Distinct lipid profiles predict improved glycemic control in obese, nondiabetic patients after a low-caloric diet intervention: the diet, obesity and genes randomized trial

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Distinct lipid profiles predict improved glycemic control in obese, nondiabetic patients after a low-caloric diet intervention : the diet, obesity and genes randomized trial. / Valsesia, Armand; Saris, Wim Hm; Astrup, Arne; Hager, Jörg; Masoodi, Mojgan.

In: American Journal of Clinical Nutrition, Vol. 104, No. 3, 2016, p. 566-575.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Valsesia, A, Saris, WH, Astrup, A, Hager, J & Masoodi, M 2016, 'Distinct lipid profiles predict improved glycemic control in obese, nondiabetic patients after a low-caloric diet intervention: the diet, obesity and genes randomized trial', American Journal of Clinical Nutrition, vol. 104, no. 3, pp. 566-575. https://doi.org/10.3945/ajcn.116.137646

APA

Valsesia, A., Saris, W. H., Astrup, A., Hager, J., & Masoodi, M. (2016). Distinct lipid profiles predict improved glycemic control in obese, nondiabetic patients after a low-caloric diet intervention: the diet, obesity and genes randomized trial. American Journal of Clinical Nutrition, 104(3), 566-575. https://doi.org/10.3945/ajcn.116.137646

Vancouver

Valsesia A, Saris WH, Astrup A, Hager J, Masoodi M. Distinct lipid profiles predict improved glycemic control in obese, nondiabetic patients after a low-caloric diet intervention: the diet, obesity and genes randomized trial. American Journal of Clinical Nutrition. 2016;104(3):566-575. https://doi.org/10.3945/ajcn.116.137646

Author

Valsesia, Armand ; Saris, Wim Hm ; Astrup, Arne ; Hager, Jörg ; Masoodi, Mojgan. / Distinct lipid profiles predict improved glycemic control in obese, nondiabetic patients after a low-caloric diet intervention : the diet, obesity and genes randomized trial. In: American Journal of Clinical Nutrition. 2016 ; Vol. 104, No. 3. pp. 566-575.

Bibtex

@article{e7234a8917c44bf287e2bdd61c0c94e1,
title = "Distinct lipid profiles predict improved glycemic control in obese, nondiabetic patients after a low-caloric diet intervention: the diet, obesity and genes randomized trial",
abstract = "BACKGROUND: An aim of weight loss is to reduce the risk of type 2 diabetes (T2D) in obese subjects. However, the relation with long-term glycemic improvement remains unknown.OBJECTIVE: We evaluated the changes in lipid composition during weight loss and their association with long-term glycemic improvement.DESIGN: We investigated the plasma lipidome of 383 obese, nondiabetic patients within a randomized, controlled dietary intervention in 8 European countries at baseline, after an 8-wk low-caloric diet (LCD) (800-1000 kcal/d), and after 6 mo of weight maintenance.RESULTS: After weight loss, a lipid signature identified 2 groups of patients who were comparable at baseline but who differed in their capacities to lose weight and improve glycemic control. Six months after the LCD, one group had significant glycemic improvement [homeostasis model assessment of insulin resistance (HOMA-IR) mean change: -0.92; 95% CI: -1.17, -0.67)]. The other group showed no improvement in glycemic control (HOMA-IR mean change: -0.26; 95% CI: -0.64, +0.13). These differences were sustained for ≥1 y after the LCD. The same conclusions were obtained with other endpoints (Matsuda index and fasting insulin and glucose concentrations). Significant differences between the 2 groups were shown in leptin gene expression in adipose tissue biopsies. Significant differences were also observed in weight-related endpoints (body mass index, weight, and fat mass). The lipid signature allowed prediction of which subjects would be considered to be insulin resistant after 6 mo of weight maintenance [validation's receiver operating characteristic (ROC) area under the curve (AUC): 71%; 95% CI: 62%, 81%]. This model outperformed a clinical data-only model (validation's ROC AUC: 61%; 95% CI: 50%, 71%; P = 0.01).CONCLUSIONS: In this study, we report a lipid signature of LCD success (for weight and glycemic outcome) in obese, nondiabetic patients. Lipid changes during an 8-wk LCD allowed us to predict insulin-resistant patients after 6 mo of weight maintenance. The determination of the lipid composition during an LCD enables the identification of nonresponders and may help clinicians manage metabolic outcomes with further intervention, thereby improving the long-term outcome and preventing T2D. This trial was registered at clinicaltrials.gov as NCT00390637.",
author = "Armand Valsesia and Saris, {Wim Hm} and Arne Astrup and J{\"o}rg Hager and Mojgan Masoodi",
note = "CURIS 2016 NEXS 212",
year = "2016",
doi = "10.3945/ajcn.116.137646",
language = "English",
volume = "104",
pages = "566--575",
journal = "American Journal of Clinical Nutrition",
issn = "0002-9165",
publisher = "American Society for Nutrition",
number = "3",

}

RIS

TY - JOUR

T1 - Distinct lipid profiles predict improved glycemic control in obese, nondiabetic patients after a low-caloric diet intervention

T2 - the diet, obesity and genes randomized trial

AU - Valsesia, Armand

AU - Saris, Wim Hm

AU - Astrup, Arne

AU - Hager, Jörg

AU - Masoodi, Mojgan

N1 - CURIS 2016 NEXS 212

PY - 2016

Y1 - 2016

N2 - BACKGROUND: An aim of weight loss is to reduce the risk of type 2 diabetes (T2D) in obese subjects. However, the relation with long-term glycemic improvement remains unknown.OBJECTIVE: We evaluated the changes in lipid composition during weight loss and their association with long-term glycemic improvement.DESIGN: We investigated the plasma lipidome of 383 obese, nondiabetic patients within a randomized, controlled dietary intervention in 8 European countries at baseline, after an 8-wk low-caloric diet (LCD) (800-1000 kcal/d), and after 6 mo of weight maintenance.RESULTS: After weight loss, a lipid signature identified 2 groups of patients who were comparable at baseline but who differed in their capacities to lose weight and improve glycemic control. Six months after the LCD, one group had significant glycemic improvement [homeostasis model assessment of insulin resistance (HOMA-IR) mean change: -0.92; 95% CI: -1.17, -0.67)]. The other group showed no improvement in glycemic control (HOMA-IR mean change: -0.26; 95% CI: -0.64, +0.13). These differences were sustained for ≥1 y after the LCD. The same conclusions were obtained with other endpoints (Matsuda index and fasting insulin and glucose concentrations). Significant differences between the 2 groups were shown in leptin gene expression in adipose tissue biopsies. Significant differences were also observed in weight-related endpoints (body mass index, weight, and fat mass). The lipid signature allowed prediction of which subjects would be considered to be insulin resistant after 6 mo of weight maintenance [validation's receiver operating characteristic (ROC) area under the curve (AUC): 71%; 95% CI: 62%, 81%]. This model outperformed a clinical data-only model (validation's ROC AUC: 61%; 95% CI: 50%, 71%; P = 0.01).CONCLUSIONS: In this study, we report a lipid signature of LCD success (for weight and glycemic outcome) in obese, nondiabetic patients. Lipid changes during an 8-wk LCD allowed us to predict insulin-resistant patients after 6 mo of weight maintenance. The determination of the lipid composition during an LCD enables the identification of nonresponders and may help clinicians manage metabolic outcomes with further intervention, thereby improving the long-term outcome and preventing T2D. This trial was registered at clinicaltrials.gov as NCT00390637.

AB - BACKGROUND: An aim of weight loss is to reduce the risk of type 2 diabetes (T2D) in obese subjects. However, the relation with long-term glycemic improvement remains unknown.OBJECTIVE: We evaluated the changes in lipid composition during weight loss and their association with long-term glycemic improvement.DESIGN: We investigated the plasma lipidome of 383 obese, nondiabetic patients within a randomized, controlled dietary intervention in 8 European countries at baseline, after an 8-wk low-caloric diet (LCD) (800-1000 kcal/d), and after 6 mo of weight maintenance.RESULTS: After weight loss, a lipid signature identified 2 groups of patients who were comparable at baseline but who differed in their capacities to lose weight and improve glycemic control. Six months after the LCD, one group had significant glycemic improvement [homeostasis model assessment of insulin resistance (HOMA-IR) mean change: -0.92; 95% CI: -1.17, -0.67)]. The other group showed no improvement in glycemic control (HOMA-IR mean change: -0.26; 95% CI: -0.64, +0.13). These differences were sustained for ≥1 y after the LCD. The same conclusions were obtained with other endpoints (Matsuda index and fasting insulin and glucose concentrations). Significant differences between the 2 groups were shown in leptin gene expression in adipose tissue biopsies. Significant differences were also observed in weight-related endpoints (body mass index, weight, and fat mass). The lipid signature allowed prediction of which subjects would be considered to be insulin resistant after 6 mo of weight maintenance [validation's receiver operating characteristic (ROC) area under the curve (AUC): 71%; 95% CI: 62%, 81%]. This model outperformed a clinical data-only model (validation's ROC AUC: 61%; 95% CI: 50%, 71%; P = 0.01).CONCLUSIONS: In this study, we report a lipid signature of LCD success (for weight and glycemic outcome) in obese, nondiabetic patients. Lipid changes during an 8-wk LCD allowed us to predict insulin-resistant patients after 6 mo of weight maintenance. The determination of the lipid composition during an LCD enables the identification of nonresponders and may help clinicians manage metabolic outcomes with further intervention, thereby improving the long-term outcome and preventing T2D. This trial was registered at clinicaltrials.gov as NCT00390637.

U2 - 10.3945/ajcn.116.137646

DO - 10.3945/ajcn.116.137646

M3 - Journal article

C2 - 27510538

VL - 104

SP - 566

EP - 575

JO - American Journal of Clinical Nutrition

JF - American Journal of Clinical Nutrition

SN - 0002-9165

IS - 3

ER -

ID: 164517886