Impact of a diabetes-designed meal delivery service on changes in hemoglobin A1c and quality of life in patients with diabetes.

BACKGROUND: Over 34 million Americans have diabetes, and nutrition therapy is essential in self-management. AIMS: The primary aim of the study was to evaluate the impact of meals designed for patients with type 2 diabetes (T2D) through a meal delivery program. The primary outcome was a 3-month change in hemoglobin A1c (HbA1c). Secondary outcomes included a 3-month change in weight, blood pressure, high-density lipoprotein, low-density lipoprotein, and triglycerides. Furthermore, the study aimed to evaluate the impact of the meal delivery program on the participants' quality of life. METHODS: In this randomized crossover clinical trial, patients were allocated in a 1:1 fashion to treatment sequence AB or treatment sequence BA. In Phase 1, participants allocated to sequence AB received 10 meals per week for 3 months, followed by a 3-month washout period and a 3-month standard intervention period with no meals. Participants allocated to sequence BA received 3 months of standard intervention with no meals followed by a 3-month washout period and a 3-month period with 10 meals per week. A quality-of-life survey was obtained during weeks 0, 12, 24, and 36. RESULTS: The mean 3-month change in HbA1c (primary outcome) was nearly a half point lower with meal delivery (-0.44% [95% CI: -0.85%, -0.03%]; P = 0.037). The estimated mean 3-month change in quality of life was approximately 2 points lower (better) with meal delivery (-2.2 points [95% CI: -4.2, -0.3]; P = .027). There were no statistically significant differences in secondary outcomes with meal delivery (all P ≥ 0.15). CONCLUSIONS: A meal delivery system for patients with T2D improves glycemic control and quality of life.

Biochemical Analysis of the Lipoprotein Lipase Truncation Variant, LPLS447X, Reveals Increased Lipoprotein Uptake.

Lipoprotein lipase (LPL) is responsible for the hydrolysis of triglycerides from circulating lipoproteins. Whereas most identified mutations in the LPL gene are deleterious, one mutation, LPLS447X, causes a gain of function. This mutation truncates two amino acids from LPL's C-terminus. Carriers of LPLS447X have decreased VLDL levels and increased HDL levels, a cardioprotective phenotype. LPLS447X is used in Alipogene tiparvovec, the gene therapy product for individuals with familial LPL deficiency. It is unclear why LPLS447X results in a serum lipid profile more favorable than that of LPL. In vitro reports vary as to whether LPLS447X is more active than LPL. We report a comprehensive, biochemical comparison of purified LPLS447X and LPL dimers. We found no difference in specific activity on synthetic and natural substrates. We also did not observe a difference in the Ki for ANGPTL4 inhibition of LPLS447X relative to that of LPL. Finally, we analyzed LPL-mediated uptake of fluorescently labeled lipoprotein particles and found that LPLS447X enhanced lipoprotein uptake to a greater degree than LPL did. An LPL structural model suggests that the LPLS447X truncation exposes residues implicated in LPL binding to uptake receptors.