Condition
Postprandial hyperglycaemia
3 compounds were checked against postprandial hyperglycaemia, and every one of them earned a row.
Last updated
Recorded under Hyperglycaemia, alongside 0 other indications.
Compounds with a graded row
Ordered by rung, strongest first. The rung rates the study design; the chip beside it says what the study measured. Both are needed.
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Lixisenatide
human RCT Direct outcome Approved for this condition
- Who was studied
- adults with type 2 diabetes on optimised insulin glargine with or without metformin, n=142, multicentre randomised open-label three-arm, 8 weeks; primary measure was the 4-hour postprandial plasma glucose AUC after a standardised solid breakfast
The primary endpoint was the postprandial excursion itself: lixisenatide 20 mcg once daily reduced the 4-hour post-breakfast glucose AUC more than liraglutide 1.2 mg (-108.3 mg/dL.h difference) or 1.8 mg (-83.0 mg/dL.h), with greater slowing of gastric emptying, while HbA1c ended similar across arms (about 6.1-6.2%). Symptomatic hypoglycaemia was more frequent with lixisenatide than with liraglutide in this insulin-treated population; the abstract does not quantify the rates.
Source PubMed 1 primary source read for this row
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Pramlintide
human RCT Direct outcome Approved for this condition
- Who was studied
- adults with type 2 diabetes, n=24 in a single-blind randomised crossover (12 on exogenous insulin, 12 managed with diet and/or oral agents); 5-hour intravenous pramlintide or placebo infusion with a test meal one hour in, glucose measured over the 4 hours after the meal
The measurement is exactly the post-meal excursion: plasma glucose, insulin, C-peptide and lactate over four hours after a standardised test meal during a pramlintide or placebo infusion. Postprandial glucose fell significantly only in the insulin-treated group; in the diet/oral-agent group insulin, C-peptide and lactate fell but mean glucose did not. This is an acute infusion experiment on the analogue pramlintide, not native amylin; the FDA approval is as a mealtime adjunct to insulin, and the label carries a boxed warning for severe insulin-induced hypoglycaemia.
Source PubMed 1 primary source read for this row
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Amylin
human case series Mechanistic only Not approved for this condition
- Who was studied
- six volunteers, native islet amyloid polypeptide (amylin) infused intravenously at 25 and 50 pmol/kg/min against saline, each session followed by an intravenous glucose bolus of 0.5 g/kg — a bolus, not a meal; health status of the volunteers not further characterised in the abstract
Recorded, and not evidence for this condition
No study on file has given native amylin around a meal and measured the post-meal glucose excursion, and this row is mechanistic only. In the one acute human infusion study located, the challenge was an intravenous glucose bolus rather than food: 25 pmol/kg/min changed neither glucose disposal nor the insulin response, and only 50 pmol/kg/min — circulating concentrations above 90 times normal postprandial peaks — reduced the insulin response, leading the authors to conclude circulating amylin is unlikely to influence carbohydrate metabolism in man at physiological concentrations. Almost all human amylin literature uses the analogue pramlintide rather than the native peptide, which is graded on its own row.
Source PubMed 1 primary source read for this row
Every compound checked earned a row
Nothing was checked against postprandial hyperglycaemia and set aside. That is unusual — most conditions here have a list at the bottom of this page.
What this page does not say
It reports what was measured, in whom, and how directly. It does not say what to take or at what dose, and a row here is a record of a study rather than a reason to use anything. Every rung links to the rubric that assigned it.