Trial reportThe Journal of clinical endocrinology and metabolism2022
Weight Loss, Lifestyle Intervention, and Metformin Affect Longitudinal Relationship of Insulin Secretion and Sensitivity.
Trial report in The Journal of clinical endocrinology and metabolism, 2022. The graph read 4 numbers from its abstract, feeding 2 cells of the map, but none could be read as for or against, so it casts no vote. It also reports 4 associations that do not count as treatment evidence, such as HR 0.71 (0.61 to 0.82) for diabetes risk. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
Read, but not usablea number the graph found but could not read as for or against
In time-dependent hazard models, increasing compensatory insulin secretion (hazard ratio [HR] = 0.166 per baseline SD, 95% CI 0.133, 0.206) and weight loss (HR = 0.710 per 5 kg loss, 95% CI 0.613, 0.819) predicted lower diabetes risk.
Improvements were directly related to weight loss; decreased weight significantly reduced secretory demand (b=-0.144 SD; 95% CI (-0.162, -0.125)/5 kg loss) and increased compensatory insulin secretion (b = 0.287 SD, 95% CI (0.261, 0.314)/5 kg loss).
Improvements were directly related to weight loss; decreased weight significantly reduced secretory demand (b=-0.144 SD; 95% CI (-0.162, -0.125)/5 kg loss) and increased compensatory insulin secretion (b = 0.287 SD, 95% CI (0.261, 0.314)/5 kg loss).
In time-dependent hazard models, increasing compensatory insulin secretion (hazard ratio [HR] = 0.166 per baseline SD, 95% CI 0.133, 0.206) and weight loss (HR = 0.710 per 5 kg loss, 95% CI 0.613, 0.819) predicted lower diabetes risk.
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Where it lands on the map
Rows are treatments, columns are outcomes. The coloured squares are the cells this paper feeds, coloured by the vote it casts there. Click one to jump to what this paper adds to it.
What it adds to each cell
For every cell the paper feeds: the belief in the claim with and without this paper, and this paper's estimate drawn against every other readable study in the cell. The ringed dot is this paper.
Insulin×glycemic control
No readable resultOpen on the map →What to test next →40 readable studies in this cell: 13 favour the treatment, 14 find no difference, 14 favour the comparator.
This paper's own estimate is on a different scale from the rest of the cell, so it is not drawn here.
Insulin×body weight & composition
No readable resultOpen on the map →What to test next →11 readable studies in this cell: 1 favour the treatment, 1 find no difference, 9 favour the comparator.
This paper's own estimate is on a different scale from the rest of the cell, so it is not drawn here.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Trial
- The Diabetes Prevention Program and Its Outcomes Study: NIDDK's Journey Into the Prevention of Type 2 Diabetes and Its Public Health Impact.Diabetes care · 2025Review
- Targeting inflammation-metabolism crosstalk: current status and challenges of novel therapeutic strategies for osteoarthritis.Frontiers in medicine · 2025Review
- Effects of theBMJ open diabetes research & care · 2023Article
- Metformin Monotherapy Alters the Human Plasma Lipidome Independent of Clinical Markers of Glycemic Control and Cardiovascular Disease Risk in a Type 2 Diabetes Clinical Cohort.The Journal of pharmacology and experimental therapeutics · 2023Observational
- Comparison of orlistat and orlistat plus metformin therapy between diabetic and nondiabetic groups.Revista da Associacao Medica Brasileira (1992) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The marked sentences are the ones the graph read a number from.
contextInsulin secretion and sensitivity regulate glycemia, with inadequately compensated deficiencies leading to diabetes.
objectiveWe investigated effects of weight loss, an intensive lifestyle intervention (ILS), and metformin on the relationship between insulin secretion and sensitivity using repository data from 2931 participants in the Diabetes Prevention Program clinical trial in adults at high risk of developing type 2 diabetes.
methodsInsulin secretion and sensitivity were estimated from insulin and glucose concentrations in fasting and 30-minute postload serum samples at baseline and 1, 2, and 3 years after randomization, during the active intervention phase. The nonlinear relationship of secretion and sensitivity was evaluated by standardized major axis regression to account for variability in both variables. Insulin secretory demand and compensatory insulin secretion were characterized by distances along and away from the regression line, respectively.
resultsILS and metformin decreased secretory demand while increasing compensatory insulin secretion, with greater effects of ILS. Improvements were directly related to weight loss; decreased weight significantly reduced secretory demand (b=-0.144 SD; 95% CI (-0.162, -0.125)/5 kg loss) and increased compensatory insulin secretion (b = 0.287 SD, 95% CI (0.261, 0.314)/5 kg loss). In time-dependent hazard models, increasing compensatory insulin secretion (hazard ratio [HR] = 0.166 per baseline SD, 95% CI 0.133, 0.206) and weight loss (HR = 0.710 per 5 kg loss, 95% CI 0.613, 0.819) predicted lower diabetes risk.
conclusionDiabetes risk reduction was directly related to the amount of weight loss, an effect mediated by lowered insulin secretory demand (due to increased insulin sensitivity) coupled with improved compensatory insulin secretion.
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Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.