Magnesium deficiency prevents high-fat-diet-induced obesity in mice

Steef Kurstjens; Janna A van Diepen; Caro Overmars-Bos; Wynand Alkema; René J M Bindels; Frances M Ashcroft; Cees J J Tack; Joost G J Hoenderop; Jeroen H F de Baaij

doi:10.1007/s00125-018-4680-5

Magnesium deficiency prevents high-fat-diet-induced obesity in mice

Steef Kurstjens, Janna A van Diepen, Caro Overmars-Bos, Wynand Alkema, René J M Bindels, Frances M Ashcroft, Cees J J Tack, Joost G J Hoenderop, Jeroen H F de Baaij

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

AIMS/HYPOTHESIS: Hypomagnesaemia (blood Mg2+ <0.7 mmol/l) is a common phenomenon in individuals with type 2 diabetes. However, it remains unknown how a low blood Mg2+ concentration affects lipid and energy metabolism. Therefore, the importance of Mg2+ in obesity and type 2 diabetes has been largely neglected to date. This study aims to determine the effects of hypomagnesaemia on energy homeostasis and lipid metabolism.

METHODS: Mice (n = 12/group) were fed either a low-fat diet (LFD) or a high-fat diet (HFD) (10% or 60% of total energy) in combination with a normal- or low-Mg2+ content (0.21% or 0.03% wt/wt) for 17 weeks. Metabolic cages were used to investigate food intake, energy expenditure and respiration. Blood and tissues were taken to study metabolic parameters and mRNA expression profiles, respectively.

RESULTS: We show that low dietary Mg2+ intake ameliorates HFD-induced obesity in mice (47.00 ± 1.53 g vs 38.62 ± 1.51 g in mice given a normal Mg2+-HFD and low Mg2+-HFD, respectively, p < 0.05). Consequently, fasting serum glucose levels decreased and insulin sensitivity improved in low Mg2+-HFD-fed mice. Moreover, HFD-induced liver steatosis was absent in the low Mg2+ group. In hypomagnesaemic HFD-fed mice, mRNA expression of key lipolysis genes was increased in epididymal white adipose tissue (eWAT), corresponding to reduced lipid storage and high blood lipid levels. Low Mg2+-HFD-fed mice had increased brown adipose tissue (BAT) Ucp1 mRNA expression and a higher body temperature. No difference was observed in energy expenditure between the two HFD groups.

CONCLUSIONS/INTERPRETATION: Mg2+-deficiency abrogates HFD-induced obesity in mice through enhanced eWAT lipolysis and BAT activity.

Original language	English
Pages (from-to)	2030-2042
Journal	Diabetologia
Volume	61
Issue number	9
DOIs	https://doi.org/10.1007/s00125-018-4680-5
Publication status	Published - 1 Sept 2018
Externally published	Yes

Keywords

3t3-l1 cells
diet, high-fat/adverse effects
insulin resistance/physiology
lipid metabolism/drug effects
magnesium
magnesium deficiency/metabolism
mice
obesity/etiology
real-time polymerase chain reaction

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10.1007/s00125-018-4680-5

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@article{9332773475824d85ae36ed725e04d1e0,

title = "Magnesium deficiency prevents high-fat-diet-induced obesity in mice",

abstract = "AIMS/HYPOTHESIS: Hypomagnesaemia (blood Mg2+ <0.7 mmol/l) is a common phenomenon in individuals with type 2 diabetes. However, it remains unknown how a low blood Mg2+ concentration affects lipid and energy metabolism. Therefore, the importance of Mg2+ in obesity and type 2 diabetes has been largely neglected to date. This study aims to determine the effects of hypomagnesaemia on energy homeostasis and lipid metabolism.METHODS: Mice (n = 12/group) were fed either a low-fat diet (LFD) or a high-fat diet (HFD) (10% or 60% of total energy) in combination with a normal- or low-Mg2+ content (0.21% or 0.03% wt/wt) for 17 weeks. Metabolic cages were used to investigate food intake, energy expenditure and respiration. Blood and tissues were taken to study metabolic parameters and mRNA expression profiles, respectively.RESULTS: We show that low dietary Mg2+ intake ameliorates HFD-induced obesity in mice (47.00 ± 1.53 g vs 38.62 ± 1.51 g in mice given a normal Mg2+-HFD and low Mg2+-HFD, respectively, p < 0.05). Consequently, fasting serum glucose levels decreased and insulin sensitivity improved in low Mg2+-HFD-fed mice. Moreover, HFD-induced liver steatosis was absent in the low Mg2+ group. In hypomagnesaemic HFD-fed mice, mRNA expression of key lipolysis genes was increased in epididymal white adipose tissue (eWAT), corresponding to reduced lipid storage and high blood lipid levels. Low Mg2+-HFD-fed mice had increased brown adipose tissue (BAT) Ucp1 mRNA expression and a higher body temperature. No difference was observed in energy expenditure between the two HFD groups.CONCLUSIONS/INTERPRETATION: Mg2+-deficiency abrogates HFD-induced obesity in mice through enhanced eWAT lipolysis and BAT activity.",

keywords = "3t3-l1 cells, diet, high-fat/adverse effects, insulin resistance/physiology, lipid metabolism/drug effects, magnesium, magnesium deficiency/metabolism, mice, obesity/etiology, real-time polymerase chain reaction, diabetes",

author = "Steef Kurstjens and {van Diepen}, {Janna A} and Caro Overmars-Bos and Wynand Alkema and Bindels, {Ren{\'e} J M} and Ashcroft, {Frances M} and Tack, {Cees J J} and Hoenderop, {Joost G J} and {de Baaij}, {Jeroen H F}",

year = "2018",

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doi = "10.1007/s00125-018-4680-5",

language = "English",

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T1 - Magnesium deficiency prevents high-fat-diet-induced obesity in mice

AU - Kurstjens, Steef

AU - van Diepen, Janna A

AU - Overmars-Bos, Caro

AU - Alkema, Wynand

AU - Bindels, René J M

AU - Ashcroft, Frances M

AU - Tack, Cees J J

AU - Hoenderop, Joost G J

AU - de Baaij, Jeroen H F

PY - 2018/9/1

Y1 - 2018/9/1

N2 - AIMS/HYPOTHESIS: Hypomagnesaemia (blood Mg2+ <0.7 mmol/l) is a common phenomenon in individuals with type 2 diabetes. However, it remains unknown how a low blood Mg2+ concentration affects lipid and energy metabolism. Therefore, the importance of Mg2+ in obesity and type 2 diabetes has been largely neglected to date. This study aims to determine the effects of hypomagnesaemia on energy homeostasis and lipid metabolism.METHODS: Mice (n = 12/group) were fed either a low-fat diet (LFD) or a high-fat diet (HFD) (10% or 60% of total energy) in combination with a normal- or low-Mg2+ content (0.21% or 0.03% wt/wt) for 17 weeks. Metabolic cages were used to investigate food intake, energy expenditure and respiration. Blood and tissues were taken to study metabolic parameters and mRNA expression profiles, respectively.RESULTS: We show that low dietary Mg2+ intake ameliorates HFD-induced obesity in mice (47.00 ± 1.53 g vs 38.62 ± 1.51 g in mice given a normal Mg2+-HFD and low Mg2+-HFD, respectively, p < 0.05). Consequently, fasting serum glucose levels decreased and insulin sensitivity improved in low Mg2+-HFD-fed mice. Moreover, HFD-induced liver steatosis was absent in the low Mg2+ group. In hypomagnesaemic HFD-fed mice, mRNA expression of key lipolysis genes was increased in epididymal white adipose tissue (eWAT), corresponding to reduced lipid storage and high blood lipid levels. Low Mg2+-HFD-fed mice had increased brown adipose tissue (BAT) Ucp1 mRNA expression and a higher body temperature. No difference was observed in energy expenditure between the two HFD groups.CONCLUSIONS/INTERPRETATION: Mg2+-deficiency abrogates HFD-induced obesity in mice through enhanced eWAT lipolysis and BAT activity.

AB - AIMS/HYPOTHESIS: Hypomagnesaemia (blood Mg2+ <0.7 mmol/l) is a common phenomenon in individuals with type 2 diabetes. However, it remains unknown how a low blood Mg2+ concentration affects lipid and energy metabolism. Therefore, the importance of Mg2+ in obesity and type 2 diabetes has been largely neglected to date. This study aims to determine the effects of hypomagnesaemia on energy homeostasis and lipid metabolism.METHODS: Mice (n = 12/group) were fed either a low-fat diet (LFD) or a high-fat diet (HFD) (10% or 60% of total energy) in combination with a normal- or low-Mg2+ content (0.21% or 0.03% wt/wt) for 17 weeks. Metabolic cages were used to investigate food intake, energy expenditure and respiration. Blood and tissues were taken to study metabolic parameters and mRNA expression profiles, respectively.RESULTS: We show that low dietary Mg2+ intake ameliorates HFD-induced obesity in mice (47.00 ± 1.53 g vs 38.62 ± 1.51 g in mice given a normal Mg2+-HFD and low Mg2+-HFD, respectively, p < 0.05). Consequently, fasting serum glucose levels decreased and insulin sensitivity improved in low Mg2+-HFD-fed mice. Moreover, HFD-induced liver steatosis was absent in the low Mg2+ group. In hypomagnesaemic HFD-fed mice, mRNA expression of key lipolysis genes was increased in epididymal white adipose tissue (eWAT), corresponding to reduced lipid storage and high blood lipid levels. Low Mg2+-HFD-fed mice had increased brown adipose tissue (BAT) Ucp1 mRNA expression and a higher body temperature. No difference was observed in energy expenditure between the two HFD groups.CONCLUSIONS/INTERPRETATION: Mg2+-deficiency abrogates HFD-induced obesity in mice through enhanced eWAT lipolysis and BAT activity.

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KW - insulin resistance/physiology

KW - lipid metabolism/drug effects

KW - magnesium

KW - magnesium deficiency/metabolism

KW - mice

KW - obesity/etiology

KW - real-time polymerase chain reaction

KW - diabetes

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DO - 10.1007/s00125-018-4680-5

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C2 - 29987474

SN - 0012-186X

VL - 61

SP - 2030

EP - 2042

JO - Diabetologia

JF - Diabetologia

IS - 9

ER -

Magnesium deficiency prevents high-fat-diet-induced obesity in mice

Abstract

Keywords

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Research output

Nailfold capillaroscopy and candidate-biomarker levels in systemic sclerosis-associated pulmonary hypertension: A cross-sectional study

The 3Ranker: An AI-based Algorithm for Finding Non-animal Alternative Methods

Press/Media

'Productontwikkelaars moeten zich verdiepen in de mogelijkheden van Artificial intelligence'

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