Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

Low carbohydrate diet elevates blood sphingomyelin in people with type 1 diabetes

Research output: Contribution to journalConference abstract in journalResearchpeer-review

Harvard

APA

CBE

MLA

Vancouver

Author

Bibtex

@article{be45af4059c34cdfa1548f0fea5c1882,
title = "Low carbohydrate diet elevates blood sphingomyelin in people with type 1 diabetes",
abstract = "Background and Aim: Reduction of carbohydrate intake stabilizes glucose levels in persons with type 1 diabetes (T1D). To maintain similar energy intake, a reduction in carbohydrate must be accompanied by an increase in protein and/or fat intake. However, this dietary change may affect the lipid balance and lead to an increased risk of cardiovascular events. We investigated how blood lipid levels responded to dietary changes and how these changes related to diet-induced changes in metabolic characteristics, such as body mass index (BMI), waist circumference, systolic blood pressure (SBP), glycemic variability and time spent in hypoglycemia. Materials and Methods: Ten adults with T1D (mean±SD: age 43.6±13.8 years, diabetes duration 24.5±13.4 years, BMI 24.9±2.1 kg, HbA1c 57.6±2.6 ) using insulin pumps participated in a randomized 2-period crossover study with 12-week intervention periods of Low Carbohydrate Diet ( LCD < 100 g carbohydrates/day) or High Carbohydrate Diet (HCD > 250 g carbohydrates/day) respectively, separated by a 12-week washout period. A comprehensive lipidomics analysis was done for fasting plasma samples obtained after each diet, and changes in lipid levels were compared with paired tests. Results: In total, 245 lipid levels were identified from 9 major lipid classes (Triacylglycerides, Phosphatidylcholines, Phosphatidylethanolamines, Hexosyl Ceramide, Sphingomyelins, Lysophosphatidylcholines, Ceramides, Lactosylceramide, and Lysophoshatidylethanolamine). In the high-resolution lipidomics analysis, phosphatidylcholines and sphingomyelins were elevated after LCD (not significant). A short-chain monounsaturated sphingomyelin, SM(d34:1), was elevated after LCD compared with HCD (p=0.002; see Figure). Sphingomyelins and phosphatidylcholines were inversely associated with BMI, waist circumference, SBP and glycemic variability (not significant). SM(d34:1) did not show significant association to changes in clinical measurements. Conclusion: Plasma from persons with T1D showed an increase in a monounsaturated sphingomyelin with LCD compared to HCD. Results from this randomized cross-over study warrant for more investigation on the long-term effects of diet and lipid homeostasis in T1D.",
author = "Al-Sari, {Naba Hassan} and Signe Schmidt and Tommi Suvitaival and Min Kim and Kajetan Trošt and Ajenthen Ranjan and Merete Christensen and Overgaard, {Anne Julie} and Flemming Pociot and Kirsten N{\o}rgaard and Cristina Legido-Quigley",
year = "2019",
month = "9",
doi = "10.1007/s00125-019-4946-6",
language = "English",
volume = "62",
pages = "320",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "Suppl 1",

}

RIS

TY - ABST

T1 - Low carbohydrate diet elevates blood sphingomyelin in people with type 1 diabetes

AU - Al-Sari, Naba Hassan

AU - Schmidt, Signe

AU - Suvitaival, Tommi

AU - Kim, Min

AU - Trošt, Kajetan

AU - Ranjan, Ajenthen

AU - Christensen, Merete

AU - Overgaard, Anne Julie

AU - Pociot, Flemming

AU - Nørgaard, Kirsten

AU - Legido-Quigley, Cristina

PY - 2019/9

Y1 - 2019/9

N2 - Background and Aim: Reduction of carbohydrate intake stabilizes glucose levels in persons with type 1 diabetes (T1D). To maintain similar energy intake, a reduction in carbohydrate must be accompanied by an increase in protein and/or fat intake. However, this dietary change may affect the lipid balance and lead to an increased risk of cardiovascular events. We investigated how blood lipid levels responded to dietary changes and how these changes related to diet-induced changes in metabolic characteristics, such as body mass index (BMI), waist circumference, systolic blood pressure (SBP), glycemic variability and time spent in hypoglycemia. Materials and Methods: Ten adults with T1D (mean±SD: age 43.6±13.8 years, diabetes duration 24.5±13.4 years, BMI 24.9±2.1 kg, HbA1c 57.6±2.6 ) using insulin pumps participated in a randomized 2-period crossover study with 12-week intervention periods of Low Carbohydrate Diet ( LCD < 100 g carbohydrates/day) or High Carbohydrate Diet (HCD > 250 g carbohydrates/day) respectively, separated by a 12-week washout period. A comprehensive lipidomics analysis was done for fasting plasma samples obtained after each diet, and changes in lipid levels were compared with paired tests. Results: In total, 245 lipid levels were identified from 9 major lipid classes (Triacylglycerides, Phosphatidylcholines, Phosphatidylethanolamines, Hexosyl Ceramide, Sphingomyelins, Lysophosphatidylcholines, Ceramides, Lactosylceramide, and Lysophoshatidylethanolamine). In the high-resolution lipidomics analysis, phosphatidylcholines and sphingomyelins were elevated after LCD (not significant). A short-chain monounsaturated sphingomyelin, SM(d34:1), was elevated after LCD compared with HCD (p=0.002; see Figure). Sphingomyelins and phosphatidylcholines were inversely associated with BMI, waist circumference, SBP and glycemic variability (not significant). SM(d34:1) did not show significant association to changes in clinical measurements. Conclusion: Plasma from persons with T1D showed an increase in a monounsaturated sphingomyelin with LCD compared to HCD. Results from this randomized cross-over study warrant for more investigation on the long-term effects of diet and lipid homeostasis in T1D.

AB - Background and Aim: Reduction of carbohydrate intake stabilizes glucose levels in persons with type 1 diabetes (T1D). To maintain similar energy intake, a reduction in carbohydrate must be accompanied by an increase in protein and/or fat intake. However, this dietary change may affect the lipid balance and lead to an increased risk of cardiovascular events. We investigated how blood lipid levels responded to dietary changes and how these changes related to diet-induced changes in metabolic characteristics, such as body mass index (BMI), waist circumference, systolic blood pressure (SBP), glycemic variability and time spent in hypoglycemia. Materials and Methods: Ten adults with T1D (mean±SD: age 43.6±13.8 years, diabetes duration 24.5±13.4 years, BMI 24.9±2.1 kg, HbA1c 57.6±2.6 ) using insulin pumps participated in a randomized 2-period crossover study with 12-week intervention periods of Low Carbohydrate Diet ( LCD < 100 g carbohydrates/day) or High Carbohydrate Diet (HCD > 250 g carbohydrates/day) respectively, separated by a 12-week washout period. A comprehensive lipidomics analysis was done for fasting plasma samples obtained after each diet, and changes in lipid levels were compared with paired tests. Results: In total, 245 lipid levels were identified from 9 major lipid classes (Triacylglycerides, Phosphatidylcholines, Phosphatidylethanolamines, Hexosyl Ceramide, Sphingomyelins, Lysophosphatidylcholines, Ceramides, Lactosylceramide, and Lysophoshatidylethanolamine). In the high-resolution lipidomics analysis, phosphatidylcholines and sphingomyelins were elevated after LCD (not significant). A short-chain monounsaturated sphingomyelin, SM(d34:1), was elevated after LCD compared with HCD (p=0.002; see Figure). Sphingomyelins and phosphatidylcholines were inversely associated with BMI, waist circumference, SBP and glycemic variability (not significant). SM(d34:1) did not show significant association to changes in clinical measurements. Conclusion: Plasma from persons with T1D showed an increase in a monounsaturated sphingomyelin with LCD compared to HCD. Results from this randomized cross-over study warrant for more investigation on the long-term effects of diet and lipid homeostasis in T1D.

U2 - 10.1007/s00125-019-4946-6

DO - 10.1007/s00125-019-4946-6

M3 - Conference abstract in journal

VL - 62

SP - 320

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - Suppl 1

M1 - 669

ER -

ID: 57798947