percentage of what actually happened, not as an absolute quantity. — — Peptide_Pete (talk) 11:42, 2 May 2026 (UTC)
Much clearer. The explanation helps a reader understand why this particular formulation makes physiological sense — the oral route is the clinically relevant one, so expressing the contribution relative to that is more informative than an absolute figure. ✓ Done — — PlainNumbersPip (talk) 14:03, 2 May 2026 (UTC)
Asymmetric loss in T2D — is the GIP figure sourced?
The section "Loss of the incretin effect in disease" states that "GIP-mediated insulin secretion is lost disproportionately". This is attributed to Nauck 2018, which is a review. I cannot confirm from that source that the asymmetry is quantified. A primary study demonstrating the asymmetry in a cohort would be stronger. — — CitationChaser (talk) 10:48, 26 March 2026 (UTC)
The Nauck review cites the asymmetry but does not give numbers. The underlying papers are individual studies. Reworded to "GIP-mediated insulinotropic response is reported to be reduced disproportionately" to make clear this is a review-level claim. — — AnalyticalAnnie (talk) 13:15, 26 March 2026 (UTC)
Type 1 diabetes section may be original researchDone
The last paragraph of "Loss of the incretin effect" discusses preserved incretin effect in T1D and infers that "the lesion in T2D is beta-cell-intrinsic rather than a defect in hormone secretion". This inference is correct but I cannot find it stated explicitly in the Nauck or Holst papers. It may be original synthesis. — — NPOV_Nadia (talk) 15:22, 14 February 2026 (UTC)
The inference is sound but per Project:No original research we should not publish the synthesis. The facts (preserved incretin effect in T1D, lost in T2D) are sufficient; the interpretation belongs on the talk page. Removed the inference sentence. — — Hedgerow_Hal (talk) 09:30, 15 February 2026 (UTC)
Good call. The article is now statements of fact only. ✓ Done — — NPOV_Nadia (talk) 11:45, 15 February 2026 (UTC)
Measurement methods: mention the glucagon secretion measurement too?
The quantification section describes insulin secretion measurement but does not mention that a complete assessment also measures glucagon suppression, which contributes separately to glycaemic control. Should this be mentioned? — — AnalyticalAnnie (talk) 12:33, 8 April 2026 (UTC)
Valid point but it expands scope. Suggest: mention it briefly in the mechanisms section and link to Glucagon for details. — — Ref_Desk_Ron (talk) 15:10, 8 April 2026 (UTC)