Hepatic Lipoprotein Export and Remission of Human Type 2 Diabetes after Weight Loss.
Level 2 - randomized trial
Subgroup analysis within a randomized controlled trial
PubMed 31866441 · doi:10.1016/j.cmet.2019.11.018
What was done
Investigators measured the contributions of hepatic VLDL1-triglyceride production rates and VLDL1-palmitic acid content to intra-pancreatic fat accumulation and first-phase insulin response. The study was conducted in a subgroup of participants from the Diabetes Remission Clinical Trial across 24 months of follow-up after dietary weight loss.
What was found
The abstract provides no numerical data, effect sizes, or p-values. Liver fat, VLDL1-triglyceride production, and intra-pancreatic fat decreased after weight loss and remained normalized at 24 months in participants maintaining remission. First-phase insulin response remained increased only in those in remission. Participants who relapsed showed greater increases in VLDL1-triglyceride and VLDL1-palmitic acid content, re-accumulated intra-pancreatic fat, and lost first-phase insulin response by 24 months.
Why it matters
The findings demonstrate a mechanistic pathway linking disordered hepatic lipid export and pancreatic fat re-accumulation to beta-cell dysfunction in diabetes relapse.
Limits
The abstract does not state the sample size, baseline patient characteristics, or numerical measurements. As an observational comparison between remitters and relapsers within an intervention cohort, residual confounding cannot be excluded.
Cited by
- supports Ectopic fat accumulation within the pancreas reduces the amount of insulin secreted by pancreatic beta cells.