N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism. / Ström, Kristoffer; Morales-Alamo, David; Ottosson, Filip; Edlund, Anna; Hjort, Line; Jörgensen, Sine W.; Almgren, Peter; Zhou, Yuedan; Martin-Rincon, Marcos; Ekman, Carl; Pérez-López, Alberto; Ekström, Ola; Perez-Suarez, Ismael; Mattiasson, Markus; De Pablos-Velasco, Pedro; Oskolkov, Nikolay; Ahlqvist, Emma; Wierup, Nils; Eliasson, Lena; Vaag, Allan; Groop, Leif; Stenkula, Karin G.; Fernandez, Céline; Calbet, Jose A.L.; Holmberg, Hans Christer; Hansson, Ola.

I: Scientific Reports, Vol. 8, Nr. 1, 3016, 01.12.2018.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Ström, K, Morales-Alamo, D, Ottosson, F, Edlund, A, Hjort, L, Jörgensen, SW, Almgren, P, Zhou, Y, Martin-Rincon, M, Ekman, C, Pérez-López, A, Ekström, O, Perez-Suarez, I, Mattiasson, M, De Pablos-Velasco, P, Oskolkov, N, Ahlqvist, E, Wierup, N, Eliasson, L, Vaag, A, Groop, L, Stenkula, KG, Fernandez, C, Calbet, JAL, Holmberg, HC & Hansson, O 2018, 'N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism', Scientific Reports, vol. 8, nr. 1, 3016. https://doi.org/10.1038/s41598-018-21099-1

APA

Ström, K., Morales-Alamo, D., Ottosson, F., Edlund, A., Hjort, L., Jörgensen, S. W., Almgren, P., Zhou, Y., Martin-Rincon, M., Ekman, C., Pérez-López, A., Ekström, O., Perez-Suarez, I., Mattiasson, M., De Pablos-Velasco, P., Oskolkov, N., Ahlqvist, E., Wierup, N., Eliasson, L., ... Hansson, O. (2018). N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism. Scientific Reports, 8(1), [3016]. https://doi.org/10.1038/s41598-018-21099-1

CBE

Ström K, Morales-Alamo D, Ottosson F, Edlund A, Hjort L, Jörgensen SW, Almgren P, Zhou Y, Martin-Rincon M, Ekman C, Pérez-López A, Ekström O, Perez-Suarez I, Mattiasson M, De Pablos-Velasco P, Oskolkov N, Ahlqvist E, Wierup N, Eliasson L, Vaag A, Groop L, Stenkula KG, Fernandez C, Calbet JAL, Holmberg HC, Hansson O. 2018. N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism. Scientific Reports. 8(1):Article 3016. https://doi.org/10.1038/s41598-018-21099-1

MLA

Vancouver

Author

Ström, Kristoffer ; Morales-Alamo, David ; Ottosson, Filip ; Edlund, Anna ; Hjort, Line ; Jörgensen, Sine W. ; Almgren, Peter ; Zhou, Yuedan ; Martin-Rincon, Marcos ; Ekman, Carl ; Pérez-López, Alberto ; Ekström, Ola ; Perez-Suarez, Ismael ; Mattiasson, Markus ; De Pablos-Velasco, Pedro ; Oskolkov, Nikolay ; Ahlqvist, Emma ; Wierup, Nils ; Eliasson, Lena ; Vaag, Allan ; Groop, Leif ; Stenkula, Karin G. ; Fernandez, Céline ; Calbet, Jose A.L. ; Holmberg, Hans Christer ; Hansson, Ola. / N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism. I: Scientific Reports. 2018 ; Vol. 8, Nr. 1.

RIS

TY - JOUR

T1 - N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism

AU - Ström, Kristoffer

AU - Morales-Alamo, David

AU - Ottosson, Filip

AU - Edlund, Anna

AU - Hjort, Line

AU - Jörgensen, Sine W.

AU - Almgren, Peter

AU - Zhou, Yuedan

AU - Martin-Rincon, Marcos

AU - Ekman, Carl

AU - Pérez-López, Alberto

AU - Ekström, Ola

AU - Perez-Suarez, Ismael

AU - Mattiasson, Markus

AU - De Pablos-Velasco, Pedro

AU - Oskolkov, Nikolay

AU - Ahlqvist, Emma

AU - Wierup, Nils

AU - Eliasson, Lena

AU - Vaag, Allan

AU - Groop, Leif

AU - Stenkula, Karin G.

AU - Fernandez, Céline

AU - Calbet, Jose A.L.

AU - Holmberg, Hans Christer

AU - Hansson, Ola

PY - 2018/12/1

Y1 - 2018/12/1

N2 - Obesity is a major health problem, and although caloric restriction and exercise are successful strategies to lose adipose tissue in obese individuals, a simultaneous decrease in skeletal muscle mass, negatively effects metabolism and muscle function. To deeper understand molecular events occurring in muscle during weight-loss, we measured the expressional change in human skeletal muscle following a combination of severe caloric restriction and exercise over 4 days in 15 Swedish men. Key metabolic genes were regulated after the intervention, indicating a shift from carbohydrate to fat metabolism. Nicotinamide N-methyltransferase (NNMT) was the most consistently upregulated gene following the energy-deficit exercise. Circulating levels of N1-methylnicotinamide (MNA), the product of NNMT activity, were doubled after the intervention. The fasting-fed state was an important determinant of plasma MNA levels, peaking at ~18 h of fasting and being lowest ~3 h after a meal. In culture, MNA was secreted by isolated human myotubes and stimulated lipolysis directly, with no effect on glucagon or insulin secretion. We propose that MNA is a novel myokine that enhances the utilization of energy stores in response to low muscle energy availability. Future research should focus on applying MNA as a biomarker to identify individuals with metabolic disturbances at an early stage.

AB - Obesity is a major health problem, and although caloric restriction and exercise are successful strategies to lose adipose tissue in obese individuals, a simultaneous decrease in skeletal muscle mass, negatively effects metabolism and muscle function. To deeper understand molecular events occurring in muscle during weight-loss, we measured the expressional change in human skeletal muscle following a combination of severe caloric restriction and exercise over 4 days in 15 Swedish men. Key metabolic genes were regulated after the intervention, indicating a shift from carbohydrate to fat metabolism. Nicotinamide N-methyltransferase (NNMT) was the most consistently upregulated gene following the energy-deficit exercise. Circulating levels of N1-methylnicotinamide (MNA), the product of NNMT activity, were doubled after the intervention. The fasting-fed state was an important determinant of plasma MNA levels, peaking at ~18 h of fasting and being lowest ~3 h after a meal. In culture, MNA was secreted by isolated human myotubes and stimulated lipolysis directly, with no effect on glucagon or insulin secretion. We propose that MNA is a novel myokine that enhances the utilization of energy stores in response to low muscle energy availability. Future research should focus on applying MNA as a biomarker to identify individuals with metabolic disturbances at an early stage.

U2 - 10.1038/s41598-018-21099-1

DO - 10.1038/s41598-018-21099-1

M3 - Article

C2 - 29445118

AN - SCOPUS:85042133592

VL - 8

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 3016

ER -