Epidermal Acyl-CoA-binding protein is indispensable for systemic energy homeostasis

Research output: Contribution to journalJournal articlepeer-review

Standard

Epidermal Acyl-CoA-binding protein is indispensable for systemic energy homeostasis. / Neess, Ditte; Kruse, Vibeke; Marcher, Ann Britt; Wæde, Mie Rye; Vistisen, Julie; Møller, Pauline M.; Petersen, Rikke; Brewer, Jonathan R.; Ma, Tao; Colleluori, Georgia; Severi, Ilenia; Cinti, Saverio; Gerhart-Hines, Zach; Mandrup, Susanne; Færgeman, Nils J.

In: Molecular Metabolism, Vol. 44, 101144, 2021.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Neess, D, Kruse, V, Marcher, AB, Wæde, MR, Vistisen, J, Møller, PM, Petersen, R, Brewer, JR, Ma, T, Colleluori, G, Severi, I, Cinti, S, Gerhart-Hines, Z, Mandrup, S & Færgeman, NJ 2021, 'Epidermal Acyl-CoA-binding protein is indispensable for systemic energy homeostasis', Molecular Metabolism, vol. 44, 101144. https://doi.org/10.1016/j.molmet.2020.101144

APA

Neess, D., Kruse, V., Marcher, A. B., Wæde, M. R., Vistisen, J., Møller, P. M., Petersen, R., Brewer, J. R., Ma, T., Colleluori, G., Severi, I., Cinti, S., Gerhart-Hines, Z., Mandrup, S., & Færgeman, N. J. (2021). Epidermal Acyl-CoA-binding protein is indispensable for systemic energy homeostasis. Molecular Metabolism, 44, [101144]. https://doi.org/10.1016/j.molmet.2020.101144

Vancouver

Neess D, Kruse V, Marcher AB, Wæde MR, Vistisen J, Møller PM et al. Epidermal Acyl-CoA-binding protein is indispensable for systemic energy homeostasis. Molecular Metabolism. 2021;44. 101144. https://doi.org/10.1016/j.molmet.2020.101144

Author

Neess, Ditte ; Kruse, Vibeke ; Marcher, Ann Britt ; Wæde, Mie Rye ; Vistisen, Julie ; Møller, Pauline M. ; Petersen, Rikke ; Brewer, Jonathan R. ; Ma, Tao ; Colleluori, Georgia ; Severi, Ilenia ; Cinti, Saverio ; Gerhart-Hines, Zach ; Mandrup, Susanne ; Færgeman, Nils J. / Epidermal Acyl-CoA-binding protein is indispensable for systemic energy homeostasis. In: Molecular Metabolism. 2021 ; Vol. 44.

Bibtex

@article{24f4464c66444d8a8a507c97370c3551,
title = "Epidermal Acyl-CoA-binding protein is indispensable for systemic energy homeostasis",
abstract = "Objectives: The skin is the largest sensory organ of the human body and plays a fundamental role in regulating body temperature. However, adaptive alterations in skin functions and morphology have only vaguely been associated with physiological responses to cold stress or sensation of ambient temperatures. We previously found that loss of acyl-CoA-binding protein (ACBP) in keratinocytes upregulates lipolysis in white adipose tissue and alters hepatic lipid metabolism, suggesting a link between epidermal barrier functions and systemic energy metabolism. Methods: To assess the physiological responses to loss of ACBP in keratinocytes in detail, we used full-body ACBP−/− and skin-specific ACBP−/− knockout mice to clarify how loss of ACBP affects 1) energy expenditure by indirect calorimetry, 2) response to high-fat feeding and a high oral glucose load, and 3) expression of brown-selective gene programs by quantitative PCR in inguinal WAT (iWAT). To further elucidate the role of the epidermal barrier in systemic energy metabolism, we included mice with defects in skin structural proteins (ma/ma Flgft/ft) in these studies. Results: We show that the ACBP−/− mice and skin-specific ACBP−/− knockout mice exhibited increased energy expenditure, increased food intake, browning of the iWAT, and resistance to diet-induced obesity. The metabolic phenotype, including browning of the iWAT, was reversed by housing the mice at thermoneutrality (30 °C) or pharmacological β-adrenergic blocking. Interestingly, these findings were phenocopied in flaky tail mice (ma/ma Flgft/ft). Taken together, we demonstrate that a compromised epidermal barrier induces a β-adrenergic response that increases energy expenditure and browning of the white adipose tissue to maintain a normal body temperature. Conclusions: Our findings show that the epidermal barrier plays a key role in maintaining systemic metabolic homeostasis. Thus, regulation of epidermal barrier functions warrants further attention to understand the regulation of systemic metabolism in further detail.",
keywords = "Acyl-CoA binding protein, Adipose tissue, Browning, Diet induced obesity, Energy expenditure, Epidermal barrier, Filaggrin, β-adrenergic signaling",
author = "Ditte Neess and Vibeke Kruse and Marcher, {Ann Britt} and W{\ae}de, {Mie Rye} and Julie Vistisen and M{\o}ller, {Pauline M.} and Rikke Petersen and Brewer, {Jonathan R.} and Tao Ma and Georgia Colleluori and Ilenia Severi and Saverio Cinti and Zach Gerhart-Hines and Susanne Mandrup and F{\ae}rgeman, {Nils J.}",
year = "2021",
doi = "10.1016/j.molmet.2020.101144",
language = "English",
volume = "44",
journal = "Molecular Metabolism",
issn = "2212-8778",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Epidermal Acyl-CoA-binding protein is indispensable for systemic energy homeostasis

AU - Neess, Ditte

AU - Kruse, Vibeke

AU - Marcher, Ann Britt

AU - Wæde, Mie Rye

AU - Vistisen, Julie

AU - Møller, Pauline M.

AU - Petersen, Rikke

AU - Brewer, Jonathan R.

AU - Ma, Tao

AU - Colleluori, Georgia

AU - Severi, Ilenia

AU - Cinti, Saverio

AU - Gerhart-Hines, Zach

AU - Mandrup, Susanne

AU - Færgeman, Nils J.

PY - 2021

Y1 - 2021

N2 - Objectives: The skin is the largest sensory organ of the human body and plays a fundamental role in regulating body temperature. However, adaptive alterations in skin functions and morphology have only vaguely been associated with physiological responses to cold stress or sensation of ambient temperatures. We previously found that loss of acyl-CoA-binding protein (ACBP) in keratinocytes upregulates lipolysis in white adipose tissue and alters hepatic lipid metabolism, suggesting a link between epidermal barrier functions and systemic energy metabolism. Methods: To assess the physiological responses to loss of ACBP in keratinocytes in detail, we used full-body ACBP−/− and skin-specific ACBP−/− knockout mice to clarify how loss of ACBP affects 1) energy expenditure by indirect calorimetry, 2) response to high-fat feeding and a high oral glucose load, and 3) expression of brown-selective gene programs by quantitative PCR in inguinal WAT (iWAT). To further elucidate the role of the epidermal barrier in systemic energy metabolism, we included mice with defects in skin structural proteins (ma/ma Flgft/ft) in these studies. Results: We show that the ACBP−/− mice and skin-specific ACBP−/− knockout mice exhibited increased energy expenditure, increased food intake, browning of the iWAT, and resistance to diet-induced obesity. The metabolic phenotype, including browning of the iWAT, was reversed by housing the mice at thermoneutrality (30 °C) or pharmacological β-adrenergic blocking. Interestingly, these findings were phenocopied in flaky tail mice (ma/ma Flgft/ft). Taken together, we demonstrate that a compromised epidermal barrier induces a β-adrenergic response that increases energy expenditure and browning of the white adipose tissue to maintain a normal body temperature. Conclusions: Our findings show that the epidermal barrier plays a key role in maintaining systemic metabolic homeostasis. Thus, regulation of epidermal barrier functions warrants further attention to understand the regulation of systemic metabolism in further detail.

AB - Objectives: The skin is the largest sensory organ of the human body and plays a fundamental role in regulating body temperature. However, adaptive alterations in skin functions and morphology have only vaguely been associated with physiological responses to cold stress or sensation of ambient temperatures. We previously found that loss of acyl-CoA-binding protein (ACBP) in keratinocytes upregulates lipolysis in white adipose tissue and alters hepatic lipid metabolism, suggesting a link between epidermal barrier functions and systemic energy metabolism. Methods: To assess the physiological responses to loss of ACBP in keratinocytes in detail, we used full-body ACBP−/− and skin-specific ACBP−/− knockout mice to clarify how loss of ACBP affects 1) energy expenditure by indirect calorimetry, 2) response to high-fat feeding and a high oral glucose load, and 3) expression of brown-selective gene programs by quantitative PCR in inguinal WAT (iWAT). To further elucidate the role of the epidermal barrier in systemic energy metabolism, we included mice with defects in skin structural proteins (ma/ma Flgft/ft) in these studies. Results: We show that the ACBP−/− mice and skin-specific ACBP−/− knockout mice exhibited increased energy expenditure, increased food intake, browning of the iWAT, and resistance to diet-induced obesity. The metabolic phenotype, including browning of the iWAT, was reversed by housing the mice at thermoneutrality (30 °C) or pharmacological β-adrenergic blocking. Interestingly, these findings were phenocopied in flaky tail mice (ma/ma Flgft/ft). Taken together, we demonstrate that a compromised epidermal barrier induces a β-adrenergic response that increases energy expenditure and browning of the white adipose tissue to maintain a normal body temperature. Conclusions: Our findings show that the epidermal barrier plays a key role in maintaining systemic metabolic homeostasis. Thus, regulation of epidermal barrier functions warrants further attention to understand the regulation of systemic metabolism in further detail.

KW - Acyl-CoA binding protein

KW - Adipose tissue

KW - Browning

KW - Diet induced obesity

KW - Energy expenditure

KW - Epidermal barrier

KW - Filaggrin

KW - β-adrenergic signaling

U2 - 10.1016/j.molmet.2020.101144

DO - 10.1016/j.molmet.2020.101144

M3 - Journal article

C2 - 33346070

AN - SCOPUS:85098995871

VL - 44

JO - Molecular Metabolism

JF - Molecular Metabolism

SN - 2212-8778

M1 - 101144

ER -

ID: 258826399